﻿FN Clarivate Analytics Web of Science
VR 1.0
PT J
AU Kloth, M
   Ruesseler, V
   Engel, C
   Koenig, K
   Peifer, M
   Mariotti, E
   Kuenstlinger, H
   Florin, A
   Rommerscheidt-Fuss, U
   Koitzsch, U
   Wodtke, C
   Ueckeroth, F
   Holzapfel, S
   Aretz, S
   Propping, P
   Loeffler, M
   Merkelbach-Bruse, S
   Odenthal, M
   Friedrichs, N
   Heukamp, LC
   Zander, T
   Buettner, R
AF Kloth, Michael
   Ruesseler, Vanessa
   Engel, Christoph
   Koenig, Katharina
   Peifer, Martin
   Mariotti, Erika
   Kuenstlinger, Helen
   Florin, Alexandra
   Rommerscheidt-Fuss, Ursula
   Koitzsch, Ulrike
   Wodtke, Claudia
   Ueckeroth, Frank
   Holzapfel, Stefanie
   Aretz, Stefan
   Propping, Peter
   Loeffler, Markus
   Merkelbach-Bruse, Sabine
   Odenthal, Margarete
   Friedrichs, Nicolaus
   Heukamp, Lukas Carl
   Zander, Thomas
   Buettner, Reinhard
TI Activating ERBB2/HER2 mutations indicate susceptibility to pan-HER
   inhibitors in Lynch and Lynch-like colorectal cancer
SO GUT
LA English
DT Article
ID COMPREHENSIVE MOLECULAR CHARACTERIZATION; MICROSATELLITE INSTABILITY;
   MISMATCH REPAIR; COLON-CANCER; GENE; ADENOCARCINOMA; TRANSFORMATION;
   TUMORIGENESIS; METHYLATION; CARCINOMAS
AB Objective Microsatellite instability (MSI) is detected in approximately 15% of all colorectal cancers (CRC) and virtually in all cases with Lynch syndrome. The MSI phenotype is caused by dysfunctional mismatch repair (MMR) and leads to accumulation of DNA replication errors. Sporadic MSI CRC often harbours BRAF(V600E); however, no consistent data exist regarding targeted treatment approaches in BRAF(wt) MSI CRC.
   Design Mutations and quantitative MSI were analysed by deep sequencing in 196 formalin fixed paraffin embedded (FFPE) specimens comprising Lynch and Lynch-like CRCs from the German Hereditary Nonpolyposis Colorectal Cancer registry. Functional relevance of recurrent ERBB2/HER2 mutations was investigated in CRC cell lines using reversible and irreversible HER-targeting inhibitors, EGFR-directed antibody cetuximab, HER2-directed antibody trastuzumab and siRNA-mediated ERBB2/HER2 knockdown.
   Results Quantification of nucleotide loss in non-coding mononucleotide repeats distinguished microsatellite status with very high accuracy (area under curve=0.9998) and demonstrated progressive losses with deeper invasion of MMR-deficient colorectal neoplasms (p=0.008). Characterisation of BRAF(wt) MSI CRC revealed hot-spot mutations in well-known oncogenic drivers, including KRAS (38.7%), PIK3CA (36.5%), and ERBB2 (15.0%). L755S and V842I substitutions in ERBB2 were highly recurrent. Functional analyses in ERBB2-mutated MSI CRC cell lines revealed a differential response to HER-targeting compounds and superiority of irreversible pan-HER inhibitors.
   Conclusions We developed a high-throughput deep sequencing approach for concomitant MSI and mutational analyses in FFPE specimens. We provided novel insights into clinically relevant alterations in MSI CRC and a rationale for targeting ERBB2/HER2 mutations in Lynch and Lynch-like CRC.
C1 [Kloth, Michael; Ruesseler, Vanessa; Koenig, Katharina; Kuenstlinger, Helen; Florin, Alexandra; Rommerscheidt-Fuss, Ursula; Koitzsch, Ulrike; Wodtke, Claudia; Ueckeroth, Frank; Merkelbach-Bruse, Sabine; Odenthal, Margarete; Friedrichs, Nicolaus; Heukamp, Lukas Carl; Buettner, Reinhard] Univ Hosp Cologne, Inst Pathol, Ctr Integrated Oncol, Cologne, Germany.
   [Engel, Christoph; Loeffler, Markus] Univ Leipzig, Inst Med Informat Stat & Epidemiol, Leipzig, Germany.
   [Peifer, Martin; Mariotti, Erika] Ctr Mol Med Cologne, Dept Translat Genom, Cologne, Germany.
   [Holzapfel, Stefanie; Aretz, Stefan; Propping, Peter] Univ Hosp Bonn, Inst Human Genet, Bonn, Germany.
   [Zander, Thomas] Univ Hosp Cologne, Dept Internal Med 1, Ctr Integrated Oncol, Kerpenerstr 62, D-50924 Cologne, Germany.
C3 University of Cologne; Leipzig University; University of Cologne;
   University of Bonn; University of Cologne
RP Zander, T (corresponding author), Univ Hosp Cologne, Dept Internal Med 1, Ctr Integrated Oncol, Kerpenerstr 62, D-50924 Cologne, Germany.
EM Thomas.Zander@uk-koeln.de
RI Aretz, Stefan/C-1241-2008; Heukamp, Lukas/A-8338-2013; Heukamp,
   Lukas/G-9967-2012
OI Peifer, Martin/0000-0002-5243-5503; Heukamp, Lukas/0000-0002-3388-3482;
   Engel, Christoph/0000-0002-7247-282X
FU Deutsche Krebshilfe
FX Deutsche Krebshilfe.
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NR 45
TC 60
Z9 64
U1 2
U2 17
PU BMJ PUBLISHING GROUP
PI LONDON
PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND
SN 0017-5749
EI 1468-3288
J9 GUT
JI Gut
PD AUG
PY 2016
VL 65
IS 8
BP 1296
EP 1305
DI 10.1136/gutjnl-2014-309026
PG 10
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA DR2TL
UT WOS:000379756700010
PM 26001389
DA 2025-01-04
ER

PT J
AU Pan, DC
   Krishnan, V
   Salinas, AK
   Kim, J
   Sun, T
   Ravid, S
   Peng, K
   Wu, D
   Nurunnabi, M
   Nelson, JA
   Niziolek, Z
   Guo, JL
   Mitragotri, S
AF Pan, Daniel C.
   Krishnan, Vinu
   Salinas, Alyssa K.
   Kim, Jayoung
   Sun, Tao
   Ravid, Sagi
   Peng, Kevin
   Wu, Debra
   Nurunnabi, Md
   Nelson, Jeffery A.
   Niziolek, Zachary
   Guo, Junling
   Mitragotri, Samir
TI Hyaluronic acid-doxorubicin nanoparticles for targeted treatment of
   colorectal cancer
SO BIOENGINEERING & TRANSLATIONAL MEDICINE
LA English
DT Article
DE colitis associated cancer; colorectal cancer; doxorubicin; hyaluronic
   acid; polymer drug conjugates
ID INFLAMMATORY-BOWEL-DISEASE; PEGYLATED LIPOSOMAL DOXORUBICIN;
   NANOLIPOSOMAL IRINOTECAN PEP02; CAPECITABINE PLUS OXALIPLATIN; III
   COLON-CANCER; GASTROINTESTINAL TOXICITY; 1ST-LINE TREATMENT; ADJUVANT
   CHEMOTHERAPY; ANTITUMOR-ACTIVITY; RANDOMIZED-TRIAL
AB Colorectal cancer, common in both men and women, occurs when tumors form in the linings of the colon. Common treatments of colorectal cancer include surgery, chemotherapy, and radiation therapy; however, many colorectal cancer treatments often damage healthy tissues and cells, inducing severe side effects. Conventional chemotherapeutic agents such as doxorubicin (Dox) can be potentially used for the treatment of colorectal cancer; however, they suffer from limited targeting and lack of selectivity. Here, we report that doxorubicin complexed to hyaluronic acid (HA) (HA-Dox) exhibits an unusual behavior of high accumulation in the intestines for at least 24 hr when injected intravenously. Intravenous administrations of HA-Dox effectively preserved the mucosal epithelial intestinal integrity in a chemical induced colon cancer model in mice. Moreover, treatment with HA-Dox decreased the expression of intestinal apoptotic and inflammatory markers. The results suggest that HA-Dox could effectively inhibit the development of colorectal cancer in a safe manner, which potentially be used a promising therapeutic option.
C1 [Pan, Daniel C.; Krishnan, Vinu; Salinas, Alyssa K.; Kim, Jayoung; Sun, Tao; Ravid, Sagi; Peng, Kevin; Wu, Debra; Nurunnabi, Md; Guo, Junling; Mitragotri, Samir] Harvard Univ, Sch Engn & Appl Sci, Wyss Inst Biol Inspired Engn, Cambridge, MA 02138 USA.
   [Nelson, Jeffery A.; Niziolek, Zachary] Harvard Univ, Fac Arts & Sci, Div Sci, Cambridge, MA 02138 USA.
C3 Harvard University; Harvard University
RP Mitragotri, S (corresponding author), Harvard Univ, Sch Engn & Appl Sci, 29 Oxford St,Pierce Hall, Cambridge, MA 02138 USA.
EM mitragotri@seas.harvard.edu
RI Guo, Junling/ABA-7604-2021; PENG, kevin/IQR-5657-2023; Sun,
   Tao/S-1310-2019; Krishnan, Vinu/J-5707-2018; Nurunnabi, Md/B-7465-2012
OI Krishnan, Vinu/0000-0003-0098-7864; Nurunnabi, Md/0000-0003-4457-3401;
   Sun, Tao/0000-0002-3853-971X; Salinas, Alyssa/0000-0001-6752-0455;
   Ravid, Sagi/0000-0003-4292-2305
FU Harvard School of Engineering and Applied Sciences; National Cancer
   Institute [2CA174650]; Harvard University; National Cancer Institute
   [R25CA174650] Funding Source: NIH RePORTER
FX Harvard School of Engineering and Applied Sciences; National Cancer
   Institute, Grant/Award Number: #2CA174650; Harvard University
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NR 140
TC 20
Z9 21
U1 1
U2 39
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
EI 2380-6761
J9 BIOENG TRANSL MED
JI Bioeng. Transl. Med.
PD JAN
PY 2021
VL 6
IS 1
AR e10166
DI 10.1002/btm2.10166
EA MAY 2020
PG 14
WC Biotechnology & Applied Microbiology; Engineering, Biomedical;
   Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biotechnology & Applied Microbiology; Engineering; Pharmacology &
   Pharmacy
GA PZ8CV
UT WOS:000535846500001
PM 33532580
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Tang, YA
   Chen, YF
   Bao, Y
   Mahara, S
   Yatim, SMJM
   Oguz, G
   Lee, PL
   Feng, M
   Cai, Y
   Tan, EY
   Fong, SS
   Yang, ZH
   Lan, P
   Wu, XJ
   Yu, Q
AF Tang, Yen-An
   Chen, Yu-feng
   Bao, Yi
   Mahara, Sylvia
   Yatim, Siti Maryam J. M.
   Oguz, Gokce
   Lee, Puay Leng
   Feng, Min
   Cai, Yu
   Tan, Ern Yu
   Fong, Sau Shung
   Yang, Zi-huan
   Lan, Ping
   Wu, Xiao-jian
   Yu, Qiang
TI Hypoxic tumor microenvironment activates GLI2 via HIF-1α and TGF-β2 to
   promote chemoresistance in colorectal cancer
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
   AMERICA
LA English
DT Article
DE HIF; GLI2; TGF-beta; tumor microenvironment; chemoresistance
ID COLON-CANCER; STEM-CELLS; TGF-BETA; INDUCIBLE FACTOR-1-ALPHA; STAGE-II;
   CHEMOTHERAPY; INHIBITION; PREDICTS; FIBROBLASTS; SUBTYPES
AB Colorectal cancer patients often relapse after chemotherapy, owing to the survival of stem or progenitor cells referred to as cancer stem cells (CSCs). Although tumor stromal factors are known to contribute to chemoresistance, it remains not fully understood how CSCs in the hypoxic tumor microenvironment escape the chemotherapy. Here, we report that hypoxia-inducible factor (HIF-1 alpha) and cancer-associated fibroblasts (CAFs)-secreted TGF-beta 2 converge to activate the expression of hedgehog transcription factor GLI2 in CSCs, resulting in increased stemness/dedifferentiation and intrinsic resistance to chemotherapy. Genetic or small-molecule inhibitor-based ablation of HIF-1 alpha/TGF-beta 2-mediated GLI2 signaling effectively reversed the chemoresistance caused by the tumor microenvironment. Importantly, high expression levels of HIF1 alpha/TGF-beta 2/GLI2 correlated robustly with the patient relapse following chemotherapy, highlighting a potential biomarker and therapeutic target for chemoresistance in colorectal cancer. Our study thus uncovers a molecular mechanism by which hypoxic colorectal tumor microenvironment promotes cancer cell sternness and resistance to chemotherapy and suggests a potentially targeted treatment approach to mitigating chemoresistance.
C1 [Tang, Yen-An; Bao, Yi; Mahara, Sylvia; Yatim, Siti Maryam J. M.; Oguz, Gokce; Lee, Puay Leng; Feng, Min; Yu, Qiang] Agcy Sci Technol & Res, Genome Inst Singapore, Canc Therapeut & Stratified Oncol, Singapore 138672, Singapore.
   [Chen, Yu-feng; Lan, Ping; Wu, Xiao-jian] Sun Yat Sen Univ, Affiliated Hosp 6, Dept Colorectal Surg, Guangzhou 510655, Guangdong, Peoples R China.
   [Chen, Yu-feng; Yang, Zi-huan; Lan, Ping; Wu, Xiao-jian] Sun Yat Sen Univ, Affiliated Hosp 6, Guangdong Prov Key Lab Colorectal & Pelv Floor Di, Guangzhou 510655, Guangdong, Peoples R China.
   [Chen, Yu-feng; Yang, Zi-huan; Lan, Ping; Wu, Xiao-jian] Sun Yat Sen Univ, Affiliated Hosp 6, Guangdong Inst Gastroenterol, Guangzhou 510655, Guangdong, Peoples R China.
   [Cai, Yu] Jinan Univ, Sch Pharm, Guangzhou 510632, Guangdong, Peoples R China.
   [Cai, Yu; Yu, Qiang] Jinan Univ, Canc Res Inst, Guangzhou 510632, Guangdong, Peoples R China.
   [Tan, Ern Yu; Fong, Sau Shung; Yu, Qiang] Tan Tock Seng Hosp, Dept Gen Surg, Singapore 308433, Singapore.
   [Yu, Qiang] Natl Univ Singapore, Yong Loo Lin Sch Med, Dept Physiol, Singapore 117597, Singapore.
   [Yu, Qiang] Duke NUS Grad Med Sch, Canc & Stem Cell Biol, Singapore 169857, Singapore.
C3 Agency for Science Technology & Research (A*STAR); A*STAR - Genome
   Institute of Singapore (GIS); Sun Yat Sen University; Sun Yat Sen
   University; Sun Yat Sen University; Jinan University; Jinan University;
   Tan Tock Seng Hospital; National University of Singapore; National
   University of Singapore
RP Yu, Q (corresponding author), Agcy Sci Technol & Res, Genome Inst Singapore, Canc Therapeut & Stratified Oncol, Singapore 138672, Singapore.; Wu, XJ (corresponding author), Sun Yat Sen Univ, Affiliated Hosp 6, Dept Colorectal Surg, Guangzhou 510655, Guangdong, Peoples R China.; Wu, XJ (corresponding author), Sun Yat Sen Univ, Affiliated Hosp 6, Guangdong Prov Key Lab Colorectal & Pelv Floor Di, Guangzhou 510655, Guangdong, Peoples R China.; Wu, XJ (corresponding author), Sun Yat Sen Univ, Affiliated Hosp 6, Guangdong Inst Gastroenterol, Guangzhou 510655, Guangdong, Peoples R China.; Yu, Q (corresponding author), Jinan Univ, Canc Res Inst, Guangzhou 510632, Guangdong, Peoples R China.; Yu, Q (corresponding author), Tan Tock Seng Hosp, Dept Gen Surg, Singapore 308433, Singapore.; Yu, Q (corresponding author), Natl Univ Singapore, Yong Loo Lin Sch Med, Dept Physiol, Singapore 117597, Singapore.; Yu, Q (corresponding author), Duke NUS Grad Med Sch, Canc & Stem Cell Biol, Singapore 169857, Singapore.
EM wuxjian@mail.sysu.edu.cn; yuq@gis.a-star.edu.sg
RI Oguz, Gokce/HPH-7335-2023; lan, ping/T-1708-2017; Tan,
   Ryan/KBA-0903-2024
OI Mahara, Sylvia/0000-0001-7261-1423; Yu, Qiang/0000-0003-2132-8278; Yu,
   Qiang/0009-0009-8474-8510; Wu, Xiaojian/0000-0001-5610-2530
FU core budget of the Agency for Science, Technology, and Research of
   Singapore, Singapore-China Collaborative Research Grant [13-711102];
   International S&T Cooperation Program of China Grant [2013DFG32990];
   National High Technology Research and Development Program (863) of China
   [2012AA02A520]
FX This work was supported by the core budget of the Agency for Science,
   Technology, and Research of Singapore, Singapore-China Collaborative
   Research Grant 13-711102 (to Q.Y. and X.-j.W.), International S&T
   Cooperation Program of China Grant 2013DFG32990 (to X.-j.W. and Q.Y.),
   and National High Technology Research and Development Program (863) of
   China Grant 2012AA02A520 (to X.-j.W.).
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NR 38
TC 204
Z9 223
U1 2
U2 44
PU NATL ACAD SCIENCES
PI WASHINGTON
PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA
SN 0027-8424
J9 P NATL ACAD SCI USA
JI Proc. Natl. Acad. Sci. U. S. A.
PD JUN 26
PY 2018
VL 115
IS 26
BP E5990
EP E5999
DI 10.1073/pnas.1801348115
PG 10
WC Multidisciplinary Sciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Science & Technology - Other Topics
GA GK5UZ
UT WOS:000436245000021
PM 29891662
OA Green Published, Bronze
DA 2025-01-04
ER

PT J
AU Zhao, X
   Feng, H
   Wang, Y
   Wu, YM
   Guo, QQ
   Feng, YL
   Ma, MT
   Guo, WD
   Song, XY
   Zhang, Y
   Han, S
   Cao, L
AF Zhao, Xin
   Feng, Hao
   Wang, Yang
   Wu, Yanmei
   Guo, Qiqiang
   Feng, Yanling
   Ma, Mengtao
   Guo, Wendong
   Song, Xiaoyu
   Zhang, Ying
   Han, Shuai
   Cao, Liu
TI Septin4 promotes cell death in human colon cancer cells by interacting
   with BAX
SO INTERNATIONAL JOURNAL OF BIOLOGICAL SCIENCES
LA English
DT Article
DE Septin4; BAX; Colon Cancer; apoptosis
ID COLORECTAL-CANCER; CASPASE ACTIVATION; CYTOCHROME-C; ARTS PROTEIN;
   APOPTOSIS; BCL-2; SEPT4/ARTS; EXPRESSION; CARCINOMA; CETUXIMAB
AB Septin4 is a tumor suppressor protein that promotes cell programmed death in various cell types through specifically antagonizing XIAP (X linked inhibitor of apoptosis), little is known its other novel binding partner and role in colorectal cancer. In this study, we found that Septin4 significantly expressed lower in human colon cancer when compared to peri-tumor benign cells, and its low expression was significantly associated with worse prognostic outcomes. Furthermore, Septin4 participated in DOX-induced colon cancer cell death in vitro. Septin4-overexpressing colon cancer cells displayed augmented apoptotic cell death and ROS production. Additionally, Septin4-knockdown cells revealed a resistance of DOX-induced cell death and reduced ROS production. Importantly, we first identified that BAX is a novel Septin4 binding partner and the interaction is enhanced under DOX treatment. Finally, Septin4-knockdown promoted colon cells growth in vivo. These observations suggest that Septin4 as an essential molecule contribute to the occurrence and development of human colon cancer and provide new technical approaches for targeted treatment of this disease.
C1 [Zhao, Xin; Guo, Qiqiang; Feng, Yanling; Ma, Mengtao; Guo, Wendong; Song, Xiaoyu; Cao, Liu] Minist Educ, Key Lab Med Cell Biol, Shenyang, Liaoning, Peoples R China.
   [Zhao, Xin; Guo, Qiqiang; Feng, Yanling; Ma, Mengtao; Guo, Wendong; Song, Xiaoyu; Cao, Liu] China Med Univ, Coll Med Sci, Inst Translat Med, Shenyang, Liaoning, Peoples R China.
   [Zhao, Xin; Guo, Qiqiang; Feng, Yanling; Ma, Mengtao; Guo, Wendong; Song, Xiaoyu; Cao, Liu] Collaborat Innovat Ctr Aging Related Dis Diag & T, Shenyang, Liaoning, Peoples R China.
   [Feng, Hao] China Med Univ, Dept Ophthalmol, Hosp 1, Shenyang, Liaoning, Peoples R China.
   [Wang, Yang; Wu, Yanmei] Panjin Liaohe Oilfield Gem Flower Hosp, Panjin, Liaoning, Peoples R China.
   [Zhang, Ying] China Med Univ, Dept Cardiol, Hosp 1, Shenyang 110122, Liaoning, Peoples R China.
   [Han, Shuai] China Med Univ, Dept Neurosurg, Hosp 1, Shenyang, Liaoning, Peoples R China.
C3 China Medical University; China Medical University; China Medical
   University; China Medical University
RP Zhang, Y (corresponding author), China Med Univ, Dept Cardiol, Hosp 1, Shenyang 110122, Liaoning, Peoples R China.; Han, S (corresponding author), China Med Univ, Dept Neurosurg, Hosp 1, Shenyang, Liaoning, Peoples R China.; Cao, L (corresponding author), China Med Univ, Inst Translat Med, 77 Puhe Rd, Shenyang 110122, Liaoning, Peoples R China.
EM yzhang02@cmu.edu.cn; hanshuai537197@sina.com; lcao@cmu.edu.cn
OI Song, Xiaoyu/0000-0002-6606-327X
FU National Key R&D Program of China [2016YFC1302400]; Ministry of
   education innovation team development plan [IRT_17R107IRT13101]; Key
   project of the National Natural Science Foundation [81130042, 31171323,
   81770001, 2015225003]; National Science Foundation of China [31300963,
   LFWK201725, 81800839, 81502400, 81502447, 81502414]; Liaoning education
   department general project [LK201627]
FX This work was supported by National Key R&D Program of China
   (2016YFC1302400). The Ministry of education innovation team development
   plan to Liu Cao (IRT_17R107&IRT13101). Key project of the National
   Natural Science Foundation to Liu Cao (81130042, 31171323, 81770001,
   2015225003) National Science Foundation of China to Xiaoyu Song
   (31300963, LFWK201725), Hao Feng (81800839), Qiqiang Guo (81502400), Yi
   Guan (81502447) and Fei Yi (81502414). Liaoning education department
   general project to Hongde Xu (LK201627).
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NR 37
TC 6
Z9 6
U1 0
U2 10
PU IVYSPRING INT PUBL
PI LAKE HAVEN
PA PO BOX 4546, LAKE HAVEN, NSW 2263, AUSTRALIA
SN 1449-2288
J9 INT J BIOL SCI
JI Int. J. Biol. Sci.
PY 2020
VL 16
IS 11
BP 1917
EP 1928
DI 10.7150/ijbs.44429
PG 12
WC Biochemistry & Molecular Biology; Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
   Topics
GA LG4HD
UT WOS:000528063100013
PM 32398959
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Xiong, M
   Wang, MS
   Yan, YH
   Chen, XW
   Guo, WW
   Xu, M
   Guo, SY
   Wang, YY
AF Xiong, Man
   Wang, Mingsen
   Yan, Youhong
   Chen, Xiaowu
   Guo, Wanwei
   Xu, Ming
   Guo, Shaoyan
   Wang, Yeyang
TI MACC1 Promotes the Progression and Is a Novel Biomarker for Predicting
   Immunotherapy Response in Colorectal Cancer
SO JOURNAL OF ONCOLOGY
LA English
DT Article
ID CERVICAL-CANCER; COLON CANCER-1; MET; CELLS; CARCINOMA; IMPACT; GROWTH;
   RNA
AB Aims. As one of the most prevalent malignant diseases in the world, the mechanisms of metastasis in colon cancer are poorly understood. The aim of this study was to investigate the role of the HGF/c-MET axis in the proliferation and metastasis in colon cancer. Methods. The effect of MACC1 on cell proliferation and metastasis was analyzed through a series of in vitro experiments. The role of MACC1 in cancer cells was demonstrated by overexpression and silencing of MACC1 in gain or loss function experiments. To investigate the relationship between MACC1 and c-MET/HGF, we detected c-MET protein expression by disrupting with or overexpressing MACC1. The bioinformatics analysis was used to investigate the correlation between MACC1 and c-MET, and the c-MET expression after the interference of HGF with MACC1 was determined. Subsequently, the function of c-MET was verified in colon cancer cells by a series of experiments. The mouse tumor transplantation model experiment is most suitable in vivo. Results. The results indicated that the overexpression of MACC1 could accelerate proliferation and facilitate metastasis in colon cancer cell lines. Furthermore, c-MET was determined to be the downstream regulator of MACC1. The addition of HGF could stimulate the expression of MACC1. With further exploration, we proved that c-MET is downstream of MACC1 in colon cancer and that overexpression of c-MET in colon cancer enhances cell proliferation and migration capability. At last, MACC1 expression level negatively correlates with the infiltration levels and several immune checkpoint biomarkers. High MACC1 expression has a lower response rate with ICIs in COAD. Conclusions. We found that, under the regulation of the MACC1/HGF/c-MET axis, the proliferation and metastasis of colorectal cancer are increased by MACC1, which can be a novel biomarker for predicting ICIs response in colorectal cancer. Our findings provide a new idea for the targeted treatment of colorectal cancer.
C1 [Xiong, Man] Guangzhou Univ Chinese Med, Sch Nursing, Guangzhou 510006, Guangdong, Peoples R China.
   [Xiong, Man; Yan, Youhong; Chen, Xiaowu; Guo, Wanwei; Xu, Ming; Guo, Shaoyan] Guangdong Second Prov Gen Hosp, Dept Gastroenterol, Guangzhou 510030, Guangdong, Peoples R China.
   [Wang, Mingsen] Tradit Chinese Med Hosp, Dept Orthoped, Puning 515300, Jieyang, Peoples R China.
   [Wang, Yeyang] Guangdong Second Prov Gen Hosp, Dept Spine Surg, Guangzhou 510030, Guangdong, Peoples R China.
C3 Guangzhou University of Chinese Medicine
RP Guo, SY (corresponding author), Guangdong Second Prov Gen Hosp, Dept Gastroenterol, Guangzhou 510030, Guangdong, Peoples R China.; Wang, YY (corresponding author), Guangdong Second Prov Gen Hosp, Dept Spine Surg, Guangzhou 510030, Guangdong, Peoples R China.
EM 1170749923@qq.com; wangyy@gd2h.org.cn
FU Science and Technology Foundation of Guangzhou [202102020108]; Doctoral
   Station Fund of Guangdong Second Provincial General Hospital
   [2019BSGZ005, 2019BSGZ006]; Youth Foundation of Guangdong Second
   Provincial General Hospital [Yq2018-013, YQ2017-011]
FX The authors acknowledge the Science and Technology Foundation of
   Guangzhou (202102020108), Doctoral Station Fund of Guangdong Second
   Provincial General Hospital (Grant nos. 2019BSGZ005 and 2019BSGZ006),
   and Youth Foundation of Guangdong Second Provincial General Hospital
   (Grant nos. Yq2018-013 and YQ2017-011).
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NR 44
TC 4
Z9 4
U1 0
U2 2
PU HINDAWI LTD
PI LONDON
PA ADAM HOUSE, 3RD FLR, 1 FITZROY SQ, LONDON, W1T 5HF, ENGLAND
SN 1687-8450
EI 1687-8469
J9 J ONCOL
JI J. Oncol.
PD JUL 14
PY 2022
VL 2022
AR 8326940
DI 10.1155/2022/8326940
PG 17
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 5N8EU
UT WOS:000872021400001
PM 35874635
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Mauri, D
   Kamposioras, K
   Matthaios, D
   Tolia, M
   Nixon, I
   Dambrosio, M
   Zarkavelis, G
   Papadimitriou, K
   Petricevic, B
   Kountourakis, P
   Kopecky, J
   Kuhar, CG
   Popovic, L
   Chilingirova, NP
   De Mello, RA
   Plavetic, ND
   Katsanos, K
   Mostert, B
   Alongi, F
   de Bari, B
   Corradini, S
   Kampletsas, E
   Gazouli, I
   Gkoura, S
   Amylidi, AL
   Valachis, A
AF Mauri, Davide
   Kamposioras, Konstantinos
   Matthaios, Dimitrios
   Tolia, Maria
   Nixon, Ioanna
   Dambrosio, Mario
   Zarkavelis, Georgios
   Papadimitriou, Konstantinos
   Petricevic, Branka
   Kountourakis, Pantelis
   Kopecky, Jindrich
   Kuhar, Cvetka Grasic
   Popovic, Lazar
   Chilingirova, Nataliya P.
   De Mello, Ramon Andrade
   Plavetic, Natalija Dedic
   Katsanos, Konstantinos
   Mostert, Bianca
   Alongi, Filippo
   de Bari, Berardino
   Corradini, Stefanie
   Kampletsas, Eleytherios
   Gazouli, Ioanna
   Gkoura, Stefania
   Amylidi, Anna-Lea
   Valachis, Antonios
TI Next-Generation Sequencing of Circulating Tumor DNA Can Optimize
   Second-Line Treatment in RAS Wild-Type Metastatic Colorectal Cancer
   after Progression on anti-EGFR Therapy: Time to Rethink Our Approach
SO ONCOLOGY RESEARCH AND TREATMENT
LA English
DT Review
DE Next-generation sequencing; Circulating tumor DNA; 2nd-line; Targeted;
   Treatments; Metastatic colorectal carcinoma; Progression
ID POSITIVE SOLID TUMORS; PLUS CETUXIMAB; MUTATIONS
AB Background: Management of Ras wild-type colorectal cancer (CRC) patients upon disease progression after the successful use of targeted treatment with anti-EGFR monoclonal antibodies and backbone chemotherapy remains a clinical challenge. Summary: Development of treatment resistance with prevalence of preexisting RAS mutated clones, RAS mutation conversion, truncation of extracellular receptor domains as well as HER2 and MET amplification are molecular events that can be difficult to follow without the use of sophisticated laboratory techniques. The clinical hurdle of re-biopsy and tumor heterogeneity can be overcome by the implementation of next-generation sequencing (NGS) to analyze circulating tumor DNA (ctDNA) and identify druggable mutations or recovery of RAS-wildness. In this opinion paper, we summarize with critical thinking the clinical approach to be followed after the failure of first-line treatment in Ras wild-type CRC tumors with the use of NGS. Rechallenge with anti-EGFR inhibitors, in case of persistent or recovery of RAS-wildness, and targeted approach of specific mutations (BRAF inhibitors), amplifications (anti-Her2 treatment), or fusion proteins (NTRK inhibitors) can by guided by the use of NGS. The use of NGS platforms for serial analysis of ctDNA is an important step to better understand the molecular landscape of metastatic CRC and guide clinical decisions. Key Messages: NGS should be considered a mainstay in clinical practice for the management of CRC patients and health authorities should consider reimbursing its use in the appropriate clinical settings. (C) 2021 S. Karger AG, Basel
C1 [Mauri, Davide; Zarkavelis, Georgios; Kampletsas, Eleytherios; Gazouli, Ioanna; Gkoura, Stefania; Amylidi, Anna-Lea] Univ Ioannina, Dept Med Oncol, Ioannina, Greece.
   [Kamposioras, Konstantinos] Christie NHS Fdn Trust, Dept Med Oncol, Manchester, Lancs, England.
   [Matthaios, Dimitrios] Gen Hosp Rhodes, Dept Oncol, Rhodes, Greece.
   [Tolia, Maria] Univ Crete, Fac Med, Dept Radiotherapy Radiat Oncol, Iraklion, Greece.
   [Nixon, Ioanna] Beatson West Scotland Canc Ctr, Scottish Sarcoma Network SSN UK Chair NCRI HN Epi, Glasgow, Lanark, Scotland.
   [Dambrosio, Mario] Clin San Carlo, Dept Med Oncol, Paderno Dugnano, Italy.
   [Papadimitriou, Konstantinos] Univ Hosp Antwerp, Antwerp, Belgium.
   [Petricevic, Branka] Klin Ottakring, Dept Hematol & Oncol, Vienna, Austria.
   [Kountourakis, Pantelis] Bank Cyprus Oncol Ctr, Med Oncol Dept, Nicosia, Cyprus.
   [Kopecky, Jindrich] Univ Hosp Hradec Kralove, Dept Clin Oncol & Radiotherapy, Hradec Kralove, Czech Republic.
   [Kuhar, Cvetka Grasic] Inst Oncol Ljubljana, Dept Med Oncol, Ljubljana, Slovenia.
   [Popovic, Lazar] Univ Novi Sad, Oncol Inst Vojvodina, Med Oncol Dept, Novi Sad, Serbia.
   [Chilingirova, Nataliya P.] Univ Pleven, Med Oncol Clin Specialized Hosp Act Treatment Onc, Sofia, Bulgaria.
   [De Mello, Ramon Andrade] Univ Algarve, Dept Biomed Sci & Med, Faro, Portugal.
   [De Mello, Ramon Andrade] Fed Univ Sao Paulo UNIFESP, Precis Oncol Grp, Sao Paulo, Brazil.
   [De Mello, Ramon Andrade] Nine July Univ UNINOVE, Sao Paulo, Brazil.
   [Plavetic, Natalija Dedic] Univ Zagreb, Univ Hosp Ctr Zagreb, Sch Med, Dept Oncol, Zagreb, Croatia.
   [Katsanos, Konstantinos] Univ Hosp Ioannina, Dept Gastroenterol, Ioannina, Greece.
   [Mostert, Bianca] Erasmus MC Canc Inst, Dept Med Oncol, Rotterdam, Netherlands.
   [Alongi, Filippo] IRCCS Sacro Cuore Don Calabria Hosp, Canc Care Ctr, Adv Radiat Oncol Dept, Verona, Italy.
   [Alongi, Filippo] Univ Brescia, Brescia, Italy.
   [de Bari, Berardino] Hosp Neuchatelois, La Chaux De Fonds, Switzerland.
   [Corradini, Stefanie] Ludwig Maximilians Univ Munchen, Dept Radiat Oncol, Univ Hosp, Munich, Germany.
   [Valachis, Antonios] Orebro Univ, Fac Med & Hlth, Dept Oncol, Orebro, Sweden.
C3 University of Ioannina; Christie NHS Foundation Trust; University of
   Crete; Beatson Oncology Centre; University of Antwerp; University
   Hospital Hradec Kralove; Institute of Oncology - Slovenia; University of
   Novi Sad; Medical University Pleven; Universidade do Algarve;
   Universidade Federal de Sao Paulo (UNIFESP); Universidade Nove de Julho;
   University of Zagreb; University Hospital Ioannina; Erasmus University
   Rotterdam; Erasmus MC; Erasmus MC Cancer Institute; IRCCS Sacro Cuore
   Don Calabria; University of Brescia; University of Munich; Orebro
   University
RP Mauri, D (corresponding author), Univ Ioannina, Dept Med Oncol, Ioannina, Greece.
EM dvd.mauri@gmail.com
RI De+Mello, Ramon/ABG-4463-2020; Kopecky, Jindrich/IQV-8052-2023;
   papadimitriou, konstantinos/IUP-5946-2023; Nixon, Iain/O-1886-2013;
   Tolia, Maria/AAM-8550-2021; Corradini, Stefanie/HLP-6817-2023
OI Gazouli, Ioanna/0000-0001-8774-136X; , MARIA/0000-0001-5822-4363;
   Mostert, Bianca/0000-0001-5193-0820; Zarkavelis,
   George/0000-0001-5961-2237; Popovic, Lazar/0000-0002-3278-6875; Kopecky,
   Jindrich/0000-0002-4126-0410
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NR 36
TC 3
Z9 3
U1 0
U2 7
PU KARGER
PI BASEL
PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND
SN 2296-5270
EI 2296-5262
J9 ONCOL RES TREAT
JI Oncol. Res. Treat.
PY 2022
VL 45
IS 4
BP 216
EP 220
DI 10.1159/000521845
PG 5
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 2R4TM
UT WOS:000821106000007
PM 34999585
OA Green Submitted, Green Accepted
DA 2025-01-04
ER

PT J
AU Puccini, A
   Seeber, A
   Berger, MD
AF Puccini, Alberto
   Seeber, Andreas
   Berger, Martin D.
TI Biomarkers in Metastatic Colorectal Cancer: Status Quo and Future
   Perspective
SO CANCERS
LA English
DT Review
DE colorectal cancer; metastatic; biomarker; precision medicine;
   personalized treatment
ID FOLFIRI PLUS CETUXIMAB; CIRCULATING-TUMOR DNA; POTENTIAL THERAPEUTIC
   TARGET; POSITIVE SOLID TUMORS; R-SPONDIN FUSIONS; III COLON-CANCER;
   MISMATCH-REPAIR; OPEN-LABEL; RAS MUTATIONS; MICROSATELLITE INSTABILITY
AB Simple Summary Despite recent progress in the treatment of metastatic colorectal cancer patients, novel therapeutic approaches are highly warranted to further improve outcome. Additionally, it is of utmost importance to define subgroups of patients who may derive the most benefit from a specific treatment, as we are moving forward in the field of personalized medicine. This review provides an overview about established biomarkers helping us to better guide treatment. Moreover, we report on emerging and potential promising biomarkers having the potential to be implemented into clinical practice in the near future. Colorectal cancer (CRC) is the third most frequent cancer worldwide, and its incidence is steadily increasing. During the last two decades, a tremendous improvement in outcome has been achieved, mainly due to the introduction of novel drugs, targeted treatment, immune checkpoint inhibitors (CPIs) and biomarker-driven patient selection. Moreover, progress in molecular diagnostics but also improvement in surgical techniques and local ablative treatments significantly contributed to this success. However, novel therapeutic approaches are needed to further improve outcome in patients diagnosed with metastatic CRC. Besides the established biomarkers for mCRC, such as microsatellite instability (MSI) or mismatch repair deficiency (dMMR), RAS/BRAF, sidedness and HER2 amplification, new biomarkers have to be identified to better select patients who derive the most benefit from a specific treatment. In this review, we provide an overview about therapeutic relevant and established biomarkers but also shed light on potential promising markers that may help us to better tailor therapy to the individual mCRC patient in the near future.
C1 [Puccini, Alberto] IRCCS Osped Policlin San Martino, Med Oncol Unit 1, I-16132 Genoa, Italy.
   [Puccini, Alberto] Univ Genoa, Sch Med, Dept Internal Med & Med Specialties DIMI, I-16132 Genoa, Italy.
   [Seeber, Andreas] Med Univ Innsbruck, Comprehens Canc Ctr Innsbruck, Dept Hematol & Oncol, A-6020 Innsbruck, Austria.
   [Berger, Martin D.] Univ Bern, Bern Univ Hosp, Dept Med Oncol, Inselspital, CH-3010 Bern, Switzerland.
C3 University of Genoa; Medical University of Innsbruck; University of
   Bern; University Hospital of Bern
RP Berger, MD (corresponding author), Univ Bern, Bern Univ Hosp, Dept Med Oncol, Inselspital, CH-3010 Bern, Switzerland.
EM martin.berger@insel.ch
RI Berger, Martin/AAR-4415-2021; Puccini, Alberto/F-3255-2018
OI Puccini, Alberto/0000-0002-2492-4043; Berger, Martin
   D./0000-0001-9224-7104; , Andreas/0000-0001-8529-7824
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NR 220
TC 12
Z9 12
U1 0
U2 4
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2072-6694
J9 CANCERS
JI Cancers
PD OCT
PY 2022
VL 14
IS 19
AR 4828
DI 10.3390/cancers14194828
PG 25
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 5F9VD
UT WOS:000866656900001
PM 36230751
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Chen, L
   Lin, Y
   Zhang, ZJ
   Yang, RS
   Bai, XS
   Liu, ZB
   Luo, ZL
   Zhou, ML
   Zhong, ZR
AF Chen, Lin
   Lin, Yan
   Zhang, Zijun
   Yang, Ruisheng
   Bai, Xiaosheng
   Liu, Zhongbing
   Luo, Zhongling
   Zhou, Meiling
   Zhong, Zhirong
TI A novel dual-prodrug carried by cyclodextrin inclusion complex for the
   targeting treatment of colon cancer
SO JOURNAL OF NANOBIOTECHNOLOGY
LA English
DT Article
DE Butyric acid; 5-Aminosalicylic acid; Prodrug; Inclusion complex; Colon
   cancer
ID DRUG-DELIVERY; ACID; NANOPARTICLES; DOXORUBICIN; EFFICACY; RECEPTOR;
   THERAPY; BREAST; GROWTH; TUMORS
AB Background: There is an obvious correlation between ulcerative colitis and colorectal cancer, and the risk of colorectal cancer in patients with ulcerative colitis is increasing. Therefore, the combination therapy of anti-inflammatory and anti-tumor drugs may show promising to inhibit colon cancer. 5-aminosalicylic acid (5-ASA) with anti-inflammatory function is effective for maintaining remission in patients with ulcerative colitis and may also reduce colorectal cancer risk. Histone deacetylase (HDAC) plays an essential role in the progression of colon cancer. Butyric acid (BA) is a kind of HDAC inhibitor and thus shows tumor suppression to colon cancer. However, the volatile and corrosive nature of BA presents challenges in practical application. In addition, its clinical application is limited due to its non-targeting ability and low bioavailability. We aimed to synthesize a novel dual-prodrug of 5-ASA and BA, referred as BBA, to synergistically inhibit colon cancer. Further, based on the fact that folate receptor (FR) is over-expressed in most solid tumors and it has been identified to be a cancer stem cell surface marker in colon cancer, we took folate as the targeting ligand and used carboxymethyl-beta-cyclodextrin (CM-beta-CD) to carry BBA and thus prepared a novel inclusion complex of BBA/FA-PEG-CM-beta-CD.
   Results: It was found that BBA/FA-PEG-CM-beta-CD showed significant inhibition in cell proliferation against colon cancer cells SW620. It showed a pro-longed in vivo circulation and mainly accumulated in tumor tissue. More importantly, BBA/FA-PEG-CM-beta-CD gave great tumor suppression effect against nude mice bearing SW620 xenografts.
   Conclusions: Therefore, BBA/FA-PEG-CM-beta-CD may have clinical potential in colon cancer therapy.
C1 [Chen, Lin; Lin, Yan; Zhang, Zijun; Yang, Ruisheng; Bai, Xiaosheng; Liu, Zhongbing; Luo, Zhongling; Zhong, Zhirong] Southwest Med Univ, Sch Pharm, Dept Pharmaceut Sci, Luzhou 646000, Sichuan, Peoples R China.
   [Chen, Lin] Nanchong Cent Hosp, Dept Pharm, North Sichuan Med Coll, Clin Med Coll 2,Nanchong Key Lab Individualized D, Nanchong 637000, Sichuan, Peoples R China.
   [Zhou, Meiling] Southwest Med Univ, Dept Pharm, Affiliated Hosp, Luzhou 646000, Sichuan, Peoples R China.
C3 Southwest Medical University; North Sichuan Medical University;
   Southwest Medical University
RP Zhong, ZR (corresponding author), Southwest Med Univ, Sch Pharm, Dept Pharmaceut Sci, Luzhou 646000, Sichuan, Peoples R China.; Zhou, ML (corresponding author), Southwest Med Univ, Dept Pharm, Affiliated Hosp, Luzhou 646000, Sichuan, Peoples R China.
EM meilzhou@163.com; zhongzhirong@126.com
RI liu, yichen/GVT-6262-2022
OI zhong, zhirong/0000-0003-1509-4540; Xia, Chen/0000-0001-8901-0827
FU Collaborative Project of Luzhou Government and Southwest Medical
   University [2020LZXNYDZ04, 2019LZXNYDJ21, 2018LZXNYDPT02]; Science and
   Technology Project of the Health Planning Committee of Sichuan [20PJ174]
FX This work was supported by the Collaborative Project of Luzhou
   Government and Southwest Medical University (2020LZXNYDZ04,
   2019LZXNYDJ21, 2018LZXNYDPT02), the Science and Technology Project of
   the Health Planning Committee of Sichuan (20PJ174).
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NR 46
TC 11
Z9 11
U1 5
U2 52
PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
EI 1477-3155
J9 J NANOBIOTECHNOL
JI J. Nanobiotechnol.
PD OCT 19
PY 2021
VL 19
IS 1
AR 329
DI 10.1186/s12951-021-01064-3
PG 22
WC Biotechnology & Applied Microbiology; Nanoscience & Nanotechnology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biotechnology & Applied Microbiology; Science & Technology - Other
   Topics
GA WJ2TO
UT WOS:000708901400001
PM 34666761
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Stefanescu, H
   Muntean, D
   Pilut, C
   Diaconu, M
   Popescu, R
   Hutanu, D
   Moise, M
   Diana, L
   Nitu, R
   Cherecheanu, AP
   Negoita, S
   Iovan, CV
   Ungureanu, E
   Calu, V
   Ciuca, I
AF Stefanescu, Horatiu
   Muntean, Delia
   Pilut, Ciprian
   Diaconu, Mircea
   Popescu, Roxana
   Hutanu, Delia
   Moise, Marius
   Diana, Lighezan
   Nitu, Razvan
   Cherecheanu, Alina Popa
   Negoita, Silvius
   Iovan, Ciprian, V
   Ungureanu, Emil
   Calu, Valentin
   Ciuca, Ioana
TI Using Blood and Plasma MicroRNAs as a Non-Invasive Biomarker in Patients
   with Colorectal Cancer
SO CLINICAL LABORATORY
LA English
DT Article
DE colorectal cancer; microRNAs; epigenetic biomarkers
ID ILL POLYTRAUMA PATIENTS; GENETIC POLYMORPHISMS; POOR-PROGNOSIS; KAPPA-B;
   EXPRESSION; PROMOTES; MIRNAS; CELLS; DAMAGE; PROLIFERATION
AB Background: A high percentage of oncological patients die yearly because of colorectal cancer (CRC). Worldwide, CRC represents the fourth leading cause of death among oncological patients. Numerous studies have been conducted in order to identify new biomarkers for the early diagnosis of patients with CRC. From this point of view, an ideal biomarker is represented by the expression of microRNAs. In this paper, we wish to summarize the expressions of microRNAs in CRC and to present the pathophysiological and genetic interactions that microRNAs have with protein systems in these patients.
   Methods: For this paper, we looked into the studies available in scientific databases such as PubMed. For the search the following keywords have been used: "miRNAs expression", "colorectal cancer", "genetic polymorphisms in CRC", and "genetic biomarkers in CRC".
   Results: Modifying the expression of microRNAs can be used successfully both in diagnosing patients with CRC and in following their response to chemotherapy. Numerous studies have shown high specificity for certain microRNA species in the case of CRC. An extraordinary advantage of these biomarkers is represented by their non-invasive sampling from urine and blood. Moreover, a series of connections of microRNAs in some mechanisms involved in the appearance and development of CRC have been shown. Therefore, microRNAs can be named as the biomarker of the future, as well as the epigenetic targeted treatment for patients with CRC.
   Conclusions: The expression of microRNAs can be successfully used in the evaluation and non-invasive monitoring of patients with CRC. However, further studies are needed regarding the expression of microRNAs and the connections these species have in the pathological mechanisms specific for CRC.
C1 [Stefanescu, Horatiu; Muntean, Delia; Pilut, Ciprian; Diaconu, Mircea; Popescu, Roxana; Moise, Marius; Diana, Lighezan; Nitu, Razvan; Ciuca, Ioana] Victor Babes Univ Med & Pharm, Fac Med, Timisoara, Romania.
   [Hutanu, Delia] West Univ Timisoara, Fac Chem Biol Geog, Timisoara, Romania.
   [Cherecheanu, Alina Popa; Negoita, Silvius; Ungureanu, Emil] Carol Davila Univ Med & Pharm, Fac Med, Bucharest, Romania.
   [Iovan, Ciprian, V] Univ Oradea, Fac Med & Pharm, Oradea, Romania.
C3 Victor Babes University of Medicine & Pharmacy, Timisoara; West
   University of Timisoara; Carol Davila University of Medicine & Pharmacy;
   University of Oradea
RP Hutanu, D (corresponding author), West Univ Timisoara, Fac Chem Biol Geog, Timisoara, Romania.
EM delia.hutanu.uvt@gmail.com
RI Popescu, Roxana/AAB-1809-2019; delia, hutanu/HSE-9303-2023; Delia,
   Muntean/J-9468-2019; NEGOITA, SILVIUS/AAG-2433-2021; Ciuca,
   Ioana/C-7235-2015; Nitu, Razvan/LWI-1635-2024; CALU,
   VALENTIN/AAN-8374-2020; Stefanescu, Eugen Horatiu/AAO-5783-2020
OI Delia, Muntean/0000-0001-9100-4530; Delia, Hutanu/0000-0002-1335-6845;
   CALU, VALENTIN/0000-0001-7710-9109; Nicolae Ciprian,
   Pilut/0009-0006-9681-8289; Ciuca, Ioana Mihaiela/0000-0002-2879-8080;
   Stefanescu, Eugen Horatiu/0000-0002-6669-7715; Popescu,
   Roxana/0000-0002-9387-1141; Popa-Cherecheanu, Alina/0000-0003-4189-6571
CR [Anonymous], GASTROENTEROL RES PR
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NR 39
TC 5
Z9 5
U1 0
U2 12
PU CLIN LAB PUBL
PI HEIDELBERG
PA IM BREITSPIEL 15, HEIDELBERG, D-69126, GERMANY
SN 1433-6510
J9 CLIN LAB
JI Clin. Lab.
PY 2018
VL 64
IS 3
BP 257
EP 262
DI 10.7754/Clin.Lab.2017.170819
PG 6
WC Medical Laboratory Technology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Medical Laboratory Technology
GA GG7KT
UT WOS:000432877800005
PM 29739108
DA 2025-01-04
ER

PT J
AU Wang, ZM
   Su, M
   Xiang, BW
   Zhao, K
   Qin, BL
AF Wang, Zhongmiao
   Su, Meng
   Xiang, Bowen
   Zhao, Kai
   Qin, Baoli
TI Circular RNA PVT1 promotes metastasis via miR-145 sponging in CRC
SO BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
LA English
DT Article
DE circPVT1; miR-145; Metastasis; Colorectal cancer
ID CANCER CELL-MIGRATION; COLORECTAL-CANCER; CIRCPVT1; INVASION; ABUNDANT;
   MARKER
AB Circular RNAs (circRNAs) are a class of covalently closed non-coding RNAs and are widely involved in various cancers including colorectal cancer (CRC). Circular RNA PVT1 (circPVT1) was reported in several malignancies but the role it plays in CRC remains unclear. In our current research, we focused on the expression and function of circPVT1) works in CRC. We found that circPVT1 was upregulated in CRC. Also, we illustrated that the upregulated circPVT1 was closely correlated with poor prognosis and bad clinicopathological features of patients with CRC. Through a loss of function experiment, we showed that a downregulation of circPVT1 suppressed CRC cells metastasis. Through online prediction, we found that circPVT1 had a microRNA response element (MRE) for miR-145. Additionally, we demonstrated that miR-145 was downregulated in CRC. Even further, we showed that miR-145 was involved in circPVT1 mediated facilitation of CRC metastasis. In a further mechanical study, we demonstrated that circPVT1 could target miR-145. Lastly, we revealed that the metastasis-promoting role of circPVT1 in CRC was partially achieved via miR-145 sponging.
   In brief, the findings of the present study illustrated that circPVT1, working as an oncogene, promotes metastasis via miR-145 sponging in CRC. CircPVT1 imiR-145 axial might be a novel point in targeting treatment of CRC. (C) 2019 The Authors. Published by Elsevier Inc.
C1 [Wang, Zhongmiao; Su, Meng; Xiang, Bowen; Zhao, Kai; Qin, Baoli] China Med Univ, Dept Internal Med, Canc Hosp, Liaoning Canc Hosp & Ins, 44 Xiaoheyan Rd, Shenyang 110042, Liaoning, Peoples R China.
C3 China Medical University
RP Qin, BL (corresponding author), China Med Univ, Dept Internal Med, Canc Hosp, Liaoning Canc Hosp & Ins, 44 Xiaoheyan Rd, Shenyang 110042, Liaoning, Peoples R China.
EM wangzhongmiao@126.com; sumeng_1980@126.com; xiangbowen90@l63.com;
   zk1292975918@163.com; qinbaoli1964@163.com
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NR 28
TC 75
Z9 79
U1 0
U2 5
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0006-291X
EI 1090-2104
J9 BIOCHEM BIOPH RES CO
JI Biochem. Biophys. Res. Commun.
PD MAY 14
PY 2019
VL 512
IS 4
BP 716
EP 722
DI 10.1016/j.bbrc.2019.03.121
PG 7
WC Biochemistry & Molecular Biology; Biophysics
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Biophysics
GA HY6RX
UT WOS:000468258500013
PM 30922567
OA hybrid
DA 2025-01-04
ER

PT J
AU Bingmer, K
   Ofshteyn, A
   Bliggenstorfer, JT
   Kethman, W
   Ammori, JB
   Charles, R
   Stein, SL
   Steinhagen, E
AF Bingmer, Katherine
   Ofshteyn, Asya
   Bliggenstorfer, Jonathan T.
   Kethman, William
   Ammori, John B.
   Charles, Ronald
   Stein, Sharon L.
   Steinhagen, Emily
TI Primary tumor location impacts survival in colorectal cancer patients
   after resection of liver metastases
SO JOURNAL OF SURGICAL ONCOLOGY
LA English
DT Article
DE colorectal cancer; hepatic metastases; right-sided colon cancer
ID SURGICAL-TREATMENT
AB Background and Objectives Right-sided colon cancers (R-CC) are associated with worse outcomes compared to left-sided colon cancers (L-CC). We hypothesize that R-CC with synchronous liver metastases who undergo resection of primary and metastatic sites have worse survival and that survival will vary significantly among R-CC, L-CC, and rectal cancer (ReC). Methods The Surveillance, Epidemiology, and End Results (SEER) database from 2010 to 2016 was used to identify colorectal cancer patients with liver metastases who underwent surgical resection of both primary and metastatic disease. Survival was analyzed by multivariate Cox regression. Results A total of 2275 patients were included; 38% R-CC, 46% L-CC, and 16% ReC. R-CC primary tumors tended to be larger than 5 cm, higher grade, and mucinous (allP < .001). Compared to patients with R-CC, both L-CC and ReC had improved overall (HR 0.72;P < .001; HR 0.75,P = .006) and disease-specific (HR 0.71,P < .001; HR 0.73,P = .008) survival. There was no difference in survival between L-CC and ReC. Conclusions Patients with R-CC have significantly worse survival than L-CC or ReC. This provides additional evidence that R-CC tumors are fundamentally different from L-CC and ReC tumors. Future studies should determine factors responsible for this disparity, and identify targeted treatment based on primary tumor location.
C1 [Bingmer, Katherine; Ofshteyn, Asya; Bliggenstorfer, Jonathan T.; Kethman, William; Ammori, John B.; Charles, Ronald; Stein, Sharon L.; Steinhagen, Emily] Univ Hosp Cleveland Med Ctr, Dept Surg, Univ Hosp Res Surg Outcomes & Effectiveness Ctr, Cleveland, OH USA.
C3 University Hospitals of Cleveland
RP Steinhagen, E (corresponding author), Dept Surg, 11100 Euclid Ave,LKS 5047, Cleveland, OH 44106 USA.
EM emily.steinhagen@uhhospitals.org
OI Bingmer, Katherine/0000-0002-0155-801X; Ammori,
   John/0000-0003-2131-0369; Kethman, William/0000-0002-8210-844X
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NR 15
TC 8
Z9 8
U1 0
U2 4
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0022-4790
EI 1096-9098
J9 J SURG ONCOL
JI J. Surg. Oncol.
PD SEP
PY 2020
VL 122
IS 4
BP 745
EP 752
DI 10.1002/jso.26061
EA JUN 2020
PG 8
WC Oncology; Surgery
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Surgery
GA MZ8NW
UT WOS:000539202400001
PM 32524637
DA 2025-01-04
ER

PT J
AU Yang, SJ
   Tseng, SY
   Wang, CH
   Young, TH
   Chen, KC
   Shieh, MJ
AF Yang, Shu-Jyuan
   Tseng, Shu-Yi
   Wang, Chung-Hao
   Young, Tai-Horng
   Chen, Ke-Cheng
   Shieh, Ming-Jium
TI Magnetic nanomedicine for CD133-expressing cancer therapy using
   locoregional hyperthermia combined with chemotherapy
SO NANOMEDICINE
LA English
DT Article
DE cancer stem cell; chemotherapy; colorectal cancer; hyperthermia;
   superparamagnetic iron oxide nanoparticles
ID STEM-CELLS; COLORECTAL-CANCER; SUPERPARAMAGNETIC NANOPARTICLES; CD133;
   SIZE; MICROSPHERES; METASTASIS
AB Aim: Cells with CD133 overexpression, a theoretical cancer stem cells (CSCs) marker, have been shown to induce colorectal cancer (CRC) initiation and relapse. Therefore, the detection and treatment of CSCs are the most important factors in overcoming CRC. Materials & methods: Herein, we developed a magnetite-based nanomedicine (superparamagnetic iron oxide@poly(sodium styrene sulfonate)/irinotecan/human serum albumin-anti-CD133 nanoparticle) using loco-regional hyperthermia combined with chemotherapy for CRC- and CSC-specific targeting treatment. Results: The designed nanoparticles were highly biocompatible and exhibited a higher temperature increase rate under radiofrequency generator irradiation. The nanoparticles could be used as a T2-weighted magnetic resonance imaging contrast media, and also applied during hyperthermia and chemotherapy to display a synergistic anticancer effect. Conclusion: Therefore, the superparamagnetic iron oxide@poly(sodium styrene sulfonate)/irinotecan/human serum albumin-anti-CD133 nanoparticles are a powerful candidate for future antitumor strategies.
C1 [Yang, Shu-Jyuan; Tseng, Shu-Yi; Young, Tai-Horng; Chen, Ke-Cheng; Shieh, Ming-Jium] Natl Taiwan Univ, Inst Biomed Engn, Coll Med, 1,Sect 1,Jen Ai Rd, Taipei 100, Taiwan.
   [Yang, Shu-Jyuan; Tseng, Shu-Yi; Young, Tai-Horng; Chen, Ke-Cheng; Shieh, Ming-Jium] Natl Taiwan Univ, Inst Biomed Engn, Coll Engn, 1,Sect 1,Jen Ai Rd, Taipei 100, Taiwan.
   [Wang, Chung-Hao] Genee Tech Co Ltd, 2F,661 Bannan Rd, New Taipei 235, Taiwan.
   [Chen, Ke-Cheng] Natl Taiwan Univ Hosp & Coll Med, Dept Surg, 7 Chung Shan South Rd, Taipei 100, Taiwan.
   [Shieh, Ming-Jium] Natl Taiwan Univ Hosp & Coll Med, Dept Oncol, 7,Chung Shan South Rd, Taipei 100, Taiwan.
C3 National Taiwan University; National Taiwan University; National Taiwan
   University; National Taiwan University Hospital; National Taiwan
   University; National Taiwan University Hospital
RP Chen, KC; Shieh, MJ (corresponding author), Natl Taiwan Univ, Inst Biomed Engn, Coll Med, 1,Sect 1,Jen Ai Rd, Taipei 100, Taiwan.; Chen, KC; Shieh, MJ (corresponding author), Natl Taiwan Univ, Inst Biomed Engn, Coll Engn, 1,Sect 1,Jen Ai Rd, Taipei 100, Taiwan.
EM 010288@ntuh.gov.tw; soloman@ntu.edu.tw
FU Ministry of Science and Technology [MOST 106-2314-B-002 -015 -MY3,
   106-3114-E-002-004-]
FX The authors appreciate the help from the National Taiwan University
   College of Medicine and the National Taiwan University Hospital. This
   work was supported by the Ministry of Science and Technology (MOST
   106-2314-B-002 -015 -MY3 and 106-3114-E-002-004-). The authors have no
   other relevant affiliations or financial involvement with any
   organization or entity with a financial interest in or financial
   conflict with the subject matter or materials discussed in the
   manuscript apart from those disclosed.
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NR 60
TC 9
Z9 9
U1 1
U2 21
PU TAYLOR & FRANCIS LTD
PI ABINGDON
PA 2-4 PARK SQUARE, MILTON PARK, ABINGDON OR14 4RN, OXON, ENGLAND
SN 1743-5889
EI 1748-6963
J9 NANOMEDICINE-UK
JI Nanomedicine
PD SEP
PY 2020
VL 15
IS 26
BP 2543
EP 2561
DI 10.2217/nnm-2020-0222
EA OCT 2020
PG 19
WC Biotechnology & Applied Microbiology; Nanoscience & Nanotechnology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biotechnology & Applied Microbiology; Science & Technology - Other
   Topics
GA OU3IM
UT WOS:000583625500001
PM 33103961
DA 2025-01-04
ER

PT J
AU Paric, A
   Karan-Krizanac, D
   Saric, I
   Vranic, S
AF Paric, Ana
   Karan-Krizanac, Dragana
   Saric, Ivan
   Vranic, Semir
TI A Chromosome 9p24.1 Amplification in Colorectal Cancer with Metastases
   to the Kidney and Adrenal Gland: A Case Report
SO CASE REPORTS IN ONCOLOGY
LA English
DT Article
DE Colorectal cancer; Renal metastasis; Adrenal metastasis; Molecular
   profiling; Immune checkpoint inhibitors; Programmed cell death ligand 1;
   Programmed cell death ligand 2
ID PRECISION MEDICINE; COLON; DIAGNOSIS; PD-L1
AB Colorectal cancer (CRC) is the third leading cause of mortality worldwide. The Food and Drug Administration recently designated pembrolizumab, an immune checkpoint inhibitor (ICI) against a programmed death-1 receptor, as a breakthrough drug for the treatment of patients with mCRC whose tumors have deficient mismatch-repair gene expression (as evidenced by microsatellite instability-high) and patients with solid tumors with a high tumor mutational burden with >= 10 mutations/megabase. We present a patient with metastatic CRC having renal and adrenal gland metastases. Comprehensive molecular profiling performed on a site of metastatic CRC in the kidney revealed multiple genomic alterations characteristic of CRC and rare chromosome 9p24.1 amplification, resulting in a co-amplification of the PDL1, PDL2, and JAK2 genes. Although this genomic alteration may predict the response to ICI, the lack of pembrolizumab prevented the patient from receiving targeted treatment and succumbing to the disease.
C1 [Paric, Ana] Univ Hosp Ctr Mostar, Dept Oncol, Mostar, Bosnia & Herceg.
   [Karan-Krizanac, Dragana] Univ Hosp Ctr Mostar, Dept Pathol & Cytopathol, Mostar, Bosnia & Herceg.
   [Saric, Ivan] Univ Hosp Ctr Mostar, Dept Abdominal Surg, Mostar, Bosnia & Herceg.
   [Vranic, Semir] Qatar Univ Doha, Coll Med, QU Hlth, Doha, Qatar.
C3 University of Mostar; University of Mostar; University of Mostar; Qatar
   University
RP Vranic, S (corresponding author), Qatar Univ Doha, Coll Med, QU Hlth, Doha, Qatar.
EM semir.vranic@gmail.com
RI Vranic, Semir/J-4113-2012
OI Vranic, Semir/0000-0001-9743-7265
CR Aksu Gorkem, 2003, Int J Gastrointest Cancer, V34, P73, DOI 10.1385/IJGC:34:2-3:073
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   [Anonymous], 2017, FDA grants accelerated approval to pembrolizumab for first tissue/site agnostic indication
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NR 31
TC 0
Z9 0
U1 0
U2 0
PU KARGER
PI BASEL
PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND
SN 1662-6575
J9 CASE REP ONCOL
JI Case Rep. Oncol.
PY 2023
VL 16
IS 1
BP 803
EP 810
DI 10.1159/000533377
PG 8
WC Oncology
WE Emerging Sources Citation Index (ESCI)
SC Oncology
GA NW4F6
UT WOS:001203472100108
PM 37900784
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Wang, ZL
   Run, ZC
   Wang, HM
   He, XJ
   Li, J
AF Wang, Zhenlei
   Run, Zengci
   Wang, Huamin
   He, Xiaojun
   Li, Jian
TI TiO2-Ti3C2 Nanocomposites Utilize Their Photothermal Activity for
   Targeted Treatment of Colorectal Cancer
SO INTERNATIONAL JOURNAL OF NANOMEDICINE
LA English
DT Article
DE TiO 2-Ti 3 C 2; photothermal activity; colorectal cancer; photothermal
   therapy
ID MXENE; TI3C2; THERAPY; TIO2; SURVIVORS; HYBRIDS
AB Purpose: The search for effective and low-risk treatment methods for colorectal cancer (CRC) is a pressing concern, given the inherent risks and adverse reactions associated with traditional therapies. Photothermal therapy (PTT) has emerged as a promising approach for cancer treatment, offering advantages such as non-radiation, non-invasiveness, and targeted treatment. Consequently, the development of nanoparticles with high stability, biocompatibility, and photothermal effects has become a significant research focus within the field of PTT. Methods: In this study, TiO2-Ti3C2 nanocomposites were synthesized and characterized, and their photothermal conversion efficiency in the near-infrared region II (NIR-II) was determined. Then studied the in vivo and in vitro photothermal activity and anti-tumor effect of TiO2-Ti3C2 in human colorectal cancer cell lines and nude mice subcutaneous tumor model. Results: The results showed that TiO2-Ti3C2 nanocomposites have strong absorption ability in the NIR-II, and have high photothermal conversion efficiency under 1064 nm (0.5 W/cm2, 6 min) laser stimulation. In addition, in vitro experiments showed that TiO2-Ti3C2 nanocomposites significantly inhibited the invasion, migration, and proliferation of colorectal cancer cells, and induced cell apoptosis; in vivo, experiments showed that TiO2-Ti3C2 nanocomposites-mediated PTT had good biocompatibility and efficient targeted inhibition of tumor growth. Conclusion: In conclusion, TiO2-Ti3C2 nanocomposites can be used as NIR-II absorption materials in PTT to suppress the invasion, migration, and proliferation of colorectal cancer cells, induce colorectal cancer cell apoptosis, and thus inhibit the development of CRC. Therefore, TiO2-Ti3C2 nanocomposites can be used as potential anti-tumor drugs for photothermal ablation of colorectal cancer cells.
C1 [Wang, Zhenlei; Run, Zengci; Li, Jian] Zhengzhou Univ, Dept Gen Surg, Affiliated Canc Hosp, Zhengzhou 450008, Henan, Peoples R China.
   [Wang, Zhenlei; Run, Zengci; Li, Jian] Henan Canc Hosp, Zhengzhou 450008, Henan, Peoples R China.
   [Wang, Huamin] Wenzhou Med Univ, Affiliated Hosp 2, Dept Pediat, Wenzhou 325027, Zhejiang, Peoples R China.
   [Wang, Huamin] Wenzhou Med Univ, Dept Pediat, Yuying Childrens Hosp, Wenzhou 325027, Zhejiang, Peoples R China.
   [He, Xiaojun] Wenzhou Med Univ, Sch Ophthalmol & Optometry, Sch Biomed Engn, Wenzhou 325035, Zhejiang, Peoples R China.
   [Li, Jian] Zhengzhou Univ, Dept Gen Surg, Affiliated Canc Hosp, 127 Dongming Rd, Zhengzhou 450008, Henan, Peoples R China.
   [Li, Jian] Henan Canc Hosp, 127 Dongming Rd, Zhengzhou 450008, Henan, Peoples R China.
C3 Zhengzhou University; Zhengzhou University; Wenzhou Medical University;
   Wenzhou Medical University; Wenzhou Medical University; Zhengzhou
   University; Zhengzhou University
RP He, XJ (corresponding author), Wenzhou Med Univ, Sch Ophthalmol & Optometry, Sch Biomed Engn, Wenzhou 325035, Zhejiang, Peoples R China.; Li, J (corresponding author), Zhengzhou Univ, Dept Gen Surg, Affiliated Canc Hosp, 127 Dongming Rd, Zhengzhou 450008, Henan, Peoples R China.; Li, J (corresponding author), Henan Canc Hosp, 127 Dongming Rd, Zhengzhou 450008, Henan, Peoples R China.
EM 513080867@qq.com; garfycat@126.com
RI Wang, Zhenlei/R-4750-2019
FU National Natural Science Foundation of China [81902891]
FX Acknowledgments This study was supported by the National Natural Science
   Foundation of China (81902891) . Graphical abstract was created with
   Biorender.com .
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NR 35
TC 0
Z9 0
U1 3
U2 18
PU DOVE MEDICAL PRESS LTD
PI ALBANY
PA PO BOX 300-008, ALBANY, AUCKLAND 0752, NEW ZEALAND
SN 1178-2013
J9 INT J NANOMED
JI Int. J. Nanomed.
PY 2024
VL 19
BP 1041
EP 1054
DI 10.2147/IJN.S446537
PG 14
WC Nanoscience & Nanotechnology; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Science & Technology - Other Topics; Pharmacology & Pharmacy
GA GY7N6
UT WOS:001156302900001
PM 38317849
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Augustyniak, M
   Lou, EM
   Jacobs, G
   Fleming, M
   Marshall, J
   Coutinho, A
   Yoshino, T
AF Augustyniak, Monica
   Lou, Emil
   Jacobs, Ginny
   Fleming, Matthew
   Marshall, John
   Coutinho, Anelisa
   Yoshino, Takayuki
TI Learning Outcomes of "GetSMART," Education for Diagnostics and Targeted
   Treatment for HER2+Metastatic Gastric and Colorectal Cancers
SO JOURNAL OF CANCER EDUCATION
LA English
DT Article
DE Gastric cancer; Colorectal cancer; Human epidermal growth factor
   receptor 2 (HER2); Continuing medical education; Continuing health
   education; Program evaluation
AB The treatment landscape for patients affected by gastric and colorectal cancer (G&CRC) has significantly broadened over the past decade. Molecular diagnostic methods have improved with a precision oncology-driven approach to the development of treatment options tailored to specific molecular targets, including the human epidermal growth factor 2 (HER2). While scientific evidence on the role of HER2 in G&CRC has improved, there has been a lag in general understanding and applications of testing for HER2+ G&CRC and resulting targeting treatment in the wider oncology community. To better understand and address the root causes of this gap, a needs assessment deployed among 85 oncology care providers was conducted and informed the development of an accredited online educational program entitled "GetSMART." The program consisted of four modules developed and narrated by experts in gastrointestinal oncology. The educational content and assessment metrics were guided by a confidence-based assessment (CBA) model and the Moore, Green, and Gallis outcomes framework. Assessment methods consisted of quantitative pre- and post-activity tests, an evaluation embedded within the education (n = 163), and semi-structured interviews (n = 5) post-activity completion. Findings indicated that "GetSMART" enhanced participants' knowledge, confidence, and intent to change practice in relation to their (1) identification of HER2 aberrations, (2) selection of appropriate treatments for HER2+ G&CRC, and (3) ability to engage patients in shared decision-making and management of adverse events. "GetSMART" can therefore be a valuable educational resource for oncology HCPs caring for patients affected by HER2+ metastatic G&CRC, offering strategies to ensure an optimal team and patient-centered approach to the care being delivered.
C1 [Augustyniak, Monica] AXDEV Grp Inc, Brossard, PQ J4W 3H2, Canada.
   [Lou, Emil] Univ Minnesota, Masonic Canc Ctr, Minneapolis, MN USA.
   [Jacobs, Ginny] AXDEV Global Inc, Virginia Beach, VA USA.
   [Fleming, Matthew] Antidote Educ Co, Dallas, TX USA.
   [Marshall, John] Georgetown Univ, Washington, DC USA.
   [Coutinho, Anelisa] Clin AMO, Multidisciplinary Oncol Inst, Salvador, BA, Brazil.
   [Yoshino, Takayuki] Natl Canc Ctr Hosp East, Chiba, Japan.
C3 University of Minnesota System; University of Minnesota Twin Cities;
   Georgetown University; National Cancer Center - Japan
RP Augustyniak, M (corresponding author), AXDEV Grp Inc, Brossard, PQ J4W 3H2, Canada.
EM augustyniakm@axdevgroup.com; emil-lou@umn.edu; jacobsg@axdevgroup.com;
   mfleming@antidotecme.com; marshalj@georgetown.edu;
   coutinhoanelisa@gmail.com; tyoshino@east.ncc.go.jp
RI Marshall, J/LBH-2002-2024
OI Lou, Emil/0000-0002-1607-1386; Augustyniak, Monica/0000-0003-2825-5497
FU Daiichi-Sankyo; AXDEV Group Inc.; Daiichi-Sankyo to Antidote Education
   Company
FX The authors would like to acknowledge the support provided by Pam
   McFadden (Vice President, AXDEV Group Inc.) for supporting project
   administration, Patrice Lazure (Director of Research, AXDEV Group Inc.)
   for his guidance on the research components of this study, Randa Dalle
   (Project Manager, AXDEV Group Inc.) and Karen Mariano (Project Manager,
   Antidote Education Company) who supported coordination of tasks between
   collaborators and monitoring of data collection, and all the
   participants who took part in this study. An Independent Medical
   Education (IME) grant was provided by Daiichi-Sankyo to Antidote
   Education Company to support this initiative.
CR Adedokun O., 2012, J MULTIDISCIPLINARY, V8, P125, DOI [DOI 10.56645/JMDE.V8I17.336, 10.56645/jmde.v8i17.336, DOI 10.1016/J.THROMRES.2012.08.264]
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NR 15
TC 0
Z9 0
U1 2
U2 3
PU SPRINGER
PI NEW YORK
PA ONE NEW YORK PLAZA, SUITE 4600, NEW YORK, NY, UNITED STATES
SN 0885-8195
EI 1543-0154
J9 J CANCER EDUC
JI J. Cancer Educ.
PD APR
PY 2024
VL 39
IS 2
BP 118
EP 125
DI 10.1007/s13187-023-02384-8
EA DEC 2023
PG 8
WC Oncology; Education, Scientific Disciplines; Public, Environmental &
   Occupational Health
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Education & Educational Research; Public, Environmental &
   Occupational Health
GA MZ4Y3
UT WOS:001129575000001
PM 38135836
OA Green Published, hybrid
DA 2025-01-04
ER

PT J
AU Song, JJ
   Zhang, YJ
   Zhou, CL
   Zhan, JH
   Cheng, XF
   Huang, HY
   Mao, SX
   Zong, Z
AF Song, Jingjing
   Zhang, Yujun
   Zhou, Chulin
   Zhan, Jianhao
   Cheng, Xifu
   Huang, Haoyu
   Mao, Shengxun
   Zong, Zhen
TI The dawn of a new Era: mRNA vaccines in colorectal cancer immunotherapy
SO INTERNATIONAL IMMUNOPHARMACOLOGY
LA English
DT Article
DE Colorectal cancer; Cancer vaccine; mRNA vaccine; Cancer therapy;
   Immunotherapy
ID T-CELL RESPONSES; CONSENSUS MOLECULAR SUBTYPES; OUTER-MEMBRANE VESICLES;
   HUMAN TUMOR-ANTIGENS; I IFN; IMMUNE-RESPONSES; PHASE-I; MICROSATELLITE
   INSTABILITY; ARTIFICIAL-INTELLIGENCE; PROTEIN EXPRESSION
AB Colorectal cancer (CRC) is a typical cancer that accounts for 10% of all new cancer cases annually and nearly 10% of all cancer deaths. Despite significant progress in current classical interventions for CRC, these traditional strategies could be invasive and with numerous adverse effects. The poor prognosis of CRC patients highlights the evident and pressing need for more efficient and targeted treatment. Novel strategies regarding mRNA vaccines for anti-tumor therapy have also been well-developed since the successful application for the prevention of COVID-19. mRNA vaccine technology won the 2023 Nobel Prize in Physiology or Medicine, signaling a new direction in human anti-cancer treatment: mRNA medicine. As a promising new immunotherapy in CRC and other multiple cancer treatments, the mRNA vaccine has higher specificity, better efficacy, and fewer side effects than traditional strategies. The present review outlines the basics of mRNA vaccines and their advantages over other vaccines and informs an available strategy for developing efficient mRNA vaccines for CRC precise treatment. In the future, more exploration of mRNA vaccines for CRC shall be attached, fostering innovation to address existing limitations.
C1 [Song, Jingjing; Zhang, Yujun; Zhou, Chulin; Huang, Haoyu; Mao, Shengxun; Zong, Zhen] Nanchang Univ, Dept Gastrointestinal Surg, Affiliated Hosp 2, 1 Minde Rd, Nanchang 330006, Jiangxi, Peoples R China.
   [Song, Jingjing; Cheng, Xifu] Nanchang Univ, Sch Ophthalmol & Optometry, Nanchang 330006, Jiangxi, Peoples R China.
   [Zhang, Yujun; Zhan, Jianhao] Nanchang Univ, Huankui Acad, Nanchang 330006, Jiangxi, Peoples R China.
   [Zhou, Chulin] Nanchang Univ, Clin Med Coll 2, Nanchang 330006, Jiangxi, Peoples R China.
C3 Nanchang University; Nanchang University; Nanchang University; Nanchang
   University
RP Mao, SX; Zong, Z (corresponding author), Nanchang Univ, Dept Gastrointestinal Surg, Affiliated Hosp 2, 1 Minde Rd, Nanchang 330006, Jiangxi, Peoples R China.
EM maoshengxun@126.com; zongzhenmd@126.com
RI Cheng, Xifu/JBS-1163-2023; Song, Jing/HRC-8045-2023
FU National Natural Science Foundation of China [82060453, 82103645,
   82260596]; Training Plan for Academic and Technical Young Leaders of
   Major Disciplines in Jiangxi Province [20204BCJ23021]; China
   Postdoctoral Science Foundation [2023M741523]; Science and Technology
   Program of Jiangxi Provincial Health and Family Planning Commission
   [202410246]
FX The present study was supported by the National Natural Science
   Foundation of China (Grant Number: 82060453 and 82103645 and 82260596)
   Training Plan for Academic and Technical Young Leaders of Major
   Disciplines in Jiangxi Province (Grant Number: 20204BCJ23021) , The
   China Postdoctoral Science Foundation (Grant Number: 2023M741523) , and
   Science and Technology Program of Jiangxi Provincial Health and Family
   Planning Commission (202410246) .
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NR 280
TC 1
Z9 1
U1 14
U2 20
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
SN 1567-5769
EI 1878-1705
J9 INT IMMUNOPHARMACOL
JI Int. Immunopharmacol.
PD MAY 10
PY 2024
VL 132
AR 112037
DI 10.1016/j.intimp.2024.112037
EA APR 2024
PG 19
WC Immunology; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology; Pharmacology & Pharmacy
GA RC8Y7
UT WOS:001225575700001
PM 38599100
DA 2025-01-04
ER

PT J
AU Vashishat, A
   Singh, A
   Das Kurmi, B
   Das Gupta, G
   Singh, D
AF Vashishat, Abhinav
   Singh, Amrinder
   Das Kurmi, Balak
   Das Gupta, Ghanshyam
   Singh, Dilpreet
TI A short appraisal of polylactic-co-glycolic acid based polymer
   nanotechnology for colon cancer: recent advances and literature
   evidences
SO THERAPEUTIC DELIVERY
LA English
DT Review
DE colon cancer; nanotechnology; PLGA; target delivery; theranostics
ID PLGA-BASED NANOPARTICLES; COLORECTAL-CANCER; PHYSICOCHEMICAL PROPERTIES;
   PHYSICAL-PROPERTIES; DRUG-DELIVERY; THERAPY; CURCUMIN; SURGERY
AB The currently available formulations provided non-targeted treatment of colon cancer, the deadliest cancer variant. Due to biopharmaceutical hindrances, the majority of the drugs are unable to reach the target site. Polylactic-co-glycolic acid (PLGA) is one of the versatile polymers in cancer treatment, diagnostics and theranostics. The unique mechanism of surface modifications in PLGA properties in colon cancer has been a keen interest to be used in different nanoparticles for improving biopharmaceutical attributes. The ongoing use of these smart nano-carriers has allowed targeted delivery of several active components on a wide scale. The main goal of this review is to compile information on PLGA-based nanocarriers which possess several desirable properties for drug delivery applications, including biocompatibility, biodegradability and tunable drug-release kinetics.
C1 [Vashishat, Abhinav; Das Kurmi, Balak; Das Gupta, Ghanshyam] ISF Coll Pharm, Dept Pharmaceut, GT Rd, Moga 142001, Punjab, India.
   [Singh, Amrinder] Chitkara Univ, Chitkara Coll Pharm, Rajpura 140417, Punjab, India.
   [Singh, Dilpreet] Chandigarh Univ, Univ Inst Pharmaceut Sci, Mohali 140413, India.
C3 ISF College of Pharmacy; Chitkara University, Punjab; Chandigarh
   University
RP Singh, D (corresponding author), Chandigarh Univ, Univ Inst Pharmaceut Sci, Mohali 140413, India.
EM dilpreet.daman@gmail.com
RI Singh, Dilpreet/AAE-1640-2019; Kurmi, Balak Das/AFQ-8334-2022
OI Singh, Dilpreet/0000-0002-2176-9420; Vashishat,
   Abhinav/0009-0007-5793-3134; Kurmi, Balak Das/0000-0001-8470-6622
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NR 66
TC 0
Z9 0
U1 1
U2 11
PU TAYLOR & FRANCIS LTD
PI ABINGDON
PA 2-4 PARK SQUARE, MILTON PARK, ABINGDON OR14 4RN, OXON, ENGLAND
SN 2041-5990
EI 2041-6008
J9 THER DELIV
JI Ther. Deliv.
PD JUL
PY 2023
VL 14
IS 7
DI 10.4155/tde-2023-0027
PG 14
WC Pharmacology & Pharmacy
WE Emerging Sources Citation Index (ESCI)
SC Pharmacology & Pharmacy
GA O6WA8
UT WOS:001045175000001
PM 37559461
DA 2025-01-04
ER

PT J
AU Li, BQ
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   Cai, YD
AF Li, Bi-Qing
   Huang, Guo-Hua
   Huang, Tao
   Feng, Kai-Yan
   Liu, Lei
   Cai, Yu-Dong
TI Prediction of Colorectal Cancer Related Genes Based on Gene Ontology
SO CURRENT BIOINFORMATICS
LA English
DT Article
DE Colorectal cancer; Gene Ontology; incremental feature selection; JRip;
   minimum redundancy maximum relevance
ID BETA-CATENIN; SYSTEMS BIOLOGY; CYCLIN D1; EXPRESSION; APOPTOSIS;
   PHOSPHORYLATION; ACTIVATION; PREVENTION; CELLS
AB Prediction and identification of cancer related genes are among of the most challenging and important problems in bioinformatics and biomedicine. Colorectal cancer (CRC), the second most commonly diagnosed cancer worldwide, is a major cause of cancer-related death. Knowledge of CRC-related genes may help to make an early detection of CRC and develop gene-targeted treatment schemes to significantly improve a patient's prognosis and reduce the mortality. The very first and basic steps one needs to take are the screening and identification of CRC-related genes. Here, we presented a computational method to predict CRC-related genes based on JRip, a rule abstracting algorithm, and optimized its data inputs by the maximum relevance minimum redundancy (mRMR) method and incremental feature selection (IFS). 77 genes were compiled from KEGG CRC pathway and through text mining as CRC-related gene candidates, while 385 other genes were randomly selected as the non-CRC gene candidates. All these 462 genes were encoded according to their Gene Ontology annotation, each producing a 2669-dimensional vector which was drastically reduced to 52 dimensions after feature selection. A rule set including 7 criteria was revealed by our method, yielding an overall prediction accuracy of 0.9242 and MCC of 0.7259. And analysis of the rule set and optimal features may shed some light on how CRC genes can be separated from non-CRC genes based on GO terms.
C1 [Huang, Guo-Hua; Cai, Yu-Dong] Shanghai Univ, Coll Life Sci, Shanghai, Peoples R China.
   [Li, Bi-Qing; Feng, Kai-Yan; Liu, Lei] Chinese Acad Sci, Shanghai Inst Biol Sci, Key Lab Syst Biol, Shanghai, Peoples R China.
   [Huang, Tao] Mt Sinai Sch Med, Dept Genet & Genom Sci, New York, NY USA.
C3 Shanghai University; Chinese Academy of Sciences; Icahn School of
   Medicine at Mount Sinai
RP Cai, YD (corresponding author), Shanghai Univ, Inst Syst Biol, Shanghai, Peoples R China.
EM cai_yud@yahoo.com.cn
RI Yang, Fan/B-2755-2012; Huang, Guohua/A-2215-2019
OI cai, yudong/0000-0001-5664-7979
FU National Basic Research Program of China [2011CB510101, 2011CB510102];
   Innovation Program of Shanghai Municipal Education Commission [12ZZ087];
   The First-class Discipline of Universities in Shanghai
FX This work was supported by grants from National Basic Research Program
   of China (2011CB510101, 2011CB510102), and Innovation Program of
   Shanghai Municipal Education Commission (12ZZ087) and the grant of "The
   First-class Discipline of Universities in Shanghai".
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NR 61
TC 0
Z9 0
U1 0
U2 3
PU BENTHAM SCIENCE PUBL LTD
PI SHARJAH
PA EXECUTIVE STE Y-2, PO BOX 7917, SAIF ZONE, 1200 BR SHARJAH, U ARAB
   EMIRATES
SN 1574-8936
EI 2212-392X
J9 CURR BIOINFORM
JI Curr. Bioinform.
PY 2015
VL 10
IS 1
BP 22
EP 30
DI 10.2174/157489361001150309131058
PG 9
WC Biochemical Research Methods; Mathematical & Computational Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Mathematical & Computational Biology
GA CD1DB
UT WOS:000350813000006
DA 2025-01-04
ER

PT J
AU Daemen, A
   Udyavar, AR
   Sandmann, T
   Li, CF
   Bosch, LJW
   O'Gorman, W
   Li, YJ
   Au-Yeung, A
   Takahashi, C
   Kabbarah, O
   Bourgon, R
   Hegde, P
   Bais, C
   Das Thakur, M
AF Daemen, Anneleen
   Udyavar, Akshata R.
   Sandmann, Thomas
   Li, Congfen
   Bosch, Linda J. W.
   O'Gorman, William
   Li, Yijin
   Au-Yeung, Amelia
   Takahashi, Chikara
   Kabbarah, Omar
   Bourgon, Richard
   Hegde, Priti
   Bais, Carlos
   Das Thakur, Meghna
TI Transcriptomic profiling of adjuvant colorectal cancer identifies three
   key prognostic biological processes and a disease specific role for
   granzyme B
SO PLOS ONE
LA English
DT Article
ID T-CELL EXHAUSTION; REGULARIZATION PATHS; COLON-CANCER; EXPRESSION; NK;
   PHENOTYPE; GENE; RECOMMENDATIONS; FLUOROURACIL; CHEMOTHERAPY
AB Background
   Colorectal cancer (CRC) is a leading cause of cancer-related deaths, with a 5% 5-year survival rate for metastatic disease, yet with limited therapeutic advancements due to insufficient understanding of and inability to accurately capture high-risk CRC patients who are most likely to recur. We aimed to improve high-risk classification by identifying biological pathways associated with outcome in adjuvant stage II/III CRC.
   Methods and findings
   We included 1062 patients with stage III or high-risk stage II colon carcinoma from the prospective three-arm randomized phase 3 AVANT trial, and performed expression profiling to identify a prognostic signature. Data from validation cohort GSE39582, The Cancer Genome Atlas, and cell lines were used to further validate the prognostic biology. Our retrospective analysis of the adjuvant AVANT trial uncovered a prognostic signature capturing three biological functions-stromal, proliferative and immune-that outperformed the Consensus Molecular Subtypes (CMS) and recurrence prediction signatures like Oncotype Dx in an independent cohort. Importantly, within the immune component, high granzyme B (GZMB) expression had a significant prognostic impact while other individual T-effector genes were less or not prognostic. In addition, we found GZMB to be endogenously expressed in CMS2 tumor cells and to be prognostic in a T cell independent fashion. A limitation of our study is that these results, although robust and derived from a large dataset, still need to be clinically validated in a prospective study.
   Conclusions
   This work furthers our understanding of the underlying biology that propagates stage II/III CRC disease progression and provides scientific rationale for future high-risk stratification and targeted treatment evaluation in biomarker defined subpopulations of resectable high-risk CRC. Our results also shed light on an alternative GZMB source with context-specific implications on the disease's unique biology.
C1 [Daemen, Anneleen; Udyavar, Akshata R.; Sandmann, Thomas; Bourgon, Richard] Genentech Inc, Bioinformat & Computat Biol, San Francisco, CA 94080 USA.
   [Li, Congfen; Bosch, Linda J. W.; Li, Yijin; Au-Yeung, Amelia; Kabbarah, Omar; Hegde, Priti; Bais, Carlos; Das Thakur, Meghna] Genentech Inc, Oncol Biomarker Dev, San Francisco, CA 94080 USA.
   [O'Gorman, William; Takahashi, Chikara] Genentech Inc, OMNI Biomarker Dev, San Francisco, CA 94080 USA.
   [Daemen, Anneleen] ORIC Pharmaceut, Translat Med, San Francisco, CA 94080 USA.
   [Udyavar, Akshata R.] Instill Bio, Thousand Oaks, CA USA.
   [Sandmann, Thomas] Denali Therapeut, Discovery Genom, San Francisco, CA USA.
   [Bosch, Linda J. W.] Netherlands Canc Inst, Amsterdam, Netherlands.
   [Kabbarah, Omar] Zai Lab, Discovery Biol & Translat Med, San Francisco, CA USA.
   [Bourgon, Richard] Freenome, Computat Sci, San Francisco, CA USA.
   [Hegde, Priti] Fdn Med, Cambridge, MA USA.
C3 Roche Holding; Genentech; Roche Holding; Genentech; Roche Holding;
   Genentech; Netherlands Cancer Institute; Foundation Medicine
RP Daemen, A (corresponding author), Genentech Inc, Bioinformat & Computat Biol, San Francisco, CA 94080 USA.; Das Thakur, M (corresponding author), Genentech Inc, Oncol Biomarker Dev, San Francisco, CA 94080 USA.; Daemen, A (corresponding author), ORIC Pharmaceut, Translat Med, San Francisco, CA 94080 USA.
EM anneleen.daemen@oricpharma.com; das-thakur.meghna@gene.com
RI Li, Yijin/JBS-7750-2023
OI Daemen, Anneleen/0000-0001-6287-7105
FU Genentech Inc.; Dutch Cancer Society (KWF Kankerbestrijding (NL))
   [2013-5885]
FX Funding for the study was provided by Genentech Inc., a member of the
   Roche group. Support for these studies was also provided by the Dutch
   Cancer Society (KWF Kankerbestrijding (NL), Award Number 2013-5885,
   Recipient Linda J.W. Bosch). These funders provided support in the form
   of salaries for all authors, but did not have any additional role in the
   study design, data collection and analysis, decision to publish, or
   preparation of the manuscript. The specific roles of these authors are
   articulated in the `author contributions' section.
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NR 57
TC 1
Z9 1
U1 0
U2 4
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD DEC 31
PY 2021
VL 16
IS 12
AR e0262198
DI 10.1371/journal.pone.0262198
PG 21
WC Multidisciplinary Sciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Science & Technology - Other Topics
GA ZZ9AO
UT WOS:000773555700106
PM 34972191
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Li, Y
   Duo, YH
   Zhai, P
   He, LS
   Zhong, KL
   Zhang, Y
   Huang, KB
   Luo, JF
   Zhang, H
   Yu, XF
AF Li, Yang
   Duo, Yanhong
   Zhai, Peng
   He, Lisheng
   Zhong, Keli
   Zhang, Yue
   Huang, Kaibin
   Luo, Jinfeng
   Zhang, Han
   Yu, Xiaofang
TI Dual targeting delivery of miR-328 by functionalized mesoporous silica
   nanoparticles for colorectal cancer therapy
SO NANOMEDICINE
LA English
DT Article
DE bevacizumab; CPTP; colorectal cancer therapy; dopamine; EpCAM aptamer;
   mesoporous silica nanoparticles; miR-328; multifunctional nanoplatform;
   nanomedicine; targeted delivery
ID DRUG-DELIVERY; IN-VIVO; SURFACE MODIFICATION; STEM-CELLS; EXPRESSION;
   EPCAM; MICRORNA; EFFICACY; DIFFERENTIATION; BEVACIZUMAB
AB Aim: We aim to explore the regulatory mechanism of miR-328 and further develop miR-328-loaded mesoporous silica nanoparticles (MSNs) and surface-decorated with polymerized dopamine, epithelial cell adhesion molecule aptamer and bevacizumab for the dual-targeting treatment of colorectal cancer (CRC). Materials & methods: The relationship between miR-328 and CPTP and the mechanism and antitumor effect of MSNs-miR-328@PDA-PEG-Apt-Bev were evaluated. Results: We found CPTP is a direct target of miR-328. Compared with other groups, MSNs-miR-328@PDA-PEG-Apt-Bev can significantly increase the level of miR-328 and inhibit the expression of CPTP in SW480 cells. The results exhibit this multifunctional bioconjugates can achieve an increased binding ability and much higher cytotoxicity to CRC both in vitro and in vivo. Conclusion: This multifunctional nanoplatform is a promising miRNA replacement therapy for CRC.
C1 [Li, Yang; Zhang, Yue; Yu, Xiaofang] Jinan Univ, Shenzhen Peoples Hosp, Clin Med Coll 2, Dept Hepatobiliary & Pancreas Surg, Shenzhen 518020, Peoples R China.
   [Li, Yang] Jinan Univ, Shenzhen Peoples Hosp, Clin Med Coll 2, Dept Emergency, Shenzhen 518020, Peoples R China.
   [Duo, Yanhong; Zhang, Han] Shenzhen Univ, Shenzhen Engn Lab Phosphorene & Optoelect, Key Lab Optoelect Devices & Syst, Minist Educ & Guangdong Prov,Coll Optoelect Engn, Shenzhen 518060, Peoples R China.
   [Zhai, Peng] Shenzhen Univ, Sch Med, Med Expt Ctr, Shenzhen 518060, Peoples R China.
   [He, Lisheng; Luo, Jinfeng] Jinan Univ, Shenzhen Peoples Hosp, Clin Med Coll 2, Dept Pathol, Shenzhen 518020, Peoples R China.
   [Zhong, Keli; Huang, Kaibin] Jinan Univ, Shenzhen Peoples Hosp, Clin Med Coll 2, Dept Gastrointestinal Surg, Shenzhen 518020, Peoples R China.
C3 Jinan University; Jinan University; Shenzhen University; Shenzhen
   University; Jinan University; Jinan University
RP Yu, XF (corresponding author), Jinan Univ, Shenzhen Peoples Hosp, Clin Med Coll 2, Dept Hepatobiliary & Pancreas Surg, Shenzhen 518020, Peoples R China.; Zhang, H (corresponding author), Shenzhen Univ, Shenzhen Engn Lab Phosphorene & Optoelect, Key Lab Optoelect Devices & Syst, Minist Educ & Guangdong Prov,Coll Optoelect Engn, Shenzhen 518060, Peoples R China.
EM hzhang@szu.edu.cn; yuxfshui@hotmail.com
RI wang, rui/JAC-6240-2023; Li, Yang/AAM-5383-2020; Huang,
   Kaibin/AAC-6346-2019; zhang, han/I-8297-2015
FU Science, Technology & Innovation Commission of Shenzhen Municipality
   [JCYJ20160422170206664, JCYJ20160422143333572]; Science and Technology
   Planning Project of Guangdong Province [2016B050501005]
FX This work was supported by the Science, Technology & Innovation
   Commission of Shenzhen Municipality (No. JCYJ20160422170206664), the
   Science, Technology & Innovation Commission of Shenzhen Municipality
   (No. JCYJ20160422143333572) and the Science and Technology Planning
   Project of Guangdong Province (2016B050501005). The authors have no
   other relevant affiliations or financial involvement with any
   organization or entity with a financial interest in or financial
   conflict with the subject matter or materials discussed in the
   manuscript apart from those disclosed.
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NR 48
TC 42
Z9 45
U1 0
U2 68
PU FUTURE MEDICINE LTD
PI LONDON
PA UNITEC HOUSE, 3RD FLOOR, 2 ALBERT PLACE, FINCHLEY CENTRAL, LONDON, N3
   1QB, ENGLAND
SN 1743-5889
EI 1748-6963
J9 NANOMEDICINE-UK
JI Nanomedicine
PD JUL
PY 2018
VL 13
IS 14
BP 1753
EP 1772
DI 10.2217/nnm-2017-0353
PG 20
WC Biotechnology & Applied Microbiology; Nanoscience & Nanotechnology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biotechnology & Applied Microbiology; Science & Technology - Other
   Topics
GA GV8AF
UT WOS:000446356400006
PM 30084727
DA 2025-01-04
ER

PT J
AU Liu, YL
   Yang, F
   Xiao, WW
   Liu, RW
   Zhang, HY
   Li, XC
   Ajena, YH
   Lam, KS
   Leung, JW
AF Liu, Yanlei
   Yang, Fan
   Xiao, Wenwu
   Liu, Ruiwu
   Zhang, Hongyong
   Li, Xiaocen
   Ajena, Yousif H.
   Lam, Kit S.
   Leung, Joseph W.
TI Discovery of specific targeting ligands as the biomarkers for colorectal
   cancer
SO COLORECTAL CANCER
LA English
DT Article
DE biomarker; colorectal cancer; one-bead one-compound library; optical
   imaging; peptide
ID PEPTIDE LIBRARY; COMBINATORIAL; CHEMOTHERAPY; DELIVERY
AB Aim: Targeted diagnosis and therapy for colorectal cancer (CRC) is limited by the lack of specific biomarkers. Our aim was to discover CRC-specific targeting ligands using a one-bead one-compound (OBOC) combinatorial library. Method: Samples of OBOC peptide libraries were color coded, mixed and incubated with commercially available human CRC cells (HT-29 and DLD-1). Libraries with compound beads that bound to CRC cells were selected for further screening. Compound beads that bound to both CRC cells were screened with human colonic epithelial cells to select beads that bound only to CRC cells but not to human colonic epithelial cells. Chemical structures of the positive peptides were determined by Edman chemistry. CRC-targeted imaging agents were developed by conjugation of CRC binding peptide with biotin through a hydrophilic linker and then complexed with streptavidin-Cy5.5. Immunohistochemistry studies were used to evaluate CRC detection efficacy. Targeting specificity was further tested with subcutaneous CRC xenografts in nude mice. Results: Two cyclic peptides, CRC-6 and CRC-9, composed of natural and unnatural amino acids, bind specifically to CRC cells with moderately high affinity and specificity. CRC-9 is able to detect CRC cells grown on chamber slides at the concentration of 1 mu M after 30 min incubation. Tail vein injection of 1.8 nmol biotinylated peptide CRC-9, complexed with streptavidin-Cy5.5 (SA-Cy5.5), is able to target the subcutaneous CRC xenograft implants in nude mice. None of the two peptides showed cytotoxic effect on human blood cells, up to the concentration of 500 mu M. Conclusion: CRC-9 has the potential to be developed as an effective biomarker for improving the management of CRC patients by enhancing the efficiency of detection and efficacy of targeting treatment.
C1 [Liu, Yanlei; Leung, Joseph W.] UC Davis Med Ctr, Div Gastroenterol & Hepatol, Sacramento, CA 95817 USA.
   [Yang, Fan] Harvard Sch Dent Med, Dept Oral Med Infect & Immun, AGE Periodont, Boston, MA 02115 USA.
   [Xiao, Wenwu; Liu, Ruiwu; Zhang, Hongyong; Li, Xiaocen; Ajena, Yousif H.; Lam, Kit S.] Univ Calif Davis, Dept Biochem & Mol Med, Sacramento, CA 95817 USA.
   [Leung, Joseph W.] VA Northern Calif Hlth Care Syst, Dept Gastroenterol, Sacramento, CA 95655 USA.
C3 University of California System; University of California Davis; Harvard
   University; Harvard School of Dental Medicine; University of California
   System; University of California Davis
RP Leung, JW (corresponding author), UC Davis Med Ctr, Div Gastroenterol & Hepatol, Sacramento, CA 95817 USA.; Leung, JW (corresponding author), VA Northern Calif Hlth Care Syst, Dept Gastroenterol, Sacramento, CA 95655 USA.
EM jwleung@ucdavis.edu
RI Lam, Kit/JXL-8846-2024; zhao, yuanxin/KDO-9377-2024
FU NIH [5R21DK66362-2]; CW Law Biofilm Research Fund
FX The study was supported in part by NIH grant (5R21DK66362-2; JW Leung)
   and the CW Law Biofilm Research Fund. The authors have no other relevant
   affiliations or financial involvement with any organization or entity
   with a financial interest in or financial conflict with the subject
   matter or materials discussed in the manuscript apart from those
   disclosed.
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NR 35
TC 1
Z9 1
U1 0
U2 9
PU FUTURE MEDICINE LTD
PI LONDON
PA UNITEC HOUSE, 3RD FLOOR, 2 ALBERT PLACE, FINCHLEY CENTRAL, LONDON, N3
   1QB, ENGLAND
SN 1758-194X
EI 1758-1958
J9 COLORECTAL CANCER
JI Colorectal Cancer
PD DEC
PY 2017
VL 6
IS 4
BP 121
EP 130
DI 10.2217/crc-2017-0017
PG 10
WC Oncology
WE Emerging Sources Citation Index (ESCI)
SC Oncology
GA GR9FK
UT WOS:000443052900004
OA gold
DA 2025-01-04
ER

PT J
AU Mendelaar, PAJ
   Smid, M
   van Riet, J
   Angus, L
   Labots, M
   Steeghs, N
   Hendriks, MP
   Cirkel, GA
   van Rooijen, JM
   Ten Tije, AJ
   Lolkema, MP
   Cuppen, E
   Sleijfer, S
   Martens, JWM
   Wilting, SM
AF Mendelaar, Pauline A. J.
   Smid, Marcel
   van Riet, Job
   Angus, Lindsay
   Labots, Mariette
   Steeghs, Neeltje
   Hendriks, Mathijs P.
   Cirkel, Geert A.
   van Rooijen, Johan M.
   Ten Tije, Albert J.
   Lolkema, Martijn P.
   Cuppen, Edwin
   Sleijfer, Stefan
   Martens, John W. M.
   Wilting, Saskia M.
TI Whole genome sequencing of metastatic colorectal cancer reveals prior
   treatment effects and specific metastasis features
SO NATURE COMMUNICATIONS
LA English
DT Article
ID SIGNATURES; COLON; GENE
AB In contrast to primary colorectal cancer (CRC) little is known about the genomic landscape of metastasized CRC. Here we present whole genome sequencing data of metastases of 429 CRC patients participating in the pan-cancer CPCT-02 study (NCT01855477). Unsupervised clustering using mutational signature patterns highlights three major patient groups characterized by signatures known from primary CRC, signatures associated with received prior treatments, and metastasis-specific signatures. Compared to primary CRC, we identify additional putative (non-coding) driver genes and increased frequencies in driver gene mutations. In addition, we identify specific genes preferentially affected by microsatellite instability. CRC-specific 1kb-10Mb deletions, enriched for common fragile sites, and LINC00672 mutations are associated with response to treatment in general, whereas FBXW7 mutations predict poor response specifically to EGFR-targeted treatment. In conclusion, the genomic landscape of mCRC shows defined changes compared to primary CRC, is affected by prior treatments and contains features with potential clinical relevance. Molecular landscapes of metastatic colorectal cancers (mCRC) have often been restricted to coding regions or low numbers of patients. Here the authors present a whole-genome landscape of 429 mCRC patients, revealing the mutational impact of prior therapies and potential actionable targets.
C1 [Mendelaar, Pauline A. J.; Smid, Marcel; van Riet, Job; Angus, Lindsay; Lolkema, Martijn P.; Sleijfer, Stefan; Martens, John W. M.; Wilting, Saskia M.] Erasmus Univ, Erasmus MC, Canc Inst, Dept Med Oncol, Rotterdam, Netherlands.
   [Labots, Mariette] Vrije Univ Amsterdam, Amsterdam UMC, Canc Ctr Amsterdam, Dept Med Oncol, Amsterdam, Netherlands.
   [Labots, Mariette; Steeghs, Neeltje; Hendriks, Mathijs P.; Cirkel, Geert A.; van Rooijen, Johan M.; Ten Tije, Albert J.; Lolkema, Martijn P.; Sleijfer, Stefan; Martens, John W. M.] Ctr Personalized Canc Treatment, Rotterdam, Netherlands.
   [Steeghs, Neeltje] Netherlands Canc Inst, Dept Med Oncol, Amsterdam, Netherlands.
   [Hendriks, Mathijs P.] Northwest Clin, Dept Med Oncol, Alkmaar, Netherlands.
   [Cirkel, Geert A.] Meander Med Ctr, Dept Med Oncol, Amersfoort, Netherlands.
   [van Rooijen, Johan M.] Martini Hosp, Dept Med Oncol, Groningen, Netherlands.
   [Ten Tije, Albert J.] Amphia Hosp, Dept Med Oncol, Breda, Netherlands.
   [Cuppen, Edwin] Univ Med Ctr Utrecht, Ctr Mol Med, Utrecht, Netherlands.
   [Cuppen, Edwin] Univ Med Ctr Utrecht, Oncode Inst, Utrecht, Netherlands.
   [Cuppen, Edwin] Hartwig Med Fdn, Amsterdam, Netherlands.
C3 Erasmus University Rotterdam; Erasmus MC; Erasmus MC Cancer Institute;
   University of Amsterdam; Vrije Universiteit Amsterdam; Netherlands
   Cancer Institute; Meander Medisch Centrum; Martini Hospital; Amphia
   Hospital; Utrecht University; Utrecht University Medical Center; Utrecht
   University; Utrecht University Medical Center
RP Wilting, SM (corresponding author), Erasmus Univ, Erasmus MC, Canc Inst, Dept Med Oncol, Rotterdam, Netherlands.
EM s.wilting@erasmusmc.nl
RI Labots, Mariette/J-9731-2013; Hendriks, Mathijs/AGR-5663-2022; Steeghs,
   Neeltje/GQH-3468-2022; Cuppen, Edwin/H-2389-2016; Lolkema,
   M.P./AAE-2906-2019
OI Mendelaar, Pauline A.J./0000-0002-1496-9627; Labots,
   Mariette/0000-0002-7095-1771; Wilting, Saskia/0000-0002-2838-841X; van
   Riet, Job/0000-0001-7767-7923; Hendriks, Mathijs/0000-0001-6687-5393;
   Steeghs, Neeltje/0000-0003-2989-2279; Angus,
   Lindsay/0000-0002-7928-1102; Lolkema, Martijn/0000-0003-0466-2928
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NR 46
TC 43
Z9 45
U1 0
U2 7
PU NATURE PORTFOLIO
PI BERLIN
PA HEIDELBERGER PLATZ 3, BERLIN, 14197, GERMANY
EI 2041-1723
J9 NAT COMMUN
JI Nat. Commun.
PD JAN 25
PY 2021
VL 12
IS 1
AR 574
DI 10.1038/s41467-020-20887-6
PG 11
WC Multidisciplinary Sciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Science & Technology - Other Topics
GA UA0CS
UT WOS:000684834100019
PM 33495476
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Polk, N
   Budai, B
   Hitre, E
   Patocs, A
   Mersich, T
AF Polk, Nandor
   Budai, Barna
   Hitre, Erika
   Patocs, Attila
   Mersich, Tamas
TI High Neutrophil-To-Lymphocyte Ratio (NLR) and Systemic
   Immune-Inflammation Index (SII) Are Markers of Longer Survival After
   Metastasectomy of Patients With Liver-Only Metastasis of Rectal Cancer
SO PATHOLOGY & ONCOLOGY RESEARCH
LA English
DT Article
DE neutrophil-to-lymphocyte ratio; liver-only metastases of rectal cancer;
   metastasectomy; relapse-free survival; systemic immune-inflammation
   index; liver-only metastases of colon cancer; preoperative treatment
ID COLORECTAL-CANCER; PROGNOSTIC VALUE; PREOPERATIVE NEUTROPHIL;
   POOR-PROGNOSIS; RESECTION; TUMOR; COLON; EXPRESSION; PATTERN; PREDICT
AB Background: The literature data regarding colon cancer patients with liver-only metastases (CLM) show that NLR determined before metastasectomy is a prognostic marker of shorter relapse-free survival (RFS), but no results has been reported to date for rectal cancer patients with liver-only metastases (RLM). This study aimed to investigate the NLR and SII in CLM and RLM.Methods: Relapse-free (RFS) and overall survival (OS) were evaluated in 67 CLM and 103 RLM patients with a median follow-up of 46.5 and 59.8 months, respectively. Pre- and/or postoperative chemotherapy +/- targeted treatment was applied in 96% and 87% of CLM and RLM patients, respectively. The cut-off level for hematologic parameters were determined by receiver operating characteristic (ROC) analysis. Univariate analysis was performed by Kaplan-Meier method and log rank test. For multivariate analysis Cox regression was applied.Results: In univariate analysis low NLR (cut-off 2) and SII (535) were predictors of longer RFS in case of CLM (p < 0.01). In contrast, for RLM high NLR (2.42) and SII (792) were predictors of longer RFS (p < 0.001). For RLM both NLR and SII proved to be independent markers of RFS (HR 0.66 (95% CI 0.52-0.84) and 0.73 (0.57-0.91), respectively) and OS (0.76 (0.58-0.99) and 0.66 (0.5-0.87), respectively). Only NLR (1.44 (1.04-1.99)) was independent marker of RFS for CLM. The preoperative treatment has not influenced the role of NLR or SII.Conclusion: In contrast to CLM, in RLM the high NLR or SII determined before metastasectomy proved to be independent prognostic factors of longer RFS and OS.
C1 [Polk, Nandor; Mersich, Tamas] Natl Inst Oncol, Departmet Visceral Surg, Budapest, Hungary.
   [Budai, Barna; Patocs, Attila] Natl Inst Oncol, Dept Mol Genet, Budapest, Hungary.
   [Hitre, Erika] Natl Inst Oncol, Med Oncol & Clin Pharmacol Dept B, Budapest, Hungary.
   [Patocs, Attila] Natl Inst Oncol, Clin Cent Lab, Budapest, Hungary.
   [Patocs, Attila] Semmelweis Univ, Dept Lab Med, Budapest, Hungary.
C3 National Institute of Oncology Hungary; National Institute of Oncology
   Hungary; National Institute of Oncology Hungary; National Institute of
   Oncology Hungary; Semmelweis University
RP Budai, B (corresponding author), Natl Inst Oncol, Dept Mol Genet, Budapest, Hungary.
EM budai.barna@oncol.hu
FU National Laboratories Excellence program (under the National
   Tumorbiology Laboratory project) [(NLP-17)]; Hungarian Thematic
   Excellence Programme [TKP2020-NKA-26]
FX TM acknowledges financial support from the National Laboratories
   Excellence program (under the National Tumorbiology Laboratory project
   (NLP-17)) and the Hungarian Thematic Excellence Programme
   (TKP2020-NKA-26).
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NR 45
TC 11
Z9 11
U1 0
U2 5
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 1219-4956
EI 1532-2807
J9 PATHOL ONCOL RES
JI Pathol. Oncol. Res.
PD APR 27
PY 2022
VL 28
AR 1610315
DI 10.3389/pore.2022.1610315
PG 14
WC Oncology; Pathology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Pathology
GA 1H7KA
UT WOS:000796716800001
PM 35570841
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Wang, XJ
   Wu, F
   Wang, H
   Duan, XY
   Huang, R
   Tuersuntuoheti, A
   Su, LY
   Yan, SD
   Zhao, YC
   Lu, Y
   Li, K
   Yao, JJ
   Luo, ZW
   Guo, L
   Liu, JM
   Chen, X
   Lu, YL
   Hu, HJ
   Li, XC
   Bao, M
   Bi, XY
   Du, BY
   Miao, SY
   Cai, JD
   Wang, LF
   Zhou, HT
   Ying, JM
   Song, W
   Zhao, H
AF Wang, Xiaojuan
   Wu, Fan
   Wang, Han
   Duan, Xiaoyuan
   Huang, Rong
   Tuersuntuoheti, Amannisa
   Su, Luying
   Yan, Shida
   Zhao, Yuechao
   Lu, Yan
   Li, Kai
   Yao, Jinjie
   Luo, Zhiwen
   Guo, Lei
   Liu, Jianmei
   Chen, Xiao
   Lu, Yalan
   Hu, Hanjie
   Li, Xingchen
   Bao, Mandula
   Bi, Xinyu
   Du, Boyu
   Miao, Shiying
   Cai, Jiandiang
   Wang, Linfang
   Zhou, Haitao
   Ying, Jianming
   Song, Wei
   Zhao, Hong
TI PDCD6 cooperates with C-Raf to facilitate colorectal cancer progression
   via Raf/MEK/ERK activation
SO JOURNAL OF EXPERIMENTAL & CLINICAL CANCER RESEARCH
LA English
DT Article
DE PDCD6; Colorectal cancer; Growth; MAPK signaling pathway
ID CELL-PROLIFERATION; REGULATES RAF-1; ALG-2 INTERACTS; MAPK PATHWAY;
   ANNEXIN-XI; PROTEIN; INHIBITOR; APOPTOSIS; DOMAIN; DEATH
AB Background Colorectal cancer (CRC) is one of the most common malignancies, and it's expected that the CRC burden will substantially increase in the next two decades. New biomarkers for targeted treatment and associated molecular mechanism of tumorigenesis remain to be explored. In this study, we investigated whether PDCD6 plays an oncogenic role in colorectal cancer and its underlying mechanism. Methods Programmed cell death protein 6 (PDCD6) expression in CRC samples were analyzed by immunohistochemistry and immunofluorescence. The prognosis between PDCD6 and clinical features were analyzed. The roles of PDCD6 in cellular proliferation and tumor growth were measured by using CCK8, colony formation, and tumor xenograft in nude mice. RNA-sequence (RNA-seq), Mass Spectrum (MS), Co-Immunoprecipitation (Co-IP) and Western blot were utilized to investigate the mechanism of tumor progression. Immunohistochemistry (IHC) and quantitative real-time PCR (qRT-PCR) were performed to determine the correlation of PDCD6 and MAPK pathway. Results Higher expression levels of PDCD6 in tumor tissues were associated with a poorer prognosis in patients with CRC. Furthermore, PDCD6 increased cell proliferation in vitro and tumor growth in vivo. Mechanistically, RNA-seq showed that PDCD6 could affect the activation of the MAPK signaling pathway. PDCD6 interacted with c-Raf, resulting in the activation of downstream c-Raf/MEK/ERK pathway and the upregulation of core cell proliferation genes such as MYC and JUN. Conclusions These findings reveal the oncogenic effect of PDCD6 in CRC by activating c-Raf/MEK/ERK pathway and indicate that PDCD6 might be a potential prognostic indicator and therapeutic target for patients with colorectal cancer.
C1 [Wang, Xiaojuan; Wu, Fan; Wang, Han; Duan, Xiaoyuan; Huang, Rong; Tuersuntuoheti, Amannisa; Su, Luying; Zhao, Yuechao; Lu, Yan; Li, Kai; Lu, Yalan; Miao, Shiying; Wang, Linfang; Song, Wei] Chinese Acad Med Sci & Peking Union Med Coll, Inst Basic Med Sci, Dept Biochem & Mol Biol, State Key Lab Med Mol Biol, Beijing 100005, Peoples R China.
   [Wang, Xiaojuan] TsinghuaUniv, State Key Lab Membrane Biol, Tsinghua Univ Peking Univ Joint Ctr Life Sci, Sch Life Sci, Beijing 100084, Peoples R China.
   [Yan, Shida; Yao, Jinjie; Luo, Zhiwen; Guo, Lei; Liu, Jianmei; Chen, Xiao; Hu, Hanjie; Li, Xingchen; Bao, Mandula; Bi, Xinyu; Cai, Jiandiang; Zhou, Haitao; Ying, Jianming; Zhao, Hong] Chinese Acad Med Sci & Peking Union Med Coll, Dept Hepatobiliary Surg, State Key Lab Mol Oncol, Natl Canc Ctr,Natl Clin Res Ctr Canc,Canc Hosp, Beijing 100021, Peoples R China.
   [Yan, Shida; Yao, Jinjie; Luo, Zhiwen; Guo, Lei; Liu, Jianmei; Chen, Xiao; Hu, Hanjie; Li, Xingchen; Bao, Mandula; Bi, Xinyu; Cai, Jiandiang; Zhou, Haitao; Ying, Jianming; Zhao, Hong] Chinese Acad Med Sci & Peking Union Med Coll, Dept Pathol, State Key Lab Mol Oncol, Natl Canc Ctr,Natl Clin Res Ctr Canc,Canc Hosp, Beijing 100021, Peoples R China.
   [Bi, Xinyu; Zhou, Haitao; Ying, Jianming; Zhao, Hong] Chinese Acad Med Sci & Peking Union Med Coll, Key Lab Gene Editing Screening & R&D Digest Syst, Beijing 100021, Peoples R China.
   [Du, Boyu] Hubei Univ Med, Dept Med Biol, Sch Basic Med Sci, Shiyan 442000, Peoples R China.
C3 Chinese Academy of Medical Sciences - Peking Union Medical College;
   Peking Union Medical College; Chinese Academy of Medical Sciences -
   Peking Union Medical College; Peking Union Medical College; Cancer
   Institute & Hospital - CAMS; Chinese Academy of Medical Sciences -
   Peking Union Medical College; Cancer Institute & Hospital - CAMS; Peking
   Union Medical College; Chinese Academy of Medical Sciences - Peking
   Union Medical College; Peking Union Medical College; Hubei University of
   Medicine
RP Song, W (corresponding author), Chinese Acad Med Sci & Peking Union Med Coll, Inst Basic Med Sci, Dept Biochem & Mol Biol, State Key Lab Med Mol Biol, Beijing 100005, Peoples R China.; Ying, JM; Zhao, H (corresponding author), Chinese Acad Med Sci & Peking Union Med Coll, Dept Hepatobiliary Surg, State Key Lab Mol Oncol, Natl Canc Ctr,Natl Clin Res Ctr Canc,Canc Hosp, Beijing 100021, Peoples R China.; Ying, JM; Zhao, H (corresponding author), Chinese Acad Med Sci & Peking Union Med Coll, Dept Pathol, State Key Lab Mol Oncol, Natl Canc Ctr,Natl Clin Res Ctr Canc,Canc Hosp, Beijing 100021, Peoples R China.; Ying, JM; Zhao, H (corresponding author), Chinese Acad Med Sci & Peking Union Med Coll, Key Lab Gene Editing Screening & R&D Digest Syst, Beijing 100021, Peoples R China.
EM jmying@hotmail.com; songwei@ibms.pumc.edu.cn; zhaohong@cicams.ac.cn
RI Du, Boyu/LTF-8289-2024; WU, FAN/P-3132-2015; Zhao, Hong/IUQ-0043-2023;
   yan, shida/JCC-4254-2023; Wang, Zhen/KCL-5193-2024
OI Song, Wei/0000-0002-8395-9991
FU CAMS Innovation Fund for Medical Sciences [2016-I2M-1-001,
   2017-I2M-3-009, 2017-12 M-4-002]; National Key Research and Development
   Program of China [2018YFC1003500]; National Natural Science Foundation
   of China [81672472, 81672461, 31725013]; National Key Basic Research
   Program of China [2015CB943001]; State Key Project on Infection Diseases
   of China [2017ZX10201021-007-003]; State Key Laboratory Special fund
   from the Ministry of Science [2060204]
FX This work was supported by grants from the CAMS Innovation Fund for
   Medical Sciences (2016-I2M-1-001, 2017-I2M-3-009, and 2017-12 M-4-002),
   the National Key Research and Development Program of China (No.
   2018YFC1003500), the National Natural Science Foundation of China
   (81672472, 81672461, and 31725013), the National Key Basic Research
   Program of China (2015CB943001), the State Key Project on Infection
   Diseases of China (2017ZX10201021-007-003), and the State Key Laboratory
   Special fund from the Ministry of Science (2060204).
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NR 55
TC 16
Z9 17
U1 1
U2 10
PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
EI 1756-9966
J9 J EXP CLIN CANC RES
JI J. Exp. Clin. Cancer Res.
PD AUG 3
PY 2020
VL 39
IS 1
AR 147
DI 10.1186/s13046-020-01632-9
PG 15
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA NB3CX
UT WOS:000560391700001
PM 32746883
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Yan, LJ
   Chen, X
   Bian, ZL
   Gu, CY
   Ji, HZ
   Chen, LY
   Xu, HF
   Tang, QY
AF Yan, Lijun
   Chen, Xi
   Bian, Zhaolian
   Gu, Chunyan
   Ji, Hanzhen
   Chen, Liyan
   Xu, Haifeng
   Tang, Qiyun
TI A ferroptosis associated gene signature for predicting prognosis and
   immune responses in patients with colorectal carcinoma
SO FRONTIERS IN GENETICS
LA English
DT Article
DE colorectal carcinoma; ferroptosis; gene signature; prognosis; immune
   response
ID REGULATORY MECHANISMS; CANCER; EXPRESSION; SURVIVAL; IMMUNOTHERAPY;
   METABOLISM
AB Background: Colorectal carcinoma (CRC) is one of the most prevalent malignancies globally. Ferroptosis, a novel type of cell death, is critical in the development and treatment of tumors.Objective: This study was designed to establish a genetic signature for ferroptosis which has a predictive effect on the outcomes and immunotherapeutic response of CRC.Methods: Data of CRC patients were retrieved from TCGA and GEO databases. The genes associated with ferroptosis were obtained from GeneCards. The genetic signature for ferroptosis was identified by performing Cox regression analysis. Kaplan-Meier and ROC analysis were performed to assess the prognosis role of the genetic signature. CIBERSORT tool was used to identify a potential association of the genetic signature with the immune cells. The potential immunotherapeutic signatures and drug sensitivity prediction targeting this signature were also discussed. Immunohistochemistry was used to detect expression of ferroptosis-associated genes in CRC tissues and adjacent tissues.Results: A ferroptosis-associated gene signature comprised of three genes (CDKN2A, FDFT1, and ACSL6) was developed for prediction of prognosis and evaluation of immune responses in CRC. Patients in the high-risk group tended to have a poor prognosis. In CRC, the ferroptosis-associated gene signature may function as independent predictors. Additionally, the expressional levels of the immune checkpoint proteins PD-L1 and CTLA-4 were substantially increased in the high-risk group. Moreover, we can distinguish between patients based on their immunotherapeutic responses more effectively if we categorize them by this signature. Additionally, candidate compounds were identified for the differentiation of CRC subtypes.Conclusion: The ferroptosis-associated gene signature identified in this study is effective in predicting the prognosis and evaluating immunotherapeutic response in CRC patients, and provides us with novel insights into the potential effect of ferroptosis targeted treatment on CRC.
C1 [Yan, Lijun; Tang, Qiyun] Nanjing Med Univ, Affiliated Hosp 1, Inst Neuroendocrine Tumor, Dept Geriatr Gastroenterol, Nanjing, Peoples R China.
   [Yan, Lijun; Xu, Haifeng] Nantong Univ, Nantong Peoples Hosp Affiliated 3, Dept Hepatol, Nantong, Peoples R China.
   [Chen, Xi] Nanjing Med Univ, Taizhou Peoples Hosp, Taizhou Clin Med Sch, Dept Endocrinol, Taizhou, Peoples R China.
   [Bian, Zhaolian; Gu, Chunyan; Chen, Liyan] Nantong Univ, Nantong Peoples Hosp Affiliated 3, Dept Gastroenterol, Nantong, Peoples R China.
   [Ji, Hanzhen] Nantong Univ, Nantong Peoples Hosp Affiliated 3, Dept Lib, Nantong, Peoples R China.
C3 Nanjing Medical University; Nantong University; Nanjing Medical
   University; Nantong University; Nantong University
RP Tang, QY (corresponding author), Nanjing Med Univ, Affiliated Hosp 1, Inst Neuroendocrine Tumor, Dept Geriatr Gastroenterol, Nanjing, Peoples R China.; Xu, HF (corresponding author), Nantong Univ, Nantong Peoples Hosp Affiliated 3, Dept Hepatol, Nantong, Peoples R China.
EM 172905408@qq.com; tqy831@163.com
RI Chen, Liyan/B-2555-2010; Xu, Haifeng/AIC-5767-2022; lijun,
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OI lijun, yan/0000-0002-5993-273X
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NR 59
TC 7
Z9 7
U1 1
U2 9
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
EI 1664-8021
J9 FRONT GENET
JI Front. Genet.
PD SEP 8
PY 2022
VL 13
AR 971364
DI 10.3389/fgene.2022.971364
PG 16
WC Genetics & Heredity
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Genetics & Heredity
GA 4W7CI
UT WOS:000860315800001
PM 36160009
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Martínez-Pérez, J
   Torrado, C
   Domínguez-Cejudo, MA
   Valladares-Ayerbes, M
AF Martinez-Perez, Julia
   Torrado, Carlos
   Dominguez-Cejudo, Maria A.
   Valladares-Ayerbes, Manuel
TI Targeted Treatment against Cancer Stem Cells in Colorectal Cancer
SO INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
LA English
DT Review
DE cancer stem cell; colorectal cancer; molecular targeted therapies;
   clinical trial
ID I DOSE-ESCALATION; ACUTE MYELOID-LEUKEMIA; ADVANCED SOLID TUMORS;
   PHASE-I; INHIBITOR BEZ235; TRIAL; COMBINATION; IRINOTECAN; OLAPARIB;
   THERAPY
AB The cancer stem cell (SC) theory proposes that a population of SCs serves as the driving force behind fundamental tumor processes, including metastasis, recurrence, and resistance to therapy. The standard of care for patients with stage III and high-risk stage II colorectal cancer (CRC) includes surgery and adjuvant chemotherapy. Fluoropyrimidines and their combination with oxaliplatin increased the cure rates, being able to eradicate the occult metastatic SC in a fraction of patients. The treatment for unresectable metastatic CRC is based on chemotherapy, antibodies to VEGF and EGFR, and tyrosine-kinase inhibitors. Immunotherapy is used in MSI-H tumors. Currently used drugs target dividing cells and, while often effective at debulking tumor mass, these agents have largely failed to cure metastatic disease. SCs are generated either due to genetic and epigenetic alterations in stem/progenitor cells or to the dedifferentiation of somatic cells where diverse signaling pathways such as Wnt/beta-catenin, Hedgehog, Notch, TGF-beta/SMAD, PI3K/Akt/mTOR, NF-kappa B, JAK/STAT, DNA damage response, and Hippo-YAP play a key role. Anti-neoplastic treatments could be improved by elimination of SCs, becoming an attractive target for the design of novel agents. Here, we present a review of clinical trials assessing the efficacy of targeted treatment focusing on these pathways in CRC.
C1 [Martinez-Perez, Julia; Valladares-Ayerbes, Manuel] Hosp Univ Virgen Rocio HUVR, Med Oncol Dept, Ave Manuel Siurot s-n, Seville 41013, Spain.
   [Martinez-Perez, Julia; Dominguez-Cejudo, Maria A.; Valladares-Ayerbes, Manuel] Univ Seville, Hosp Univ Virgen Rocio HUVR, Inst Biomed Sevilla IBiS, Consejo Super Invest Cient CSIC, Ave Manuel Siurot S-N, Seville 41013, Spain.
   [Torrado, Carlos] Univ Texas MD Anderson Canc Ctr, Dept Invest Canc Therapeut, Houston, TX 77030 USA.
C3 Consejo Superior de Investigaciones Cientificas (CSIC); University of
   Sevilla; CSIC-JA-USE - Instituto de Biomedicina de Sevilla (IBIS);
   University of Texas System; UTMD Anderson Cancer Center
RP Valladares-Ayerbes, M (corresponding author), Hosp Univ Virgen Rocio HUVR, Med Oncol Dept, Ave Manuel Siurot s-n, Seville 41013, Spain.; Valladares-Ayerbes, M (corresponding author), Univ Seville, Hosp Univ Virgen Rocio HUVR, Inst Biomed Sevilla IBiS, Consejo Super Invest Cient CSIC, Ave Manuel Siurot S-N, Seville 41013, Spain.
EM julia0802@hotmail.com; ctorrado@mdanderson.org; mdcejudo-ibis@us.es;
   mvalaye@icloud.com
RI Valladares'Ayerbes, MANUEL/LDG-3881-2024; Valladares-Ayerbes,
   Manuel/K-8986-2014
OI Valladares-Ayerbes, Manuel/0000-0002-7950-9584
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NR 130
TC 7
Z9 7
U1 3
U2 3
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
SN 1661-6596
EI 1422-0067
J9 INT J MOL SCI
JI Int. J. Mol. Sci.
PD JUN
PY 2024
VL 25
IS 11
AR 6220
DI 10.3390/ijms25116220
PG 20
WC Biochemistry & Molecular Biology; Chemistry, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Chemistry
GA UA3C8
UT WOS:001245293400001
PM 38892410
OA gold
DA 2025-01-04
ER

PT J
AU Yan, W
   Qiu, L
   Yang, ML
   Xu, AR
   Ma, MQ
   Yuan, QZ
   Ma, XC
   Liang, WJ
   Li, XN
   Lu, YX
AF Yan, Wei
   Qiu, Lin
   Yang, Meiling
   Xu, Anran
   Ma, Manqi
   Yuan, Qinzi
   Ma, Xiaochen
   Liang, Wenjuan
   Li, Xuenong
   Lu, Yanxia
TI CXCL10 mediates CD8+T cells to facilitate vessel normalization and
   improve the efficacy of cetuximab combined with PD-1 checkpoint
   inhibitors in colorectal cancer
SO CANCER LETTERS
LA English
DT Article
DE CXCL10; VCAN; Vascular normalization; Anti-EGFR; Immunotherapy
ID TUMOR ANGIOGENESIS; IMMUNE; CHEMOKINES; VERSICAN; THERAPY
AB The immunotherapy and anti-EGFR targeted treatment occupying a pivotal position in colorectal cancer (CRC), is still limited to a group of patients who display specific molecular alterations and inevitably escape from resistance, further studies are still needed in colorectal cancer. We found that chemokine ligand 10 (CXCL10) expression correlates with intratumoral CD8+ T cell infiltration and reprograms tumor vasculatures in colorectal cancer. CXCL10 overexpression not only suppressed tumor growth but also increased CD8+ T cell infiltration and induced tumor vascular normalization in vivo. Additionally, the growth inhibition and tumor vascular normalization induced by CXCL10 can be reversed by the depletion of CD8+ T cells in vivo. Mechanically, CXCL10 interacts with VCAN to mediate tumor vascular normalization. The VCAN expression correlated inversely with the expression of CXCL10 and the infiltration of CD8+ T cells in CRC. Elevated CXCL10 expression sensitized colorectal cancer cells to cetuximab/anti-PD1 combination therapy compared with cetuximab or antiPD1 alone. We propose that CXCL10 could be used to increase the anti-EGFR therapy and immunotherapy effect, targeting both tumor vessels and immune cells in colorectal cancer.
C1 [Yang, Meiling; Xu, Anran; Ma, Manqi; Yuan, Qinzi; Liang, Wenjuan; Li, Xuenong; Lu, Yanxia] Southern Med Univ, Nanfang Hosp, Dept Pathol, Guangzhou, Guangdong, Peoples R China.
   [Yang, Meiling; Xu, Anran; Ma, Manqi; Yuan, Qinzi; Liang, Wenjuan; Li, Xuenong; Lu, Yanxia] Southern Med Univ, Sch Basic Med Sci, Dept Pathol, Guangzhou, Guangdong, Peoples R China.
   [Yang, Meiling; Xu, Anran; Ma, Manqi; Yuan, Qinzi; Liang, Wenjuan; Li, Xuenong; Lu, Yanxia] Guangdong Prov Key Lab Mol Tumor Pathol, 1023 South Shatai Rd, Guangzhou, Guangdong, Peoples R China.
   [Qiu, Lin] Jinan Univ, Med Imaging Ctr, Affiliated Hosp 1, Guangzhou, Guangdong, Peoples R China.
   [Ma, Xiaochen] Southern Med Univ, Biomat Res Ctr, Sch Biomed Engn, Guangzhou, Guangdong, Peoples R China.
   [Li, Xuenong; Lu, Yanxia] Southern Med Univ, Nanfang Hosp, Dept Pathol, Guangzhou 510515, Guangdong, Peoples R China.
C3 Southern Medical University - China; Southern Medical University -
   China; Jinan University; Southern Medical University - China; Southern
   Medical University - China
RP Li, XN; Lu, YX (corresponding author), Southern Med Univ, Nanfang Hosp, Dept Pathol, Guangzhou 510515, Guangdong, Peoples R China.
EM yanweitj@163.com; jnuql@qq.com; yangmei0848@163.com; xararar@163.com;
   395845722@qq.com; yuanqinzi@126.com; 1922136705@qq.com;
   chuanchiai@163.com; doctor_lixuenong@126.com; luzyanyar@163.com
RI Liu, Ya-Jun/ABF-9182-2022; Wei, Yan/JUV-3098-2023
FU National Natural Science Foundation of China [81502479]; Guangdong Basic
   and Applied Basic Research Foundation [2020A1515010088]
FX Funding This work was supported by the National Natural Science
   Foundation of China [81502479] and the Guangdong Basic and Applied Basic
   Research Foundation [2020A1515010088] .
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NR 44
TC 21
Z9 22
U1 4
U2 15
PU ELSEVIER IRELAND LTD
PI CLARE
PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000,
   IRELAND
SN 0304-3835
EI 1872-7980
J9 CANCER LETT
JI Cancer Lett.
PD JUL 28
PY 2023
VL 567
AR 216263
DI 10.1016/j.canlet.2023.216263
EA JUN 2023
PG 14
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA L4QS5
UT WOS:001023133900001
PM 37354983
DA 2025-01-04
ER

PT J
AU Li, XJ
   Chi, XD
   Huang, PJ
   Liang, Q
   Liu, JP
AF Li, Xuejie
   Chi, Xianda
   Huang, Pinjie
   Liang, Qiong
   Liu, Jianpei
TI Deep neural network for the prediction of KRAS, NRAS, and BRAF genotypes
   in left-sided colorectal cancer based on histopathologic images
SO COMPUTERIZED MEDICAL IMAGING AND GRAPHICS
LA English
DT Article
DE Deep neural network; Colorectal cancer; RAS; BRAF; Histopathology
ID MICROSATELLITE INSTABILITY; MUTATIONS; DIAGNOSIS; CETUXIMAB; RAS
AB Background: The KRAS, NRAS, and BRAF genotypes are critical for selecting targeted therapies for patients with metastatic colorectal cancer (mCRC). Here, we aimed to develop a deep learning model that utilizes pathologic whole-slide images (WSIs) to accurately predict the status of KRAS, NRAS, and BRAFV600E. Methods: 129 patients with left-sided colon cancer and rectal cancer from the Third Affiliated Hospital of Sun Yatsen University were assigned to the training and testing cohorts. Utilizing three convolutional neural networks (ResNet18, ResNet50, and Inception v3), we extracted 206 pathological features from H&E-stained WSIs, serving as the foundation for constructing specific pathological models. A clinical feature model was then developed, with carcinoembryonic antigen (CEA) identified through comprehensive multiple regression analysis as the key biomarker. Subsequently, these two models were combined to create a clinical-pathological integrated model, resulting in a total of three genetic prediction models. Result: 103 patients were evaluated in the training cohort (1782,302 image tiles), while the remaining 26 patients were enrolled in the testing cohort (489,481 image tiles). Compared with the clinical model and the pathology model, the combined model which incorporated CEA levels and pathological signatures, showed increased predictive ability, with an area under the curve (AUC) of 0.96 in the training and an AUC of 0.83 in the testing cohort, accompanied by a high positive predictive value (PPV 0.92). Conclusion: The combined model demonstrated a considerable ability to accurately predict the status of KRAS, NRAS, and BRAFV600E in patients with left-sided colorectal cancer, with potential application to assist doctors in developing targeted treatment strategies for mCRC patients, and effectively identifying mutations and eliminating the need for confirmatory genetic testing.
C1 [Li, Xuejie; Chi, Xianda; Liu, Jianpei] Sun Yat Sen Univ, Affiliated Hosp 3, Dept Gastrointestinal Surg, Guangzhou, Guangdong, Peoples R China.
   [Huang, Pinjie] Sun Yat sen Univ, Affiliated Hosp 3, Dept Anaesthesia, Guangzhou, Guangdong, Peoples R China.
   [Liang, Qiong] Sun Yat Sen Univ, Affiliated Hosp 3, Dept Pathol, Guangzhou, Guangdong, Peoples R China.
C3 Sun Yat Sen University; Sun Yat Sen University; Sun Yat Sen University
RP Liang, Q (corresponding author), Sun Yat sen Univ, Affiliated Hosp 3, Dept Pathol, 600 Tian He Rd, Guangzhou 510630, Peoples R China.; Liu, JP (corresponding author), Sun Yat sen Univ, Affiliated Hosp 3, Dept Gastrointestinal Surg, 600 Tian He Rd, Guangzhou 510630, Peoples R China.
EM liangq8@mail.sysu.edu.cn; liujpei2@sysu.edu.cn
OI Liu, Jianpei/0000-0003-4811-152X
FU Natural Science Foundation of Guangdong Province [2023A1515010347];
   Guangzhou Science and Technology Project [202102010141]
FX This work was supported by the Natural Science Foundation of Guangdong
   Province (No. 2023A1515010347) and the Guangzhou Science and Technology
   Project (No. 202102010141) .
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NR 32
TC 0
Z9 0
U1 3
U2 4
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0895-6111
EI 1879-0771
J9 COMPUT MED IMAG GRAP
JI Comput. Med. Imaging Graph.
PD JUL
PY 2024
VL 115
AR 102384
DI 10.1016/j.compmedimag.2024.102384
EA MAY 2024
PG 12
WC Engineering, Biomedical; Radiology, Nuclear Medicine & Medical Imaging
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Engineering; Radiology, Nuclear Medicine & Medical Imaging
GA C9K3K
UT WOS:001292474000001
PM 38759471
DA 2025-01-04
ER

PT J
AU Dashti, H
   Dehzangi, I
   Bayati, M
   Breen, J
   Beheshti, A
   Lovell, N
   Rabiee, HR
   Alinejad-Rokny, H
AF Dashti, Hamed
   Dehzangi, Iman
   Bayati, Masroor
   Breen, James
   Beheshti, Amin
   Lovell, Nigel
   Rabiee, Hamid R.
   Alinejad-Rokny, Hamid
TI Integrative analysis of mutated genes and mutational processes reveals
   novel mutational biomarkers in colorectal cancer
SO BMC BIOINFORMATICS
LA English
DT Article
DE Colorectal cancer; Cancer subtype identification; Somatic point
   mutations; Motif analysis; Gene prioritization; Therapeutic targets;
   Personalized medicine
ID COLON; CLASSIFICATION; PROLIFERATION; SIGNATURES; PHENOTYPE; PROGNOSIS;
   ONTOLOGY; ATLAS; CELLS; APC
AB Background Colorectal cancer (CRC) is one of the leading causes of cancer-related deaths worldwide. Recent studies have observed causative mutations in susceptible genes related to colorectal cancer in 10 to 15% of the patients. This highlights the importance of identifying mutations for early detection of this cancer for more effective treatments among high risk individuals. Mutation is considered as the key point in cancer research. Many studies have performed cancer subtyping based on the type of frequently mutated genes, or the proportion of mutational processes. However, to the best of our knowledge, combination of these features has never been used together for this task. This highlights the potential to introduce better and more inclusive subtype classification approaches using wider range of related features to enable biomarker discovery and thus inform drug development for CRC. Results In this study, we develop a new pipeline based on a novel concept called 'gene-motif', which merges mutated gene information with tri-nucleotide motif of mutated sites, for colorectal cancer subtype identification. We apply our pipeline to the International Cancer Genome Consortium (ICGC) CRC samples and identify, for the first time, 3131 gene-motif combinations that are significantly mutated in 536 ICGC colorectal cancer samples. Using these features, we identify seven CRC subtypes with distinguishable phenotypes and biomarkers, including unique cancer related signaling pathways, in which for most of them targeted treatment options are currently available. Interestingly, we also identify several genes that are mutated in multiple subtypes but with unique sequence contexts. Conclusion Our results highlight the importance of considering both the mutation type and mutated genes in identification of cancer subtypes and cancer biomarkers. The new CRC subtypes presented in this study demonstrates distinguished phenotypic properties which can be effectively used to develop new treatments. By knowing the genes and phenotypes associated with the subtypes, a personalized treatment plan can be developed that considers the specific phenotypes associated with their genomic lesion.
C1 [Dashti, Hamed; Bayati, Masroor; Rabiee, Hamid R.] Sharif Univ Technol, Dept Comp Engn, Bioinformat & Computat Biol Lab, Tehran 11365, Iran.
   [Dehzangi, Iman] Rutgers State Univ, Ctr Computat & Integrat Biol CCIB, Camden, NJ 08102 USA.
   [Breen, James] South Australian Hlth & Med Res Inst, Adelaide, SA 5000, Australia.
   [Breen, James] Univ Adelaide, Robinson Res Inst, Adelaide, SA 5006, Australia.
   [Breen, James] Univ Adelaide, Bioinformat Hub, Adelaide, SA 5006, Australia.
   [Beheshti, Amin] Macquarie Univ, Dept Comp, Sydney, NSW 2109, Australia.
   [Lovell, Nigel] UNSW Sydney, Tyree Inst Hlth Engn, Sydney, NSW 2052, Australia.
   [Lovell, Nigel] UNSW Sydney, Grad Sch Biomed Engn, Sydney, NSW 2052, Australia.
   [Alinejad-Rokny, Hamid] UNSW Sydney, Grad Sch Biomed Engn, BioMed Machine Learning Lab, Sydney, NSW 2052, Australia.
   [Alinejad-Rokny, Hamid] Univ New South Wales, UNSW Data Sci Hub, Sydney, NSW 2052, Australia.
   [Alinejad-Rokny, Hamid] Macquarie Univ, AI Enabled Proc AIP Res Ctr, Hlth Data Analyt Program, Sydney, NSW 2109, Australia.
C3 Sharif University of Technology; Rutgers University System; Rutgers
   University New Brunswick; Rutgers University Camden; South Australian
   Health & Medical Research Institute (SAHMRI); Robinson Research
   Institute; University of Adelaide; University of Adelaide; Macquarie
   University; University of New South Wales Sydney; University of New
   South Wales Sydney; University of New South Wales Sydney; University of
   New South Wales Sydney; Macquarie University
RP Rabiee, HR (corresponding author), Sharif Univ Technol, Dept Comp Engn, Bioinformat & Computat Biol Lab, Tehran 11365, Iran.; Alinejad-Rokny, H (corresponding author), UNSW Sydney, Grad Sch Biomed Engn, BioMed Machine Learning Lab, Sydney, NSW 2052, Australia.; Alinejad-Rokny, H (corresponding author), Univ New South Wales, UNSW Data Sci Hub, Sydney, NSW 2052, Australia.; Alinejad-Rokny, H (corresponding author), Macquarie Univ, AI Enabled Proc AIP Res Ctr, Hlth Data Analyt Program, Sydney, NSW 2109, Australia.
EM RABIEE@sharif.edu; h.alinejad@ieee.org
RI Lovell, Nigel/AGF-6679-2022; Breen, Jimmy/HHZ-1361-2022; Beheshti,
   Amin/ADI-5438-2022; Rabiee, Hamid/L-7866-2017
OI Beheshti, Amin/0000-0002-5988-5494; dehzangi, Iman/0000-0001-8577-0271;
   Breen, James/0000-0001-6184-0925
FU UNSW Scientia Program Fellowship; Australian Research Council Discovery
   Early Career Researcher Award (DECRA) [DE220101210]; Australian Research
   Council Discovery Project [DP160101960]; WA Department of Health
   Near-Miss Merit Award; Australian Research Council [DE220101210] Funding
   Source: Australian Research Council
FX This work was supported by the UNSW Scientia Program Fellowship and the
   Australian Research Council Discovery Early Career Researcher Award
   (DECRA) under grant DE220101210 to HAR. This work was also supported by
   a grant to Prof Alistair Forrest from an Australian Research Council
   Discovery Project grant (DP160101960) and WA Department of Health
   Near-Miss Merit Award to HAR.
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NR 92
TC 11
Z9 11
U1 1
U2 3
PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1471-2105
J9 BMC BIOINFORMATICS
JI BMC Bioinformatics
PD APR 19
PY 2022
VL 23
IS 1
AR 138
DI 10.1186/s12859-022-04652-8
PG 24
WC Biochemical Research Methods; Biotechnology & Applied Microbiology;
   Mathematical & Computational Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology;
   Mathematical & Computational Biology
GA 0O9HH
UT WOS:000783833600001
PM 35439935
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Yde, J
   Larsen, HM
   Laurberg, S
   Krogh, K
   Moeller, HB
AF Yde, Jonathan
   Larsen, Helene M.
   Laurberg, Soren
   Krogh, Klaus
   Moeller, Hanne B.
TI Chronic diarrhoea following surgery for colon cancer-frequency, causes
   and treatment options
SO INTERNATIONAL JOURNAL OF COLORECTAL DISEASE
LA English
DT Review
DE Colon cancer surgery; Diarrhoea; Bile acid malabsorption; Complications
   to colon cancer
ID BILE-ACID MALABSORPTION; QUALITY-OF-LIFE; IRRITABLE-BOWEL-SYNDROME;
   INTESTINAL BACTERIAL OVERGROWTH; ANTERIOR RESECTION SYNDROME; RANDOMIZED
   CLINICAL-TRIAL; CHRONIC WATERY DIARRHEA; GLUCAGON-LIKE PEPTIDE-1;
   COLORECTAL-CANCER; ILEAL-RESECTION
AB Purpose The growing population of survivors after colon cancer warrants increased attention to the long-term outcome of surgical treatment. The change in bowel anatomy after resection disrupts normal gastrointestinal function and may cause symptoms. Thus, many patients surviving colon cancer have to cope with bowel dysfunction for the rest of their lives. We here aim to provide an overview of the literature on this topic.
   Methods We review long-term functional outcomes of surgical treatment for colon cancer, the underlying pathology, and treatment options.
   Results Common symptoms include constipation, urge for defecation and diarrhoea. Causes of diarrhoea after colon cancer surgery are sparsely studied, but they probably include bile acid malabsorption, small intestinal bacterial overgrowth and disruption of the ileal brake. Specific diagnosis should be made to allow individual treatment based on the underlying pathology. Studies on treatment of functional problems after surgery for colon cancer are extremely few, but some lessons can be drawn from the treatment of other patient groups having undergone colon surgery.
   Conclusion Diarrhoea is likely a common long-term complication after colon cancer surgery. Attention to this complication and a specific diagnosis will aid the targeted treatment of patients suffering from this complication.
C1 [Yde, Jonathan; Moeller, Hanne B.] Aarhus Univ, Dept Biomed, Wilhelm Meyers Alle 3,Bldg 1233, DK-8000 Aarhus, Denmark.
   [Larsen, Helene M.; Laurberg, Soren] Aarhus Univ Hosp, Dept Surg, Aarhus, Denmark.
   [Krogh, Klaus] Aarhus Univ Hosp, Dept Gastroenterol & Hepatol, Aarhus, Denmark.
   [Larsen, Helene M.; Laurberg, Soren; Krogh, Klaus] Aarhus Univ Hosp, Danish Canc Soc, Ctr Res & Late Adverse Effects Canc Pelv Organs, Aarhus, Denmark.
C3 Aarhus University; Aarhus University; Aarhus University; Danish Cancer
   Society; Aarhus University
RP Moeller, HB (corresponding author), Aarhus Univ, Dept Biomed, Wilhelm Meyers Alle 3,Bldg 1233, DK-8000 Aarhus, Denmark.
EM HBMO@biomed.au.dk
OI Krogh, Klaus/0000-0001-9168-2403; Yde, Jonathan/0000-0001-5158-7743
FU AUFF starting Grant; Aage and Johanne Louis-Hansens Foundation; Danish
   Cancer Society
FX The work was supported by an AUFF starting Grant, Aage and Johanne
   Louis-Hansens Foundation, and The Danish Cancer Society.
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NR 97
TC 43
Z9 47
U1 3
U2 16
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0179-1958
EI 1432-1262
J9 INT J COLORECTAL DIS
JI Int. J. Colorectal Dis.
PD JUN
PY 2018
VL 33
IS 6
BP 683
EP 694
DI 10.1007/s00384-018-2993-y
PG 12
WC Gastroenterology & Hepatology; Surgery
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology; Surgery
GA GF4KA
UT WOS:000431930400002
PM 29589108
DA 2025-01-04
ER

PT J
AU Elmorshedy, YM
   Teleb, M
   Sallam, MA
   Elkhodairy, KA
   Bahey-El-Din, M
   Ghareeb, DA
   Abdulmalek, SA
   Monaim, SAHA
   Bekhit, AA
   Elzoghby, AO
   Albericio, F
   Khattab, SN
AF Elmorshedy, Yomna M.
   Teleb, Mohamed
   Sallam, Marwa A.
   Elkhodairy, Kadria A.
   Bahey-El-Din, Mohammed
   Ghareeb, Doaa A.
   Abdulmalek, Shaymaa A.
   Monaim, Shimaa A. H. Abdel
   Bekhit, Adnan A.
   Elzoghby, Ahmed O.
   Albericio, Fernando
   Khattab, Sherine N.
TI Engineered Microencapsulated Lactoferrin Nanoconjugates for Oral
   Targeted Treatment of Colon Cancer
SO BIOMACROMOLECULES
LA English
DT Article
ID ETHYL 2-CYANO-2-(HYDROXYIMINO)ACETATE OXYMA; IN-VITRO; REPLACE
   1-HYDROXYBENZOTRIAZOLE; LIPID NANOPARTICLES; BOVINE LACTOFERRIN;
   DELIVERY-SYSTEMS; DRUG-DELIVERY; ATORVASTATIN; DOCETAXEL; COMBINATION
AB Despite current progress in the development of targeted therapies for cancer treatment, there is a lack in convenient therapeutics for colorectal cancer (CRC). Lactoferrin nanoparticles (Lf NPs) are a promising drug delivery system in cancer therapy. However, numerous obstacles impede their oral delivery, including instability against stomach enzymes and premature uptake during passage through the small intestine. Microencapsulation of Lf NPs offer a great solution for these obstacles. It can protect Lf NPs and their drug payloads from degradation in the upper gastrointestinal tract (GIT), reduce burst drug release, and improve the release profile of the encapsulated NPs triggered by stimuli in the colon. Here, we developed nanoparticle-in-microparticle delivery systems (NIMDs) for the oral delivery of docetaxel (DTX) and atorvastatin (ATR). The NPs were obtained by dual conjugation of DTX and ATR into the Lf backbone, which was further microencapsulated into calcium-crosslinked microparticles using polysaccharide-protein hybrid copolymers. The NIMDs showed no detectable drug release in the upper GIT compared to NPs. Furthermore, sustained release of the NPs from the NIMDs in rat cecal content was observed. Moreover, the in vivo study demonstrated the superiority of the NIMDs over NPs in CRC treatment by suppressing p-AKT, p-ERK1/2, and NF -KB. This study provides the proof of concept for using NIMDs to enhance the effect of protein NPs in CRC treatment.
C1 [Elmorshedy, Yomna M.; Elzoghby, Ahmed O.] Alexandria Univ, Canc Nanotechnol Res Lab CNRL, Fac Pharm, Dept Ind Pharm, Alexandria 21521, Egypt.
   [Teleb, Mohamed; Elkhodairy, Kadria A.; Bekhit, Adnan A.] Alexandria Univ, Canc Nanotechnol Res Lab CNRL, Fac Pharm, Dept Pharmaceut Chem, Alexandria 21521, Egypt.
   [Sallam, Marwa A.] Alexandria Univ, Fac Pharm, Dept Ind Pharm, Alexandria 21521, Egypt.
   [Bahey-El-Din, Mohammed] Alexandria Univ, Fac Pharm, Dept Microbiol & Immunol, Alexandria 21521, Egypt.
   [Ghareeb, Doaa A.; Abdulmalek, Shaymaa A.] Alexandria Univ, Fac Sci, Biochem Dept, Bioscreening & Preclin Trial Lab, Alexandria 21321, Egypt.
   [Ghareeb, Doaa A.; Abdulmalek, Shaymaa A.] Ctr Excellence Drug Preclin Studies CE DPS, Pharmaceut & Fermentat Ind Dev Ctr, City Sci Res & Technol Applicat, New Borg El Arab 21934, Egypt.
   [Monaim, Shimaa A. H. Abdel] Univ KwaZulu Natal, Sch Chem & Phys, Durban 4001, South, Haiti.
   [Bekhit, Adnan A.] Univ Bahrain, Coll Hlth & Sport Sci, Pharm Program Allied Hlth Dept, Sakhir 32038, Bahrain.
   [Albericio, Fernando] Univ KwaZulu Natal, Sch Chem & Phys, ZA-4001 Durban, South Africa.
   [Albericio, Fernando] CIBER BBN, Networking Ctr Bioengn Biomat & Nanomed, Barcelona 08028, Spain.
   [Albericio, Fernando] Univ Barcelona, Dept Organ Chem, Barcelona 08028, Spain.
   [Elzoghby, Ahmed O.] Brigham & Womens Hosp, Harvard Med Sch, Dept Med, Div Engn Med, Boston, MA 02115 USA.
   [Khattab, Sherine N.] Alexandria Univ, Fac Sci, Chem Dept, Alexandria 21321, Egypt.
C3 Egyptian Knowledge Bank (EKB); Alexandria University; Egyptian Knowledge
   Bank (EKB); Alexandria University; Egyptian Knowledge Bank (EKB);
   Alexandria University; Egyptian Knowledge Bank (EKB); Alexandria
   University; Egyptian Knowledge Bank (EKB); Alexandria University;
   Egyptian Knowledge Bank (EKB); City of Scientific Research &
   Technological Applications (SRTA-City); University of Bahrain;
   University of Kwazulu Natal; CIBER - Centro de Investigacion Biomedica
   en Red; CIBERBBN; University of Barcelona; Harvard University; Harvard
   Medical School; Brigham & Women's Hospital; Egyptian Knowledge Bank
   (EKB); Alexandria University
RP Elzoghby, AO (corresponding author), Alexandria Univ, Canc Nanotechnol Res Lab CNRL, Fac Pharm, Dept Ind Pharm, Alexandria 21521, Egypt.; Elzoghby, AO (corresponding author), Brigham & Womens Hosp, Harvard Med Sch, Dept Med, Div Engn Med, Boston, MA 02115 USA.; Khattab, SN (corresponding author), Alexandria Univ, Fac Sci, Chem Dept, Alexandria 21321, Egypt.
EM ahmed_elzoghby@alexu.edu.eg; Sh.n.khattab@gmail.com
RI Bekhit, Adnan/CAH-8933-2022; Albericio, Fernando/AEN-8081-2022;
   Elzoghby, Ahmed/ABD-8837-2021; Sallam, Marwa/AAY-9786-2021; Albericio,
   Fernando/B-4383-2013; Ghareeb, Doaa/R-6914-2016; Khattab,
   Sherine/G-4985-2018; Bahey-El-Din, Mohammed/L-5206-2015
OI Elzoghby, Ahmed/0000-0002-5193-7536; Albericio,
   Fernando/0000-0002-8946-0462; Bekhit, Adnan/0000-0003-3865-0677;
   Ghareeb, Doaa/0000-0003-3327-4377; Khattab, Sherine/0000-0002-3162-6386;
   elmorshedy, yomna/0000-0002-2079-6566; Bahey-El-Din,
   Mohammed/0000-0003-3457-9084
FU Science, Technology & Innovation Funding Authority (STDF), Cairo, Egypt
   through the Innovation Grant [34857]
FX The authors thank the Science, Technology & Innovation Funding Authority
   (STDF), Cairo, Egypt, for funding this work through the Innovation Grant
   (Proposal ID 34857).
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NR 62
TC 11
Z9 12
U1 1
U2 19
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 1525-7797
EI 1526-4602
J9 BIOMACROMOLECULES
JI Biomacromolecules
PD MAY 8
PY 2023
VL 24
IS 5
BP 2149
EP 2163
DI 10.1021/acs.biomac.3c00037
EA APR 2023
PG 15
WC Biochemistry & Molecular Biology; Chemistry, Organic; Polymer Science
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Chemistry; Polymer Science
GA F6BJ3
UT WOS:000971766200001
PM 37039769
DA 2025-01-04
ER

PT J
AU Wang, Y
   Zhang, JY
   Zheng, S
AF Wang, Yong
   Zhang, Jingyu
   Zheng, Shuang
TI The role of XBP-1-mediated unfolded protein response in colorectal
   cancer progression-a regulatory mechanism associated with
   lncRNA-miRNA-mRNA network
SO CANCER CELL INTERNATIONAL
LA English
DT Article
DE Colorectal cancer; XBP-1; Endoplasmic reticulum stress; KCNQ1OT1; XIST
ID ENDOPLASMIC-RETICULUM; XBP-1; STRESS; APOPTOSIS; AUTOPHAGY; XBP1S
AB Background We aim to identify the expression and analyze the molecular action of dysregulated lncRNA-miRNA mediated by XBP-1 in colorectal cancer (CRC). Methods Here, we identified XBP-1-mediated dysregulated lncRNAs and miRNAs in CRC by bioinformatics analysis. The expression level of lncRNAs and miRNA was measured using quantitative real time PCR, and the expression of XBP-1, as well as apoptosis-related proteins, were detected by western blot. CCK-8 and TUNEL assays were performed to determine cell proliferation and apoptosis, respectively. Luciferase reporter assay was conducted to verify the binding relationship among lncRNA-miRNA-XBP-1. BALB/c nude mice were inoculated subcutaneously with HCT116 cells to establish tumor-bearing mice model. Histological analysis was carried out by HE staining and immunohistochemical staining. Results Six downregulated lncRNAs (SLFNL1-AS1, KCNQ1OT1, NEAT1, XIST, AC016876.2, AC026362.1), four dysregulated miRNAs (miR-500a-3p, miR-370-3p, miR-2467-3p, miR-512-3p) and upregulated XBP-1 were identified in CRC cell lines. Gain- and loss-of-function experiments showed that overexpression of KCNQ1OT1/XIST promoted cell proliferation and suppressed cell apoptosis. In addition, overexpression of KCNQ1OT1/XIST partly abolished the inhibitory effects of XBP-1u knockdown or tunicamycin, an activator of endoplasmic reticulum stress, on CRC cell viability loss and apoptosis. Furthermore, KCNQ1OT1/XIST aggravated tumor growth in vivo by regulating endoplasmic reticulum stress and cell apoptosis. Conclusions This study has constructed lncRNA-miRNA-mRNA networks based on XBP-1 in CRC, and disclosed the regulatory mechanism of action, providing a set of pivotal biomarkers for future molecular investigation and targeted treatment of CRC.
C1 [Wang, Yong] Nanjing Med Univ, Dept Colorectal Surg, Affiliated Hosp 1, Nanjing 210029, Jiangsu, Peoples R China.
   [Zhang, Jingyu] Second Peoples Hosp Lianyungang, Dept Gastrointestinal Oncol, Lianyungang 200023, Jiangsu, Peoples R China.
   [Zheng, Shuang] Wenzhou Med Univ, Taizhou Peoples Hosp 1, Dept Gen Surg, Huangyan Hosp, 218 Hengjie Rd, Taizhou City 318020, Zhejiang, Peoples R China.
C3 Nanjing Medical University; Wenzhou Medical University
RP Zheng, S (corresponding author), Wenzhou Med Univ, Taizhou Peoples Hosp 1, Dept Gen Surg, Huangyan Hosp, 218 Hengjie Rd, Taizhou City 318020, Zhejiang, Peoples R China.
EM zszheng2021@163.com
RI Hai, Yong/L-2679-2019
OI , Shuang/0000-0003-0393-0505
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NR 35
TC 5
Z9 6
U1 1
U2 5
PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
EI 1475-2867
J9 CANCER CELL INT
JI Cancer Cell Int.
PD SEP 14
PY 2021
VL 21
IS 1
AR 488
DI 10.1186/s12935-021-02167-5
PG 14
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA UQ1RI
UT WOS:000695847800001
PM 34521445
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Martín-García, D
   Téllez, T
   Redondo, M
   García-Aranda, M
AF Martin-Garcia, Desiree
   Tellez, Teresa
   Redondo, Maximino
   Garcia-Aranda, Marilina
TI The use of SP/Neurokinin-1 as a Therapeutic Target in Colon and Rectal
   Cancer
SO CURRENT MEDICINAL CHEMISTRY
LA English
DT Review
DE Substance P, neurokinin-1 receptor; aprepitant; pharmacological
   repositioning; targeted treatment; colorectal cancer
ID CHEMOTHERAPY-INDUCED NAUSEA; TRUNCATED NEUROKININ-1 RECEPTOR;
   SUBSTANCE-P RECEPTOR; COLORECTAL-CANCER; SERRATED POLYPS; DNA
   METHYLATION; MICROSATELLITE INSTABILITY; MOLECULAR-GENETICS;
   CLINICAL-PRACTICE; NK-1 RECEPTOR
AB Different studies have highlighted the role of Substance P / Neurokinin 1 Receptor (SP/NK-1R) axis in multiple hallmarks of cancer including cell transformation, proliferation, and migration as well as angiogenesis and metastasis of a wide range of solid tumors including colorectal cancer. Until now, the selective high-affinity antagonist of human SP/NK1-R aprepitant (Emend) has been authorized by the Food and Drug Administration as a low dosage medication to manage and treat chemotherapy-induced nausea. However, increasing evidence in recent years support the potential utility of high doses of aprepitant as an antitumor agent and thus, opening the possibility to the pharmacological repositioning of SP/NK1-R antagonists as an adjuvant therapy to conventional cancer treatments. In this review, we summarize current knowledge on the molecular basis of colorectal cancer as well as the pathophysiological importance of SP/NK1-R and the potential utility of SP/NK-1R axis as a therapeutic target in this malignancy.
C1 [Martin-Garcia, Desiree; Tellez, Teresa; Redondo, Maximino; Garcia-Aranda, Marilina] Univ Malaga, Biochem & Immunol, Malaga, Spain.
   [Garcia-Aranda, Marilina] Hosp Costa Sol, Res & Innovat Unit, Marbella 29602, Spain.
C3 Universidad de Malaga
RP Redondo, M (corresponding author), Univ Malaga, Biochem & Immunol, Malaga, Spain.
EM maximino.redondo.sspa@juntadeandalucia.es
OI Martin-Garcia, Desiree/0009-0009-5007-0529
FU European Social Fund-Operational Program of Andalusia 2014-2020
   [RH-0055-2020]; University of Malaga-Consejeria de Transformacion
   Economica, Industria, Conocimiento y Universidades-Junta de Andalucia
   [UMA20-FEDER-JA-161]; Instituto de Salud Carlos III [PI18/01181,
   PI21/00252]; European Regional Development fund
FX The researcher Marilina Garcia-Aranda is the benefactor of a
   postdoctoral contract financed by the European Social Fund-Operational
   Program of Andalusia 2014-2020 for the "Incorporation of Research
   Personnel with a PhD degree in the field of Health Sciences and
   Technologies in R&D and Innovation Centers of the Public Health System
   of Andalusia"(RH-0055-2020). This work was partially supported by grants
   from the University of Malaga-Consejeria de Transformacion Economica,
   Industria, Conocimiento y Universidades-Junta de Andalucia
   (UMA20-FEDER-JA-161) and from Instituto de Salud Carlos III(PI18/01181,
   PI21/00252) and were cofunded by the European Regional Development fund.
   The funders had no role in study design, data collection and analysis,
   decision to publish, or in the preparation of the manuscript.
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NR 170
TC 1
Z9 1
U1 1
U2 4
PU BENTHAM SCIENCE PUBL LTD
PI SHARJAH
PA EXECUTIVE STE Y-2, PO BOX 7917, SAIF ZONE, 1200 BR SHARJAH, U ARAB
   EMIRATES
SN 0929-8673
EI 1875-533X
J9 CURR MED CHEM
JI Curr. Med. Chem.
PY 2024
VL 31
IS 39
BP 6487
EP 6509
DI 10.2174/0109298673261625230924114406
PG 23
WC Biochemistry & Molecular Biology; Chemistry, Medicinal; Pharmacology &
   Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Pharmacology & Pharmacy
GA G1K0K
UT WOS:001314282800005
PM 37861026
DA 2025-01-04
ER

PT J
AU Sutphin, PD
   Ganguli, S
AF Sutphin, Patrick D.
   Ganguli, Suvranu
TI Interventional Treatment of Hepatic Metastases from Colorectal Cancer
SO SEMINARS IN INTERVENTIONAL RADIOLOGY
LA English
DT Article
DE colorectal cancer; colorectal liver metastases; ablation;
   radioembolization
ID LONG-TERM SURVIVAL; PERCUTANEOUS RADIOFREQUENCY ABLATION; LOCAL TUMOR
   PROGRESSION; DRUG-ELUTING BEAD; LIVER METASTASES; Y-90
   RADIOEMBOLIZATION; COLON-CANCER; PHASE-II; OUTCOMES; MARGINS
AB Modern systemic therapies provide a significant survival benefit in metastatic colorectal cancer. Despite these advances, the durability of response remains limited and nearly all patients progress on systemic treatment. Colorectal liver metastases (CLM) develop in approximately half of patients with metastatic disease and contribute to mortality in most patients. In selected patients, surgical resection of hepatic metastases prolongs survival, indicating the benefits of the targeted treatment of CLM through alternate means. Minimally invasive interventional treatments offer the promise of treating CLM in a wider range of patients than those eligible for surgical resection. Thermal ablation and intra-arterial therapies, including chemoembolization and radioembolization, are commonly used in the treatment of CLM. Each of these treatment modalities will be discussed in detail with an emphasis on the available clinical data for each interventional treatment for CLM.
C1 [Sutphin, Patrick D.] Harvard Med Sch, Massachusetts Gen Hosp, Dept Radiol, Div Intervent Radiol, Boston, MA 02114 USA.
   [Ganguli, Suvranu] Boston Univ, Med Sch, Boston Med Ctr, Dept Radiol,Div Intervent Radiol, Boston, MA 02215 USA.
C3 Harvard University; Massachusetts General Hospital; Harvard Medical
   School; Boston Medical Center; Boston University
RP Sutphin, PD (corresponding author), Harvard Med Sch, Massachusetts Gen Hosp, Dept Radiol, Div Intervent Radiol, Boston, MA 02114 USA.
EM psutphin@partners.org
OI Ganguli, Suvranu/0000-0002-3426-4907
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NR 52
TC 1
Z9 1
U1 1
U2 11
PU THIEME MEDICAL PUBL INC
PI NEW YORK
PA 333 SEVENTH AVE, NEW YORK, NY 10001 USA
SN 0739-9529
EI 1098-8963
J9 SEMIN INTERVENT RAD
JI Semin. Interv. Radiol.
PD DEC
PY 2020
VL 37
IS 05
BP 492
EP 498
DI 10.1055/s-0040-171919
PG 7
WC Radiology, Nuclear Medicine & Medical Imaging
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Radiology, Nuclear Medicine & Medical Imaging
GA PD3SO
UT WOS:000597608900007
PM 33328705
OA Green Published
DA 2025-01-04
ER

PT J
AU Liu, FY
   Xu, YM
   Yang, GW
   Guo, YH
   Nian, JY
AF Liu, Fangyu
   Xu, Yongmei
   Yang, Guowang
   Guo, Yuhong
   Nian, Jiayun
TI Portal vein thrombosis after cetuximab and 5-fluorouracil therapy in a
   patient with advanced colon cancer and decompensated cirrhosis: a case
   report and review of the literature
SO WORLD JOURNAL OF SURGICAL ONCOLOGY
LA English
DT Review
DE Advanced colon cancer; Decompensated cirrhosis; Cetuximab;
   5-fluorouracil; Portal vein thrombosis
ID MARY JOSEPHS NODULE; COLORECTAL-CANCER; METASTASIS; BURDEN
AB BackgroundTreatment options for advanced colon cancer are mainly combinations of chemotherapy and targeted drugs. However, poor physical health and medication intolerance limit the choice of anticancer drugs. Colon cancer with cirrhosis is a particular patient group that poses a challenge to clinical treatment.Case presentationThis article presents a case of a patient in the decompensated stage of cirrhosis who was diagnosed with advanced colon cancer. The initial presentation was a nodule on his navel named the Sister Mary Joseph's nodule, which was later confirmed by biopsy and PET-CT as one of the metastases of colon cancer. The patient was treated with cetuximab and 5-fluorouracil at a below-guideline dose; however, portal vein thrombosis developed and led to death. This entire process, from diagnosis to death, occurred within a span of three months.ConclusionCancers with cirrhosis are a special group that deserves more attention. There is no unified treatment guideline for these patients, especially those with extrahepatic primary tumors. We should be more cautious when choosing treatment for such patients in the future. Both chemotherapy and targeted treatment may potentially induce portal vein thrombosis, which appears to have a higher incidence and worse prognosis than cancers without cirrhosis.
C1 [Liu, Fangyu; Xu, Yongmei; Yang, Guowang; Guo, Yuhong; Nian, Jiayun] Capital Med Univ, Beijing Hosp Tradit Chinese Med, Beijing, Peoples R China.
C3 Capital Medical University
RP Guo, YH; Nian, JY (corresponding author), Capital Med Univ, Beijing Hosp Tradit Chinese Med, Beijing, Peoples R China.
EM docgyh@163.com; nianjiayun@126.com
FU Beijing Municipal Administration of Hospitals Incubating Program; 
   [PZ2023010]
FX Beijing Municipal Administration of Hospitals Incubating Program
   (PZ2023010).
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NR 28
TC 0
Z9 0
U1 2
U2 3
PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
EI 1477-7819
J9 WORLD J SURG ONCOL
JI World J. Surg. Oncol.
PD SEP 23
PY 2023
VL 21
IS 1
AR 302
DI 10.1186/s12957-023-03175-7
PG 6
WC Oncology; Surgery
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Surgery
GA S4RY9
UT WOS:001071068400001
PM 37741975
OA gold, Green Published, Green Submitted
DA 2025-01-04
ER

PT J
AU Bazzichetto, C
   Milella, M
   Zampiva, I
   Simionato, F
   Amoreo, CA
   Buglioni, S
   Pacelli, C
   Le Pera, L
   Colombo, T
   Bria, E
   Zeuli, M
   Del Bufalo, D
   Sperduti, I
   Conciatori, F
AF Bazzichetto, Chiara
   Milella, Michele
   Zampiva, Ilaria
   Simionato, Francesca
   Amoreo, Carla Azzurra
   Buglioni, Simonetta
   Pacelli, Chiara
   Le Pera, Loredana
   Colombo, Teresa
   Bria, Emilio
   Zeuli, Massimo
   Del Bufalo, Donatella
   Sperduti, Isabella
   Conciatori, Fabiana
TI Interleukin-8 in Colorectal Cancer: A Systematic Review and
   Meta-Analysis of Its Potential Role as a Prognostic Biomarker
SO BIOMEDICINES
LA English
DT Review
DE IL-8; tumor-stroma interactions; advanced CRC; chemotherapy;
   anti-angiogenic drugs; prognosis
ID REDUCED CLINICAL BENEFIT; IL-8; PROLIFERATION; BEVACIZUMAB; EXPRESSION;
   SURVIVAL
AB Among soluble actors that have emerged as druggable factors, the chemokine interleukin-8 (IL-8) has emerged as a possible determinant of response to immunotherapy and targeted treatment in several cancer types; however, its prognostic/predictive role in colorectal cancer (CRC) remains to be established. We: (i) conducted a systematic review of published literature on IL-8 expression in CRC; (ii) searched public transcriptomics databases; (iii) investigated IL-8 expression, by tumor and infiltrating cells, in a series of CRC samples; and (iv) carried out a meta-analysis of published literature correlating IL-8 expression and CRC prognosis. IL-8 possesses an important role as a mediator of the bidirectional crosstalk between tumor/stromal cells. Transcriptomic analysis indicated that specific IL-8 transcripts were significantly overexpressed in CRC compared to normal colon mucosa. Moreover, in our series we observed a statistically significant correlation between PTEN-loss and IL-8 expression by infiltrating mononuclear and tumor cells. In total, 12 papers met our meta-analysis inclusion criteria, demonstrating that high IL-8 levels significantly correlated with shorter overall survival and progression-free survival. Sensitivity analysis demonstrated a highly significant correlation with outcome for circulating, but not for tissue-detected, IL-8. IL-8 is overexpressed in CRC tissues and differentially produced by tumor or stromal components depending on CRC genetic background. Moreover, circulating IL-8 represents a strong prognostic factor in CRC, suggesting its use in the refining of prognostic CRC assessment and potentially the tailoring of therapeutic strategies in individual CRC patients.
C1 [Bazzichetto, Chiara; Del Bufalo, Donatella; Conciatori, Fabiana] IRCCS Regina Elena Natl Canc Inst, Preclin Models & New Therapeut Agents Unit, I-00144 Rome, Italy.
   [Bazzichetto, Chiara; Zeuli, Massimo; Conciatori, Fabiana] IRCCS Regina Elena Natl Canc Inst, Med Oncol 1, I-00144 Rome, Italy.
   [Milella, Michele; Zampiva, Ilaria] Univ Verona, Sch Med, Dept Med, Sect Oncol, I-37134 Verona, Italy.
   [Milella, Michele; Zampiva, Ilaria] Verona Univ Hosp Trust, I-37134 Verona, Italy.
   [Simionato, Francesca] San Bortolo Gen Hosp, Dept Oncol, I-36100 Vicenza, Italy.
   [Amoreo, Carla Azzurra; Buglioni, Simonetta] IRCCS Regina Elena Natl Canc Inst, Pathol Unit, I-00144 Rome, Italy.
   [Pacelli, Chiara] Sapienza Univ Rome, Dept Biochem Sci A Rossi Fanelli, I-00185 Rome, Italy.
   [Le Pera, Loredana] Ist Super San ISS, Serv Grandi Strumentaz & Core Facil, I-00161 Rome, Italy.
   [Colombo, Teresa] Natl Res Council IBPM CNR, Inst Mol Biol & Pathol, I-00185 Rome, Italy.
   [Bria, Emilio] Univ Cattolica Sacro Cuore, Fdn Polidin Univ Agostino Gemelli IRCCS, Med Oncol, I-00168 Rome, Italy.
   [Sperduti, Isabella] IRCCS Regina Elena Natl Canc Inst, Biostat Unit, I-00144 Rome, Italy.
C3 University of Verona; University of Verona; Azienda Ospedaliera
   Universitaria Integrata Verona; ULSS 8 Berica; Ospedale San Bortolo di
   Vicenza; Sapienza University Rome; Consiglio Nazionale delle Ricerche
   (CNR); Istituto di Biologia e Patologia Molecolari (IBPM-CNR); Catholic
   University of the Sacred Heart; IRCCS Policlinico Gemelli
RP Bazzichetto, C (corresponding author), IRCCS Regina Elena Natl Canc Inst, Preclin Models & New Therapeut Agents Unit, I-00144 Rome, Italy.; Bazzichetto, C (corresponding author), IRCCS Regina Elena Natl Canc Inst, Med Oncol 1, I-00144 Rome, Italy.; Milella, M (corresponding author), Univ Verona, Sch Med, Dept Med, Sect Oncol, I-37134 Verona, Italy.; Milella, M (corresponding author), Verona Univ Hosp Trust, I-37134 Verona, Italy.
EM chiara.bazzichetto@ifo.it; michele.milella@univr.it
RI Zampiva, Ilaria/AAB-8421-2022; Del Bufalo, Donatella/AAC-1594-2021;
   Milella, Michele/ABH-8606-2020; AMOREO, CARLA/K-5375-2018; Le Pera,
   Loredana/ABD-3398-2020; Bria, Emilio/A-8574-2019; Colombo,
   Teresa/P-2959-2018; Bazzichetto, Chiara/ABI-2020-2020; Sperduti,
   Isabella/K-8902-2016; Conciatori, Fabiana/AAU-2657-2020
OI Bria, Emilio/0000-0002-2333-704X; Zampiva, Ilaria/0000-0003-4858-3965;
   Colombo, Teresa/0000-0003-2415-7507; Bazzichetto,
   Chiara/0000-0002-1648-3700; Le Pera, Loredana/0000-0002-0076-9878;
   Sperduti, Isabella/0000-0001-5115-3099; Conciatori,
   Fabiana/0000-0002-8579-5222; buglioni, simonetta/0000-0002-5066-1523;
   Pacelli, Chiara/0000-0002-5565-3100
FU Italian Ministry of Health; Fondazione AIRC per la Ricerca sul Cancro
   [AIRC IG 20583]; Ministero dell'Universita e della Ricerca (MUR)
   [B39J21037270006]; Fondazione AIRC per la Ricerca sul Cancro (FIRC);
   Ministero della Salute-Fondazione Italiana per lo studio delle Malattie
   del Pancreas (FIMP) [FIMPCUP_J38D19000690001]; Bando Interno Ricerca
   Corrente IRE 2021
FX This research was financially supported through funding from the
   institutional "Ricerca Corrente" granted by the Italian Ministry of
   Health. The work was also funded by Bando Interno Ricerca Corrente IRE
   2021 (Fabiana Conciatori), Fondazione AIRC per la Ricerca sul Cancro
   (Emilio Bria, AIRC IG 20583), Ministero dell'Universita e della Ricerca
   (MUR) (Michele Milella, PRIN 2020, grant number B39J21037270006), and
   Ministero della Salute-Fondazione Italiana per lo studio delle Malattie
   del Pancreas (FIMP) (Michele Milella, FIMPCUP_J38D19000690001). Ilaria
   Zampiva was supported by a postdoctoral fellowship through Fondazione
   AIRC per la Ricerca sul Cancro (FIRC).
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NR 49
TC 17
Z9 19
U1 0
U2 3
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2227-9059
J9 BIOMEDICINES
JI Biomedicines
PD OCT
PY 2022
VL 10
IS 10
AR 2631
DI 10.3390/biomedicines10102631
PG 18
WC Biochemistry & Molecular Biology; Medicine, Research & Experimental;
   Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Research & Experimental Medicine;
   Pharmacology & Pharmacy
GA 5O6WM
UT WOS:000872610900001
PM 36289899
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Shimura, T
   Sharma, P
   Sharma, GG
   Banwait, JK
   Goel, A
AF Shimura, Tadanobu
   Sharma, Priyanka
   Sharma, Geeta G.
   Banwait, Jasjit K.
   Goel, Ajay
TI Enhanced anti-cancer activity of andrographis with oligomeric
   proanthocyanidins through activation of metabolic and ferroptosis
   pathways in colorectal cancer
SO SCIENTIFIC REPORTS
LA English
DT Article
ID ACQUIRED-RESISTANCE; HEME OXYGENASE-1; CURCUMIN; CELLS; EXPRESSION;
   COMBINATION; SUPPRESSION; SENSITIZES; PANICULATA; INDUCTION
AB The high degree of morbidity and mortality in colorectal cancer (CRC) patients is largely due to the development of chemoresistance against conventional chemotherapeutic drugs. In view of the accumulating evidence that various dietary botanicals offer a safe, inexpensive and multi-targeted treatment option, herein, we hypothesized that a combination of Andrographis paniculata and Oligomeric Proanthocyanidins (OPCs) might interact together with regard to anti-tumorigenic activity in CRC. As a result, we demonstrated the enhanced anti-cancer activity between these two botanical extracts in terms of their ability to inhibit cancer cell growth, suppress colony formation and induce apoptosis. Furthermore, we validated these findings in subcutaneous xenograft model and in patient derived primary epithelial 3D organoids. Transcriptomic profiling identified involvement of metabolic pathways and ferroptosis-associated genes, including HMOX1, GCLC and GCLM, that may be responsible for the increased anti-tumorigenic activity by the two compounds. Collectively, our study provides novel evidence in support of the combinatorial use of andrographis and OPCs as a potential therapeutic option, perhaps as an adjunctive treatment to classical drugs, in patients with colorectal cancer.
C1 [Shimura, Tadanobu; Sharma, Priyanka; Banwait, Jasjit K.; Goel, Ajay] Baylor Univ, Med Ctr, Baylor Scott & White Res Inst, Ctr Gastrointestinal Res, Dallas, TX 75226 USA.
   [Shimura, Tadanobu; Sharma, Priyanka; Banwait, Jasjit K.; Goel, Ajay] Baylor Univ, Med Ctr, Charles A Sammons Canc Ctr, Dallas, TX 75226 USA.
   [Sharma, Priyanka; Sharma, Geeta G.; Goel, Ajay] City Hope Comprehens Canc Ctr, Beckman Res Inst, Dept Mol Diag & Expt Therapeut, Duarte, CA 91016 USA.
   [Goel, Ajay] City Hope Comprehens Canc Ctr, Beckman Res Inst, Dept Mol Diag & Expt Therapeut, Biotech Innovat, 1218 S Fifth Ave,Suite 2226, Monrovia, CA 91016 USA.
C3 Baylor University Medical Center; Baylor University; Baylor Health Care
   System; Baylor University; Baylor University Medical Center; City of
   Hope; Beckman Research Institute of City of Hope
RP Goel, A (corresponding author), Baylor Univ, Med Ctr, Baylor Scott & White Res Inst, Ctr Gastrointestinal Res, Dallas, TX 75226 USA.; Goel, A (corresponding author), Baylor Univ, Med Ctr, Charles A Sammons Canc Ctr, Dallas, TX 75226 USA.; Goel, A (corresponding author), City Hope Comprehens Canc Ctr, Beckman Res Inst, Dept Mol Diag & Expt Therapeut, Duarte, CA 91016 USA.; Goel, A (corresponding author), City Hope Comprehens Canc Ctr, Beckman Res Inst, Dept Mol Diag & Expt Therapeut, Biotech Innovat, 1218 S Fifth Ave,Suite 2226, Monrovia, CA 91016 USA.
EM ajgoel@coh.org
RI Goel, Ajay/ADO-9623-2022; Sharma, Geeta/AAM-6130-2020; Sharma,
   Priyanka/ABC-6532-2021
OI Banwait, Jasjit Kaur/0000-0002-1643-3375; Sharma,
   Priyanka/0000-0001-9270-8492
FU National Cancer Institute, National Institutes of Health [CA184792,
   CA187956, CA227602, CA072851, CA202797]
FX This work was supported by CA184792, CA187956, CA227602, CA072851 and
   CA202797, grants from the National Cancer Institute, National Institutes
   of Health.
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NR 47
TC 36
Z9 39
U1 4
U2 38
PU NATURE PORTFOLIO
PI BERLIN
PA HEIDELBERGER PLATZ 3, BERLIN, 14197, GERMANY
SN 2045-2322
J9 SCI REP-UK
JI Sci Rep
PD APR 6
PY 2021
VL 11
IS 1
AR 7548
DI 10.1038/s41598-021-87283-y
PG 14
WC Multidisciplinary Sciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Science & Technology - Other Topics
GA UA1MY
UT WOS:000684931200006
PM 33824419
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Li, HS
   Feng, HR
   Zhang, T
   Wu, JW
   Shen, XN
   Xu, SY
   Xu, LH
   Wang, SD
   Zhang, YQ
   Jia, WQ
   Ji, XP
   Cheng, X
   Zhao, R
AF Li, Haosheng
   Feng, Haoran
   Zhang, Tao
   Wu, Junwei
   Shen, Xiaonan
   Xu, Shuiyu
   Xu, Lianghui
   Wang, Shaodong
   Zhang, Yaqi
   Jia, Wenqing
   Ji, Xiaopin
   Cheng, Xi
   Zhao, Ren
TI CircHAS2 activates CCNE2 to promote cell proliferation and sensitizes
   the response of colorectal cancer to anlotinib
SO MOLECULAR CANCER
LA English
DT Article
DE Colorectal cancer; circRNAs; Anlotinib; Biomarker; Translation
ID PATIENT-DERIVED ORGANOIDS; MISMATCH REPAIR; LUNG ADENOCARCINOMA;
   BREAST-CANCER; NONCODING RNA; CHEMOTHERAPY; DIAGNOSIS; ROLES; CERNA; CEA
AB Background Tyrosine kinase inhibitors (TKIs) are crucial in the targeted treatment of advanced colorectal cancer (CRC). Anlotinib, a multi-target TKI, has previously been demonstrated to offer therapeutic benefits in previous studies. Circular RNAs (circRNAs) have been implicated in CRC progression and their unique structural stability serves as promising biomarkers. The detailed molecular mechanisms and specific biomarkers related to circRNAs in the era of targeted therapies, however, remain obscure.Methods The whole transcriptome RNA sequencing and function experiments were conducted to identify candidate anlotinib-regulated circRNAs, whose mechanism was confirmed by molecular biology experiments. CircHAS2 was profiled in a library of patient-derived CRC organoids (n = 22) and patient-derived CRC tumors in mice. Furthermore, a prospective phase II clinical study of 14 advanced CRC patients with anlotinib-based therapy was commenced to verify drug sensitivity (ClinicalTrials.gov identifier: NCT05262335).Results Anlotinib inhibits tumor growth in vitro and in vivo by downregulating circHAS2. CircHAS2 modulates CCNE2 activation by acting as a sponge for miR-1244, and binding to USP10 to facilitate p53 nuclear export as well as degradation. In parallel, circHAS2 serves as a potent biomarker predictive of anlotinib sensitivity, both in patient-derived organoids and xenograft models. Moreover, the efficacy of anlotinib inclusion into the treatment regimen yields meaningful clinical responses in patients with high levels of circHAS2. Our findings offer a promising targeted strategy for approximately 52.9% of advanced CRC patients who have high circHAS2 levels.Conclusions CircHAS2 promotes cell proliferation via the miR-1244/CCNE2 and USP10/p53/CCNE2 bidirectional axes. Patient-derived organoids and xenograft models are employed to validate the sensitivity to anlotinib. Furthermore, our preliminary Phase II clinical study, involving advanced CRC patients treated with anlotinib, confirmed circHAS2 as a potential sensitivity marker.
C1 [Li, Haosheng; Feng, Haoran; Zhang, Tao; Xu, Shuiyu; Xu, Lianghui; Wang, Shaodong; Zhang, Yaqi; Jia, Wenqing; Ji, Xiaopin; Cheng, Xi; Zhao, Ren] Shanghai Jiao Tong Univ, Ruijin Hosp, Sch Med, Dept Gen Surg, Shanghai, Peoples R China.
   [Li, Haosheng; Feng, Haoran; Zhang, Tao; Xu, Lianghui; Jia, Wenqing; Ji, Xiaopin; Cheng, Xi; Zhao, Ren] Shanghai Jiao Tong Univ, Ruijin Hosp, Shanghai Inst Digest Surg, Sch Med, Shanghai, Peoples R China.
   [Wu, Junwei] Shanghai Jiao Tong Univ, Ruijin Hosp, Sch Med, Dept Oncol, Shanghai, Peoples R China.
   [Shen, Xiaonan] Shanghai Jiao Tong Univ, Ruijin Hosp, Sch Med, Dept Gastroenterol, Shanghai, Peoples R China.
C3 Shanghai Jiao Tong University; Shanghai Jiao Tong University; Shanghai
   Jiao Tong University; Shanghai Jiao Tong University
RP Ji, XP; Cheng, X; Zhao, R (corresponding author), Shanghai Jiao Tong Univ, Ruijin Hosp, Sch Med, Dept Gen Surg, Shanghai, Peoples R China.; Ji, XP; Cheng, X; Zhao, R (corresponding author), Shanghai Jiao Tong Univ, Ruijin Hosp, Shanghai Inst Digest Surg, Sch Med, Shanghai, Peoples R China.
EM surgeonjee@hotmail.com; drchengxi@126.com; rjzhaoren@139.com
RI Wu, Junwei/IUM-6922-2023; 王, 绍东/GSO-2648-2022; feng,
   haoran/JJF-9894-2023; chen, xinyu/HNR-2708-2023
OI Li, Haosheng/0000-0001-5446-9929
FU National Natural Science Foundation of China; Peer Escort Program in the
   Academic Department of the Resident Committee at Ruijin Hospital;
   Shanghai Jiao Tong University School of Medicine
FX The authors appreciate the support from Peer Escort Program in the
   Academic Department of the Resident Committee at Ruijin Hospital,
   affiliated with the Shanghai Jiao Tong University School of Medicine. We
   also thank Home for Researchers editorial team
   (www.home-for-researchers.com) for language editing.
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NR 53
TC 0
Z9 0
U1 7
U2 8
PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
EI 1476-4598
J9 MOL CANCER
JI Mol. Cancer
PD MAR 21
PY 2024
VL 23
IS 1
AR 59
DI 10.1186/s12943-024-01971-7
PG 19
WC Biochemistry & Molecular Biology; Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Oncology
GA LZ1N7
UT WOS:001190544900001
PM 38515149
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Noreen, S
   Pervaiz, F
   Ijaz, M
   Hanif, MF
   Hamza, JR
   Mahmood, H
   Shoukat, H
   Maqbool, I
   Ashraf, MA
AF Noreen, Sobia
   Pervaiz, Fahad
   Ijaz, Muhammad
   Hanif, Muhammad Farhan
   Hamza, Jam Riyan
   Mahmood, Hassan
   Shoukat, Hina
   Maqbool, Irsah
   Ashraf, Muhammad Azeem
TI pH-sensitive docetaxel-loaded chitosan/thiolated hyaluronic acid
   polymeric nanoparticles for colorectal cancer
SO NANOMEDICINE
LA English
DT Article
DE colon targeting; mucoadhesive studies; nanoparticles; pH-sensitive drug
   release; thiolated hyaluronic acid
ID IN-VITRO EVALUATION; MUCOADHESIVE POLYMER; DELIVERY-SYSTEMS; VIVO
   EVALUATION; DRUG; CYCLODEXTRIN; MICROSPHERES
AB Aim: This study aimed to develop and evaluate pH-sensitive docetaxel-loaded thiolated hyaluronic acid (HA-SH) nanoparticles (NPs) for targeted treatment of colon cancer. Materials & methods: HA-SH, synthesized via oxidation and subsequent covalent linkage to cysteamine, served as the precursor for developing HA-SH NPs through polyelectrolyte complexation involving chitosan and thiol-bearing HA. Results & conclusion: HA-SH NPs displayed favorable characteristics, with small particle sizes (184-270 nm), positive zeta potential (15.4-18.6 mV) and high entrapment efficiency (91.66-95.02%). In vitro, NPs demonstrated potent mucoadhesion and enhanced cytotoxicity compared with free docetaxel. In vivo assessments confirmed safety and biocompatibility, suggesting HA-SH NPs as promising pH-sensitive drug carriers with enhanced antitumor activity for colorectal cancer treatments.
C1 [Noreen, Sobia; Pervaiz, Fahad; Hanif, Muhammad Farhan; Shoukat, Hina; Maqbool, Irsah] Islamia Univ Bahawalpur, Fac Pharm, Dept Pharmaceut, Bahawalpur 63100, Punjab, Pakistan.
   [Noreen, Sobia; Ijaz, Muhammad] Univ Innsbruck, Inst Pharm, Ctr Chem & Biomed, Dept Pharmaceut Technol, A-6020 Innsbruck, Austria.
   [Ijaz, Muhammad; Mahmood, Hassan] COMSATS Univ Islamabad, Lahore Campus, Lahore 54000, Punjab, Pakistan.
   [Hamza, Jam Riyan] Univ Minnesota, Dept Chem & Biochem, Duluth, MN 55812 USA.
   [Ashraf, Muhammad Azeem] Univ Management & Technol, Lahore 54770, Pakistan.
C3 Islamia University of Bahawalpur; University of Innsbruck; COMSATS
   University Islamabad (CUI); University of Minnesota System; University
   of Minnesota Duluth; University of Management & Technology (UMT)
RP Pervaiz, F (corresponding author), Islamia Univ Bahawalpur, Fac Pharm, Dept Pharmaceut, Bahawalpur 63100, Punjab, Pakistan.
EM fahad.pervaiz@iub.edu.pk
RI Pervaiz, Fahad/JVN-2172-2024; Noreen, Sobia/AAT-8296-2021; Ijaz,
   Muhammad/IUN-3825-2023
OI Noreen, Sobia/0000-0002-4407-6002; Pervaiz, Fahad/0000-0003-1941-082X
FU Higher Education Commission (HEC) indigenous Pakistan
FX This research work was supported by the Higher Education Commission
   (HEC) indigenous Pakistan. The funder did not have any role in the study
   design, data collection and analysis or preparation of the manuscript.
   The authors have no other relevant affiliations or financial involvement
   with any organization or entity with a financial interest in or
   financial conflict with the subject matter or materials discussed in the
   manuscript apart from those disclosed.
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NR 70
TC 1
Z9 1
U1 6
U2 22
PU TAYLOR & FRANCIS LTD
PI ABINGDON
PA 2-4 PARK SQUARE, MILTON PARK, ABINGDON OR14 4RN, OXON, ENGLAND
SN 1743-5889
EI 1748-6963
J9 NANOMEDICINE-UK
JI Nanomedicine
PD APR
PY 2024
VL 19
IS 9
BP 755
EP 777
DI 10.2217/nnm-2023-0318
EA FEB 2024
PG 23
WC Biotechnology & Applied Microbiology; Nanoscience & Nanotechnology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biotechnology & Applied Microbiology; Science & Technology - Other
   Topics
GA LO4V4
UT WOS:001158072000001
PM 38334078
DA 2025-01-04
ER

PT J
AU Zhou, J
   Yu, WQ
   Xia, J
   Li, SY
   Xie, LS
   Wang, X
AF Zhou, Jin
   Yu, Wenqian
   Xia, Jing
   Li, Shiyi
   Xie, Linshen
   Wang, Xin
TI Not all Rectal Cancer Patients Could Benefit From the Surgery on the
   Primary Site
SO CANCER CONTROL
LA English
DT Article
DE rectal cancer; surgery on primary site; prognosis; propensity score
   matching; precise treatment
ID COLORECTAL-CANCER; RESECTION; SURVIVAL
AB AimPrevious studies have provided evidence that primary site surgery can improve the prognosis of rectal cancer patients, even in those with advanced age and distant metastasis, though results have been inconsistent. The current study aims to determine if all rectal cancer patients are likely to benefit from surgery in terms of overall survival.MethodsThis study examined the impact of primary site surgery on the prognosis of rectal cancer patients diagnosed between 2010 and 2019 using multivariable Cox regression analysis. The study also stratified patients by age group, M stage, chemotherapy, radiotherapy, and number of distant metastatic organs. The propensity score matching method was used to balance observed covariates between patients who received and did not receive surgery. The Kaplan-Meier method was used to analyze the data, and the log-rank test was used to determine differences between patients who did and did not undergo surgery.ResultsThe study included 76,941 rectal cancer patients, with a median survival of 81.0 months (95% CI: 79.2-82.8 months). Of these patients, 52,360 (68.1%) received primary site surgery, and they tended to be younger, have higher differentiated grade, earlier T, N, M stage, and lower rates of bone, brain, lung, and liver metastasis, chemotherapy, and radiotherapy than those without surgery. Multivariable Cox regression analysis revealed that surgery had a protective effect on the prognosis of rectal cancer patients, including those with advanced age, distant metastasis, and multiple organ metastasis, but not in patients with four organ metastases. The results were also confirmed using propensity score matching.ConclusionNot all rectal cancer patients could benefit from the surgery on the primary site, especially the patients with more than four distant metastases. The results could help the clinicians to tailor targeted treatment regimens and provide a guideline for making surgical decisions.
C1 [Zhou, Jin] Hosp Chengdu Univ Tradit Chinese Med, Dept Anorectal Surg, Chengdu, Sichuan, Peoples R China.
   [Yu, Wenqian; Wang, Xin] Sichuan Univ, West China Sch Publ Hlth, Dept Epidemiol & Biostat, Chengdu, Peoples R China.
   [Yu, Wenqian; Xia, Jing; Li, Shiyi; Xie, Linshen; Wang, Xin] Sichuan Univ, West China Hosp 4, Dept Epidemiol & Biostat, Chengdu, Peoples R China.
   [Yu, Wenqian; Wang, Xin] Sichuan Univ, West China Sch Publ Hlth, West China PUMC C C Chen Inst Hlth, Chengdu, Peoples R China.
   [Xia, Jing; Li, Shiyi; Xie, Linshen] Sichuan Univ, West China Sch Publ Hlth, Prevent Med, Chengdu, Peoples R China.
   [Wang, Xin] Sichuan Univ, West China Sch Publ Hlth, Dept Epidemiol & Biostat, South Renmin Rd, Chengdu 610041, Peoples R China.
   [Xie, Linshen; Wang, Xin] Sichuan Univ, West China Hosp 4, South Renmin Rd, Chengdu 610041, Peoples R China.
   [Xie, Linshen] Sichuan Univ, West China Sch Publ Hlth, South Renmin Rd, Chengdu 610041, Peoples R China.
C3 Chengdu University of Traditional Chinese Medicine; Sichuan University;
   Sichuan University; Sichuan University; Sichuan University; Sichuan
   University; Sichuan University; Sichuan University
RP Wang, X (corresponding author), Sichuan Univ, West China Sch Publ Hlth, Dept Epidemiol & Biostat, South Renmin Rd, Chengdu 610041, Peoples R China.; Xie, LS; Wang, X (corresponding author), Sichuan Univ, West China Hosp 4, South Renmin Rd, Chengdu 610041, Peoples R China.; Xie, LS (corresponding author), Sichuan Univ, West China Sch Publ Hlth, South Renmin Rd, Chengdu 610041, Peoples R China.
EM linshenxie@163.com; wangxinmarine@12.com
RI Shiyi, Li/HPE-1321-2023; Wang, Xin/N-8865-2018
OI Wang, Xin/0000-0001-9325-3194
FU National Natural Science Foundation of China [81903398]; research
   start-up fund for the introduction of talents of Sichuan University
   [YJ2021112]; Medical youth Innovation research project of Sichuan
   Province [Q21016]
FX The author(s) disclosed receipt of the following financial support for
   the research, authorship, and/or publication of this article: The study
   was supported by the National Natural Science Foundation of China
   (81903398), The research start-up fund for the introduction of talents
   of Sichuan University (YJ2021112), Medical youth Innovation research
   project of Sichuan Province (Q21016).
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NR 25
TC 1
Z9 1
U1 1
U2 2
PU SAGE PUBLICATIONS INC
PI THOUSAND OAKS
PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA
SN 1073-2748
EI 1526-2359
J9 CANCER CONTROL
JI Cancer Control
PD MAY 23
PY 2023
VL 30
AR 10732748231180056
DI 10.1177/10732748231180056
PG 10
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA I8LY1
UT WOS:001005257100001
PM 37279737
OA Green Submitted, Green Published, gold
DA 2025-01-04
ER

PT J
AU Naidoo, M
   Piercey, O
   Tie, J
AF Naidoo, Mahendra
   Piercey, Oliver
   Tie, Jeanne
TI Circulating Tumour DNA and Colorectal Cancer: the Next Revolutionary
   Biomarker?
SO CURRENT ONCOLOGY REPORTS
LA English
DT Review
DE ctDNA; Adjuvant chemotherapy; Colorectal cancer; Biomarker; Minimal
   residual disease; Metastatic; Molecular resistance
ID III COLON-CANCER; FOLFIRI PLUS BEVACIZUMAB; MINIMAL RESIDUAL DISEASE;
   CELL-FREE DNA; FOLLOW-UP; STAGE-II; ACQUIRED-RESISTANCE;
   CLINICAL-PRACTICE; ADJUVANT THERAPY; OPEN-LABEL
AB Purpose of Review Improving outcomes for patients with colorectal cancer in both the adjuvant and metastatic setting has been challenging. Here, we review the current and future directions for using ctDNA in clinical practice. Recent Findings Circulating tumour DNA (ctDNA) with its ability to detect minimal residual disease is beginning to refine the way we assess recurrence risk in the adjuvant setting. We can potentially tailor treatments to reduce recurrence risk and minimize treatment toxicity. In the metastatic setting, ctDNA can provide a less invasive method of detecting clinically important genetic changes to guide molecularly targeted treatment and to identify mechanisms of molecular resistance. ctDNA can be a surrogate marker for treatment response and help guide the timing of anti-EGFR rechallenge. We await the results of the randomized clinical trials assessing clinical utility of ctDNA in both the adjuvant and metastatic setting before incorporating ctDNA into clinical practice.
C1 [Naidoo, Mahendra; Piercey, Oliver; Tie, Jeanne] Peter MacCallum Canc Ctr, Dept Med Oncol, 305 Grattan St, Melbourne, Vic 3000, Australia.
   [Tie, Jeanne] Walter & Eliza Hall Inst Med Res, Div Personalised Oncol, Melbourne, Vic 3052, Australia.
   [Tie, Jeanne] Western Hlth, Dept Med Oncol, Melbourne, Vic 3021, Australia.
   [Tie, Jeanne] Univ Melbourne, Sir Peter MacCallum Dept Oncol, Melbourne, Vic 3010, Australia.
C3 Peter Maccallum Cancer Center; Western Health; Peter Maccallum Cancer
   Center; University of Melbourne
RP Naidoo, M (corresponding author), Peter MacCallum Canc Ctr, Dept Med Oncol, 305 Grattan St, Melbourne, Vic 3000, Australia.
EM mahendra.naidoo@petermac.org; opiercey@gmail.com; tie.j@wehi.edu.au
RI piercey, oliver/LOQ-9049-2024
OI Piercey, Oliver/0000-0003-2220-2570
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NR 71
TC 1
Z9 2
U1 0
U2 8
PU SPRINGER
PI NEW YORK
PA ONE NEW YORK PLAZA, SUITE 4600, NEW YORK, NY, UNITED STATES
SN 1523-3790
EI 1534-6269
J9 CURR ONCOL REP
JI Curr. Oncol. Rep.
PD DEC
PY 2021
VL 23
IS 12
AR 140
DI 10.1007/s11912-021-01137-4
PG 13
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA WR6BU
UT WOS:000714583600005
PM 34735665
DA 2025-01-04
ER

PT J
AU Ibrahim, IAA
   Alzahrani, AR
   Alanazi, IM
   Shahzad, N
   Shahid, I
   Falemban, AH
   Azlina, MFN
   Arulselvan, P
AF Ibrahim, Ibrahim Abdel Aziz
   Alzahrani, Abdullah R.
   Alanazi, Ibrahim M.
   Shahzad, Naiyer
   Shahid, Imran
   Falemban, Alaa Hisham
   Azlina, Mohd Fahami Nur
   Arulselvan, Palanisamy
TI Carbohydrate polymers-based surface modified nano delivery systems for
   enhanced target delivery to colon cancer - A review
SO INTERNATIONAL JOURNAL OF BIOLOGICAL MACROMOLECULES
LA English
DT Review
DE Surface modification; Carbohydrate polymers; Colon cancer; Chitosan;
   Enhanced delivery; Solid lipid nanoparticles; Pectin; Guar gum
ID SOLID LIPID NANOPARTICLES; DEPENDENT CELLULAR UPTAKE; IRON-OXIDE
   NANOPARTICLES; DRUG-DELIVERY; GOLD NANOPARTICLES; GRAPHENE OXIDE;
   MAGNETIC NANOPARTICLES; IN-VITRO; 5-FLUOROURACIL; CHITOSAN
AB Carbohydrate polymers-based surface-modified nano-delivery systems have gained significant attention in recent years for enhancing targeted delivery to colon cancer. These systems leverage carbohydrate polymers' unique properties, such as biocompatibility, biodegradability, and controlled release. These properties make them suitable candidates for drug delivery applications. Nano-delivery systems loaded with bioactive compounds are well-studied for targeted colorectal cancer delivery. However, those drugs' target reach is still limited in various nano-delivery systems. To overcome this limitation, surface modification of nanoparticles with carbohydrate polymers like chitosan, pectin, alginate, and guar gum showed enhanced target-reaching capacity along with enhanced anticancer efficacy. Recently, a chitosan-decorated PLGA nanoparticle was constructed with tannic acid and vitamin E and showed long-term release of specific targets along with higher anticancer efficacy. Similarly, Chitosan-conjugated glucuronic acid-coated silica nanoparticles loaded with capecitabine were studied against colon cancer and found to be the pH-responsive controlled release of capecitabine with higher anticancer efficacy. Surface-modified carbohydrate polymers have promising potential for improving colon cancer target delivery. By leveraging the unique properties of these polymers, such as surface modification, pH responsiveness, mucoadhesion, controlled drug release, and combination therapy, researchers are working toward developing more effective and targeted treatment strategies for colon cancer.
C1 [Ibrahim, Ibrahim Abdel Aziz; Alzahrani, Abdullah R.; Alanazi, Ibrahim M.; Shahzad, Naiyer; Shahid, Imran; Falemban, Alaa Hisham] Umm Al Qura Univ, Fac Med, Dept Pharmacol & Toxicol, Mecca, Saudi Arabia.
   [Azlina, Mohd Fahami Nur] Univ Kebangsaan Malaysia, Fac Med, Dept Pharmacol, Bangi, Malaysia.
   [Arulselvan, Palanisamy] Saveetha Univ, Saveetha Inst Med & Tech Sci SIMATS, Saveetha Sch Engn, Dept Chem, Chennai 602105, Tamil Nadu, India.
   [Ibrahim, Ibrahim Abdel Aziz] Umm Al Qura Univ, Dept Pharmacol & Toxicol, Mecca, Saudi Arabia.
C3 Umm Al Qura University; Universiti Kebangsaan Malaysia; Saveetha
   Institute of Medical & Technical Science; Saveetha School of
   Engineering; Umm Al Qura University
RP Ibrahim, IAA (corresponding author), Umm Al Qura Univ, Dept Pharmacol & Toxicol, Mecca, Saudi Arabia.
EM iamustafa@uqu.edu.sa
RI Ibrahim, Ibrahim/AAE-4458-2022; Hisham, Alaa/HDO-1159-2022; shahid,
   imran/ADK-4329-2022; ARULSELVAN, PALANISAMY/M-6388-2014; Alzahrani,
   Abdullah/ITT-0849-2023; Mohamad, Nur-Vaizura/ABA-2933-2021; Shahzad,
   Naiyer/AAD-9394-2022
OI Shahid, Imran/0000-0002-9832-3224; Alzahrani, Abdullah Rzgallah
   R/0000-0001-7782-0574
FU Deputyship for Research & Innovation, Ministry of Education in Saudi
   Arabia [IFP22UQU4331277DSR124]
FX The authors extend their appreciation to the Deputyship for Research &
   Innovation, Ministry of Education in Saudi Arabia for funding this
   research work through the project number: IFP22UQU4331277DSR124.
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NR 114
TC 11
Z9 11
U1 19
U2 65
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
SN 0141-8130
EI 1879-0003
J9 INT J BIOL MACROMOL
JI Int. J. Biol. Macromol.
PD DEC 31
PY 2023
VL 253
AR 126581
DI 10.1016/j.ijbiomac.2023.126581
EA SEP 2023
PN 2
PG 9
WC Biochemistry & Molecular Biology; Chemistry, Applied; Polymer Science
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Chemistry; Polymer Science
GA T5KA6
UT WOS:001078362600001
PM 37652322
DA 2025-01-04
ER

PT J
AU Deng, XQ
   Zhang, HB
   Wang, GF
   Xu, D
   Zhang, WY
   Wang, QS
   Cui, YL
AF Deng, Xiao-Qing
   Zhang, Hong-Bo
   Wang, Gui-Fang
   Xu, Dong
   Zhang, Wen-Yan
   Wang, Qiang-Song
   Cui, Yuan-Lu
TI Colon-specific microspheres loaded with puerarin reduce tumorigenesis
   and metastasis in colitis-associated colorectal cancer
SO INTERNATIONAL JOURNAL OF PHARMACEUTICS
LA English
DT Article
DE Puerarin; Microspheres; pH-responsive; Colon-specific drug delivery;
   Colitis-associated colorectal cancer
ID ALGINATE MICROPARTICLES; IN-VITRO; DRUG; INFLAMMATION; RELEASE; DESIGN
AB Colitis-associated colorectal cancer (CAC) is a common malignancy that develops in chronically inflamed mucosa and is usually accompanied by metastases at other sites. Puerarin, a natural isoflavone isolated from the root of the Pueraria lobata (Willd.) Ohwi, has potential anti-colon cancer activity. However, the poor solubility and low bioavailability of puerarin has restricted its application in the pharmaceutical industry. In the present study, pH-responsive alginate microspheres loaded with puerarin were prepared by emulsification/internal gelation for targeted treatment of colitis-associated colorectal cancer. Herein, puerarin, as an active drug, could participate in the construction of alginate microspheres with hydrogen bonding. The microspheres exhibited pH-responsive release behavior with little release of puerarin in simulated gastric fluid and high amounts (approximately 55%) of release in simulated colonic fluid. A fluorescence tracer indicated microspheres had high retention time of more than 20 h in the colon. Meanwhile, puerarin-loaded alginate microspheres not only significantly decreased the inflammatory response by downregulating the levels of pro-tumorigenic cytokines, but they reduced tumorigenesis and metastasis by inhibiting epithelial-mesenchymal transitions in AOM/DSS-induced colitis-associated colorectal cancer in mice. The overall results suggested that puerarin-loaded alginate microspheres could effectively inhibit development of colonic tumors, which could be developed as a promising therapeutic strategy for colitis-associated colorectal cancer.
C1 [Deng, Xiao-Qing; Wang, Gui-Fang; Xu, Dong; Zhang, Wen-Yan; Cui, Yuan-Lu] Tianjin Univ Tradit Chinese Med, Res Ctr Tradit Chinese Med, Tianjin State Key Lab Modern Chinese Med, Tianjin 301617, Peoples R China.
   [Zhang, Hong-Bo] Nankai Hosp, Tianjin Hosp ITCWM, Dept Med Oncol, Tianjin 300100, Peoples R China.
   [Wang, Qiang-Song] Chinese Acad Med Sci, Inst Biomed Engn, Tianjin Key Lab Biomed Mat, Tianjin 300192, Peoples R China.
   [Wang, Qiang-Song] Peking Union Med Coll, Tianjin 300192, Peoples R China.
C3 Tianjin University of Traditional Chinese Medicine; Chinese Academy of
   Medical Sciences - Peking Union Medical College; Institute of BioMedical
   Engineering - CAMS; Chinese Academy of Medical Sciences - Peking Union
   Medical College; Peking Union Medical College
RP Cui, YL (corresponding author), Tianjin Univ Tradit Chinese Med, Res Ctr Tradit Chinese Med, Tianjin State Key Lab Modern Chinese Med, Tianjin 301617, Peoples R China.; Wang, QS (corresponding author), Chinese Acad Med Sci, Inst Biomed Engn, Tianjin Key Lab Biomed Mat, Tianjin 300192, Peoples R China.; Wang, QS (corresponding author), Peking Union Med Coll, Tianjin 300192, Peoples R China.
EM wangqs@bme.cams.cn; cuiyl@tju.edu.cn
RI Cui, Yuan-Lu/A-3705-2013; zhang, hongbo/AAR-5498-2021
OI Cui, Yuan-Lu/0000-0003-4392-3713
FU National Natural Science Foundation of China [81473542, 81741119,
   31500761]
FX 3This work was supported by the National Natural Science Foundation of
   China (81473542, 81741119, 31500761).
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NR 50
TC 37
Z9 46
U1 6
U2 73
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
SN 0378-5173
EI 1873-3476
J9 INT J PHARMACEUT
JI Int. J. Pharm.
PD OCT 30
PY 2019
VL 570
AR 118644
DI 10.1016/j.ijpharm.2019.118644
PG 11
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA JE9UM
UT WOS:000491033000011
PM 31465837
DA 2025-01-04
ER

PT J
AU Trombino, S
   Serini, S
   Cassano, R
   Calviello, G
AF Trombino, Sonia
   Serini, Simona
   Cassano, Roberta
   Calviello, Gabriella
TI Xanthan gum-based materials for omega-3 PUFA delivery: Preparation,
   characterization and antineoplastic activity evaluation
SO CARBOHYDRATE POLYMERS
LA English
DT Article
DE Colon cancer cells; Carrier delivery; Hydrogels; Omega-3; Targeted
   treatment; Xanthan gum
ID ALPHA-LINOLENIC ACID; BREAST-CANCER CELLS; POLYUNSATURATED FATTY-ACIDS;
   SOLID LIPID NANOPARTICLES; DHA INDUCES APOPTOSIS; COLORECTAL-CANCER;
   COLON-CANCER; DOCOSAHEXAENOIC ACID; PROSTATE-CANCER; IN-VITRO
AB Xanthan gum-based microspheres and hydrogels, useful for targeted colorectal release of omega-3 polyunsaturated fatty acids (PUFAs), were successfully prepared and characterized. In particular, the microsphere size, as well as the high hydrogel swelling degree at pH 7.4, and the omega-3 PUFA loading efficiency of both the materials suggested their suitability for colorectal delivery. Moreover, the antioxidant efficiency of the xanthan gum based materials suggests their ability to protect the omega-PUFA cargo. We demonstrated that a-linolenic acid (ALA 18:3 omega-3) carried by the materials increased significantly its ability to reduce colorectal cancer cell growth in vitro. On the contrary, docosahexaenoic acid (DHA, 22:6 omega-3) enclosed in the hydrogel formulation did not enhance its already high anti-neoplastic potential. The improved anti-neoplastic efficacy of ALA enclosed in both the xanthan gum-based formulations further supports the hypothesis of a potential use of this omega-3 PUFA as a suitable and more sustainable alternative to the fish-derived DHA.
C1 [Trombino, Sonia; Cassano, Roberta] Univ Calabria, Dept Pharm Hlth & Nutr Sci, I-87036 Cosenza, Italy.
   [Serini, Simona; Calviello, Gabriella] Univ Cattolica Sacro Cuore, Inst Gen Pathol, Rome, Italy.
   [Serini, Simona; Calviello, Gabriella] Fdn Policlin Univ A Gemelli IRCCS, Rome, Italy.
C3 University of Calabria; Catholic University of the Sacred Heart; IRCCS
   Policlinico Gemelli; Catholic University of the Sacred Heart; IRCCS
   Policlinico Gemelli
RP Cassano, R (corresponding author), Univ Calabria, Dept Pharm Hlth & Nutr Sci, I-87036 Cosenza, Italy.
EM roberta.cassano@unical.it
RI Serini, Simona/AFS-0703-2022; Cannataro, Roberto/ABH-6608-2020
OI SERINI, Simona/0000-0002-6894-1443
FU Universita Cattolica del S. Cuore, Roma, Italia, within its program of
   promotion and diffusion of scientific research [Linea D1 2015, Linea D1
   2016, Linea D.3.2 2013, D.3.2 2015]
FX This work was supported in part by: 1) grants Linea D1 2015 and Linea D1
   2016, Linea D.3.2 2013 and D.3.2 2015 to G.C. from Universita Cattolica
   del S. Cuore, Roma, Italia, within its program of promotion and
   diffusion of scientific research.
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NR 73
TC 31
Z9 32
U1 7
U2 62
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 0144-8617
EI 1879-1344
J9 CARBOHYD POLYM
JI Carbohydr. Polym.
PD MAR 15
PY 2019
VL 208
BP 431
EP 440
DI 10.1016/j.carbpol.2019.01.001
PG 10
WC Chemistry, Applied; Chemistry, Organic; Polymer Science
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Chemistry; Polymer Science
GA HH3LF
UT WOS:000455620300049
PM 30658821
DA 2025-01-04
ER

PT J
AU Eilertsen, IA
   Sveen, A
   Stromme, JM
   Skotheim, RI
   Nesbakken, A
   Lothe, RA
AF Eilertsen, Ina A.
   Sveen, Anita
   Stromme, Jonas M.
   Skotheim, Rolf I.
   Nesbakken, Arild
   Lothe, Ragnhild A.
TI Alternative splicing expands the prognostic impact of <i>KRAS</i> in
   microsatellite stable primary colorectal cancer
SO INTERNATIONAL JOURNAL OF CANCER
LA English
DT Article
DE KRAS; alternative splicing; colorectal cancer; microsatellite stable;
   prognosis
ID CONSENSUS MOLECULAR SUBTYPES; K-RAS 4A; HUMAN-COLON; GENE
AB KRAS mutation is a well-known marker for poor response to targeted treatment and patient prognosis in microsatellite stable (MSS) colorectal cancer (CRC). However, variation in clinical outcomes among patients wild-type for KRAS underlines that this is not a homogeneous population. Here, we evaluated the prognostic impact of KRAS alternative splicing in relation to mutation status in a single-hospital series of primary MSS CRCs (N = 258). Using splicing-sensitive microarrays and RNA sequencing, the relative expression of KRAS-4A versus KRAS-4B transcript variants was confirmed to be down-regulated in CRC compared to normal colonic mucosa (N = 41; p <= 0.001). This was independent of mutation status, however, gene set enrichment analysis revealed that the effect of splicing on KRAS signaling was specific to the KRAS wild-type subgroup, in which low relative KRAS-4A expression was associated with a higher level of KRAS signaling (p = 0.005). In concordance, the prognostic value of KRAS splicing was also dependent on mutation status, and for patients with Stage I-III KRAS wild-type MSS CRC, low relative KRAS-4A expression was associated with inferior overall survival (HR: 2.36, 95% CI: 1.07-5.18, p = 0.033), a result not found in mutant cases (p(interaction) = 0.026). The prognostic association in the wild-type subgroup was independent of clinicopathological factors, including cancer stage in multivariable analysis (HR: 2.68, 95% CI: 1.18-6.09, p = 0.018). This suggests that KRAS has prognostic value beyond mutation status in MSS CRC, and highlights the importance of molecular heterogeneity in the clinically relevant KRAS wild-type subgroup.
C1 [Eilertsen, Ina A.; Sveen, Anita; Stromme, Jonas M.; Skotheim, Rolf I.; Lothe, Ragnhild A.] Oslo Univ Hosp, Inst Canc Res, Dept Mol Oncol, POB 4953 Nydalen, N-0424 Oslo, Norway.
   [Eilertsen, Ina A.; Sveen, Anita; Stromme, Jonas M.; Skotheim, Rolf I.; Nesbakken, Arild; Lothe, Ragnhild A.] Oslo Univ Hosp, KG Jebsen Colorectal Canc Res Ctr, Oslo, Norway.
   [Eilertsen, Ina A.; Sveen, Anita; Nesbakken, Arild; Lothe, Ragnhild A.] Univ Oslo, Inst Clin Med, Fac Med, Oslo, Norway.
   [Stromme, Jonas M.; Skotheim, Rolf I.] Univ Oslo, Fac Math & Nat Sci, Dept Informat, Oslo, Norway.
   [Nesbakken, Arild] Oslo Univ Hosp, Dept Gastrointestinal Surg, Oslo, Norway.
C3 University of Oslo; University of Oslo; University of Oslo; University
   of Oslo; University of Oslo
RP Lothe, RA (corresponding author), Oslo Univ Hosp, Inst Canc Res, Dept Mol Oncol, POB 4953 Nydalen, N-0424 Oslo, Norway.
EM ragnhild.a.lothe@rr-research.no
RI ; Skotheim, Rolf I./H-6192-2017
OI Sveen, Anita/0000-0001-8219-6251; Skotheim, Rolf I./0000-0002-5609-4048;
   Lothe, Ragnhild A./0000-0002-1693-1032
FU Stiftelsen Kristian Gerhard Jebsen; Norwegian Cancer Society
   [6824048-2016, 182759-2016]; Research Council of Norway (FRIPRO
   Toppforsk) [250993]
FX Grant sponsor: Stiftelsen Kristian Gerhard Jebsen; Grant sponsor:
   Norwegian Cancer Society; Grant number: 6824048-2016, 182759-2016; Grant
   sponsor: Research Council of Norway (FRIPRO Toppforsk); Grant number:
   250993
CR Abubaker J, 2009, J PATHOL, V219, P435, DOI 10.1002/path.2625
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NR 25
TC 22
Z9 23
U1 0
U2 5
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0020-7136
EI 1097-0215
J9 INT J CANCER
JI Int. J. Cancer
PD FEB 15
PY 2019
VL 144
IS 4
BP 841
EP 847
DI 10.1002/ijc.31809
PG 7
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA HF2XD
UT WOS:000454099100016
PM 30121958
OA Green Published, hybrid
DA 2025-01-04
ER

PT J
AU Cortese, M
   Torchiaro, E
   D'Andrea, A
   Petti, C
   Invrea, F
   Franco, L
   Donini, C
   Leuci, V
   Leto, SM
   Vurchio, V
   Cottino, F
   Isella, C
   Arena, S
   Vigna, E
   Bertotti, A
   Trusolino, L
   Sangiolo, D
   Medico, E
AF Cortese, Marco
   Torchiaro, Erica
   D'Andrea, Alice
   Petti, Consalvo
   Invrea, Federica
   Franco, Letizia
   Donini, Chiara
   Leuci, Valeria
   Leto, Simonetta Maria
   Vurchio, Valentina
   Cottino, Francesca
   Isella, Claudio
   Arena, Sabrina
   Vigna, Elisa
   Bertotti, Andrea
   Trusolino, Livio
   Sangiolo, Dario
   Medico, Enzo
TI Preclinical efficacy of a HER2 synNotch/CEA-CAR combinatorial
   immunotherapy against colorectal cancer with HER2 amplification
SO MOLECULAR THERAPY
LA English
DT Article
ID CARCINOEMBRYONIC ANTIGEN CEA; CELL-LINE NK-92; T-CELLS; EXPRESSION;
   RECEPTOR; IDENTIFICATION; ACTIVATION; SAFETY; TRIAL; COLON
AB HER2 amplification occurs in approximately 5% of colorectal cancer (CRC) cases and is associated only partially with clinical response to combined human epidermal growth factor receptor 2 (HER2)/epidermal growth factor receptor (EGFR)targeted treatment. An alternative approach based on adoptive cell therapy using T cells engineered with anti-HER2 chimeric antigen receptor (CAR) proved to be toxic due to on-target/off-tumor activity. Here we describe a combinatorial strategy to safely target HER2 amplification and carcinoembryonic antigen (CEA) expression in CRC using a synNotch-CAR-based artificial regulatory network. The natural killer (NK) cell line NK-92 was engineered with an antiHER2 synNotch receptor driving the expression of a CAR against CEA only when engaged. After being transduced and sorted for HER2-driven CAR expression, cells were cloned. The clone with optimal performances in terms of specificity and amplitude of CAR induction demonstrated significant activity in vitro and in vivo specifically against HER2-amplified (HER2amp)/CEA+ CRC models, with no effects on cells with physiological HER2 levels. The HER2-synNotch/CEACAR-NK system provides an innovative, scalable, and safe off-the-shelf cell therapy approach with potential against HER2amp CRC resistant or partially responsive to HER2/ EGFR blockade.
C1 [Cortese, Marco; Torchiaro, Erica; D'Andrea, Alice; Petti, Consalvo; Invrea, Federica; Franco, Letizia; Donini, Chiara; Leuci, Valeria; Leto, Simonetta Maria; Vurchio, Valentina; Cottino, Francesca; Isella, Claudio; Arena, Sabrina; Vigna, Elisa; Bertotti, Andrea; Trusolino, Livio; Sangiolo, Dario; Medico, Enzo] FPO IRCCS, Candiolo Canc Inst, I-10060 Candiolo, TO, Italy.
   [Cortese, Marco; Torchiaro, Erica; D'Andrea, Alice; Petti, Consalvo; Donini, Chiara; Leuci, Valeria; Isella, Claudio; Arena, Sabrina; Vigna, Elisa; Bertotti, Andrea; Trusolino, Livio; Sangiolo, Dario; Medico, Enzo] Univ Turin, Dept Oncol, I-10060 Candiolo, TO, Italy.
C3 IRCCS Fondazione del Piemonte per l'Oncologia; University of Turin
RP Cortese, M; Medico, E (corresponding author), FPO IRCCS, Candiolo Canc Inst, I-10060 Candiolo, TO, Italy.
EM enzo.medico@unito.it
RI Medico, Enzo/AAC-3185-2021; leuci, valeria/D-5554-2019; Donini,
   Chiara/AAC-1685-2021; Petti, Consalvo/K-9367-2016; Trusolino,
   Livio/A-3896-2011; Torchiaro, Erica/AAW-3628-2020; Sangiolo,
   Dario/ADQ-1991-2022; Arena, Sabrina/H-4985-2012
OI ARENA, Sabrina/0000-0002-1318-2494
FU Italian Ministry of Health (CART Italia Project) [RCR-2019-23669115];
   Progetto di Rete ACC 2019-RCR 2020; Progetto CAR-T_2 RCR-2023-23684268;
   Ricerca Corrente 2024; GR-2016 - 02362726; Fondazione Piemontese per la
   Ricerca sul Cancro-ONLUS (5x1000 Ministero della Salute 2015 "
   Immunogenomics "; SEE -HER; Associazione Italiana per la Ricerca sul
   Cancro (5 per Mille Metastasis [21091]; BRIDGE 2022 [27321]; IG-2017
   [20259]
FX This research was funded by Italian Ministry of Health (CART Italia
   Project RCR-2019-23669115 [E.M.] ; "Progetto di Rete ACC 2019 "-RCR 2020
   [E.M] ; " Progetto CAR-T_2 RCR-2023-23684268 [E.M.] ; Ricerca Corrente
   2024 [E.M.] ; GR-2016 - 02362726 [C.I.] ) ; Fondazione Piemontese per la
   Ricerca sul Cancro-ONLUS (5x1000 Ministero della Salute 2015 "
   Immunogenomics " [E.M., L.T.] and 2017 " SEE -HER " [E.M] ) ;
   Associazione Italiana per la Ricerca sul Cancro (5 per Mille
   Metastasis-ID 21091 [E.M.,L.T.,A.B.] ; under BRIDGE 2022-ID 27321 [S.A.]
   ; IG-2017 ID 20259 [D.S.] )
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NR 89
TC 1
Z9 1
U1 5
U2 5
PU CELL PRESS
PI CAMBRIDGE
PA 50 HAMPSHIRE ST, FLOOR 5, CAMBRIDGE, MA 02139 USA
SN 1525-0016
EI 1525-0024
J9 MOL THER
JI Mol. Ther.
PD AUG 7
PY 2024
VL 32
IS 8
BP 2741
EP 2761
DI 10.1016/j.ymthe.2024.06.023
EA AUG 2024
PG 21
WC Biotechnology & Applied Microbiology; Genetics & Heredity; Medicine,
   Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biotechnology & Applied Microbiology; Genetics & Heredity; Research &
   Experimental Medicine
GA C8A6D
UT WOS:001291544800001
PM 38894542
OA hybrid, Green Accepted
DA 2025-01-04
ER

PT J
AU Peker, YS
   Can, MF
   Ozerhan, IH
   Yagci, G
   Zeybek, N
   Kavakli, K
   Gurkok, S
   Gozubuyuk, A
   Genc, O
   Erdem, G
   Ozet, A
   Gerek, M
   Peker, Y
AF Peker, Yasar Subutay
   Can, Mehmet Fatih
   Ozerhan, Ismail Hakki
   Yagci, Gokhan
   Zeybek, Nazif
   Kavakli, Kutan
   Gurkok, Sedat
   Gozubuyuk, Alper
   Genc, Onur
   Erdem, Gokhan
   Ozet, Ahmet
   Gerek, Mustafa
   Peker, Yusuf
TI BRAF Inhibitors for BRAF V600E Mutant Colorectal Cancers: Literature
   Survey and Case Report
SO CASE REPORTS IN SURGERY
LA English
DT Article
ID MUTATIONS; DABRAFENIB; TRAMETINIB; METASTASES; RESECTION; MELANOMA;
   SURVIVAL; THERAPY; RAS
AB The main method of fighting against colon cancer is targeted treatment. BRAF inhibitors, which are accepted as standard treatment for V600E mutant malign melanomas, are the newest approach for targeted treatment of V600E mutant colorectal cancers. In this case report, we share our experience about the use of BRAF inhibitor vemurafenib on a V600E mutant metastatic right colon adenocarcinoma patient. A 59-year-old male with only lung multiple metastatic V600E mutant right colon cancer presented to our clinic. The patient was evaluated and FOLFOX + bevacizumab treatment was initiated, which was then continued with vemurafenib. A remarkable response was achieved with vemurafenib treatment in which the drug resistance occurred approximately in the sixth month. Even though the patient benefited majorly from vemurafenib, he died on the 20th month of the diagnosis. The expected overall survival for metastatic V600E mutant colon adenocarcinoma patients is 4.7 months. BRAF inhibitors provide new treatment alternatives for V600E mutant colorectal cancers, with prolonged overall survival. BRAF inhibitors in combination with MEK inhibitors are reported as feasible treatment to overcome BRAF inhibitor drug resistance on which phase studies are still in progress. To conclude, BRAF inhibitors alone or in combination with other drugs provide a chance for curing BRAF V600E mutant colorectal cancer patients.
C1 [Peker, Yasar Subutay; Can, Mehmet Fatih; Ozerhan, Ismail Hakki; Zeybek, Nazif] Univ Med Sci, Gulhane Training & Res Hosp, Dept Gen Surg, Ankara, Turkey.
   [Yagci, Gokhan] Guven Hosp, Dept Gen Surg, Ankara, Turkey.
   [Kavakli, Kutan; Gurkok, Sedat; Gozubuyuk, Alper; Genc, Onur] Univ Med Sci, Gulhane Training & Res Hosp, Dept Thorac Surg, Ankara, Turkey.
   [Erdem, Gokhan] Liv Hosp, Dept Med Oncol, Istanbul, Turkey.
   [Ozet, Ahmet] Gazi Univ Hosp, Dept Med Oncol, Ankara, Turkey.
   [Gerek, Mustafa] Univ Med Sci, Dept Otorhinolaryngol, Ankara, Turkey.
   [Peker, Yusuf] Gulhane Mil Med Acad, Dept Gen Surg, Ankara, Turkey.
C3 Gulhane Training & Research Hospital; Guven Hastanesi; Gulhane Training
   & Research Hospital; Ankara Liv Hospital; Gazi University; Gulhane
   Military Medical Academy
RP Peker, YS (corresponding author), Univ Med Sci, Gulhane Training & Res Hosp, Dept Gen Surg, Ankara, Turkey.
EM subutaypeker@gmail.com
RI Özet, ahmet/ABC-9831-2021; Peker, Yüksel/A-7550-2016; Can,
   Mehmet/F-6959-2011; kavaklı, kaan/AFP-0928-2022; özerhan,
   ismail/H-8689-2012
OI PEKER, YASAR SUBUTAY/0000-0001-6059-0629
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NR 31
TC 0
Z9 0
U1 1
U2 7
PU HINDAWI LTD
PI LONDON
PA ADAM HOUSE, 3RD FLR, 1 FITZROY SQ, LONDON, W1T 5HF, ENGLAND
SN 2090-6900
EI 2090-6919
J9 CASE REP SURG
JI Case Rep. Surg.
PY 2018
VL 2018
AR 8782328
DI 10.1155/2018/8782328
PG 6
WC Surgery
WE Emerging Sources Citation Index (ESCI)
SC Surgery
GA GE6KJ
UT WOS:000431334900001
PM 29850361
OA gold, Green Published, Green Submitted
DA 2025-01-04
ER

PT J
AU Salem, ME
   Battaglin, F
   Goldberg, RM
   Puccini, A
   Shields, AF
   Arguello, D
   Korn, WM
   Marshall, JL
   Grothey, A
   Lenz, HJ
AF Salem, Mohamed E.
   Battaglin, Francesca
   Goldberg, Richard M.
   Puccini, Alberto
   Shields, Anthony F.
   Arguello, David
   Korn, W. Michael
   Marshall, John L.
   Grothey, Axel
   Lenz, Heinz-Josef
TI Molecular Analyses of Left- and Right-Sided Tumors in Adolescents and
   Young Adults with Colorectal Cancer
SO ONCOLOGIST
LA English
DT Article
DE Colorectal cancer; Adolescents and young adults; Tumor sidedness;
   Molecular profiling
ID DNA-REPAIR DEFECTS; GENOMIC LANDSCAPE; COLON; MUTATIONS; IMMUNOTHERAPY;
   PREVALENCE; HEREDITARY; POLYMERASE; DEFICIENT; GERMLINE
AB Background The incidence of colorectal cancer (CRC), particularly left-sided tumors (LT), in adolescents and young adults (AYA) is rising. Epigenetic events appear to play an important role in tumorigenesis and cancer progression, especially in younger patients. We compared molecular features of LT to right-sided tumors (RT) in AYA. Materials and Methods A total of 246 LT and 56 RT were identified in a cohort of 612 AYA with primary CRC. Tumors were examined by next-generation sequencing (NGS), protein expression, and gene amplification. Tumor mutational burden (TMB) and microsatellite instability (MSI) were determined based on NGS data. Results RT showed higher mutation rates compared with LT in several genes including BRAF (10.3% vs. 2.8%), KRAS (64.1% vs. 45.5%), PIK3CA (27% vs. 11.2%), and RNF43 (24.2% vs. 2.9%). Notably, additional mutations in distinct genes involved in histone modification and chromatin remodeling, as well as genes associated with DNA repair and cancer-predisposing syndromes, were characteristic of RT; most frequently KMT2D (27.8% vs. 3.4%), ARID1A (53.3% vs. 21.4%), MSH6 (11.1% vs. 2.3%), MLH1 (10.5% vs. 2.3%), MSH2 (10.5% vs. 1.2%), POLE (5.9% vs. 0.6%), PTEN (10.8% vs. 2.3%), and BRCA1 (5.4% vs. 0.6%). MSI was seen in 20.8% of RT versus 4.8% of LT. RT had a higher frequency of TMB-high regardless of MSI status. Conclusion Molecular profiling of AYA CRC revealed different molecular characteristics in RT versus LT. Epigenetic mechanisms and alteration in DNA repair genes warrant further investigation and may be a promising treatment target for CRC in AYA. Implications for Practice Colorectal cancer (CRC) in adolescents and young adults (AYA) comprises a distinct entity with different clinicopathologic features and prognosis compared with older patients. Molecular profiling of right- and left-sided tumors in AYA is needed to gain novel insight into CRC biology and to tailor targeted treatment in this age group. This study found that right- and left-sided CRC show distinct molecular features in AYA, overall and in subgroups based on microsatellite instability status. Alterations in DNA double-strand break repair and homologous recombination repair, as well as epigenetic mechanisms, appear to play a critical role. The present molecular profiling data may support the development of personalized treatment strategies in the AYA population.
C1 [Salem, Mohamed E.] Atrium Hlth, Levine Canc Inst, Dept Med Oncol, Charlotte, NC USA.
   [Battaglin, Francesca; Puccini, Alberto; Lenz, Heinz-Josef] Univ Southern Calif, Keck Sch Med, Div Med Oncol, Norris Comprehens Canc Ctr, Los Angeles, CA 90007 USA.
   [Goldberg, Richard M.] West Virginia Univ, Canc Inst, Morgantown, WV 26506 USA.
   [Puccini, Alberto] Univ Genoa, Med Oncol Unit 1, IRCCS, Osped Policlin San Martino, Genoa, Italy.
   [Shields, Anthony F.] Wayne State Univ, Dept Oncol, Karmanos Canc Inst, Detroit, MI USA.
   [Arguello, David; Korn, W. Michael] Caris Life Sci, Phoenix, AZ USA.
   [Korn, W. Michael] Univ Calif San Francisco, San Francisco, CA 94143 USA.
   [Marshall, John L.] Ruesch Ctr, Washington, DC USA.
   [Marshall, John L.] Georgetown Lombardi Comprehens Canc Ctr, Washington, DC USA.
   [Grothey, Axel] West Canc Ctr, Germantown, TN USA.
C3 University of Southern California; West Virginia University; University
   of Genoa; Wayne State University; Barbara Ann Karmanos Cancer Institute;
   University of California System; University of California San Francisco
RP Salem, ME (corresponding author), Levine Canc Inst, Dept Med Oncol, 1021 Morehead Med Dr, Charlotte, NC 28204 USA.
EM Mohamed.Salem@atriumhealth.org
RI Puccini, Alberto/F-3255-2018; Battaglin, Francesca/C-2746-2017
OI Puccini, Alberto/0000-0002-2492-4043; Battaglin,
   Francesca/0000-0002-9869-0163
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NR 54
TC 34
Z9 34
U1 0
U2 2
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 1083-7159
EI 1549-490X
J9 ONCOLOGIST
JI Oncologist
PD MAY
PY 2020
VL 25
IS 5
BP 404
EP 413
DI 10.1634/theoncologist.2019-0552
EA DEC 2019
PG 10
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA LP5ZC
UT WOS:000502888900001
PM 31848314
OA Bronze, Green Published
DA 2025-01-04
ER

PT J
AU Akbari, F
   Peymani, M
   Salehzadeh, A
   Ghaedi, K
AF Akbari, Fatemeh
   Peymani, Maryam
   Salehzadeh, Ali
   Ghaedi, Kamran
TI Identification of modules based on integrative analysis for drug
   prediction in colorectal cancer
SO GENE REPORTS
LA English
DT Article
DE Integrative analysis; Prognosis; Drug resistance; Module; Eigengene
ID PROGNOSIS; GENES; SIGNATURE; PACKAGE
AB One of the most important topics in Colorectal Cancer (CRC) is identifying the genes that play a crucial role in cancer progression. Therefore, recognizing the important genes during the CRC progression and their effects in drug resistance could be useful for targeted treatment. In this study, by utilizing The Cancer Genome Atlas (TCGA) data, the genes that had significant differential expression in stage IV compared to stage I were identified. Then, the Weighted Gene Co-expression Network Analysis (WGCNA) method was used to achieve appropriate modules, and 147 patients in stages I and IV from TCGA were clustered based on obtained genes from the differential expression. In the next part, eigengene related to each module was identified, and the association between eigengenes and drug resistance was assessed based on the GDSC data. The results that the expression showed of 648 genes significantly changed in stage IV compared to stage I. Based on these genes, three modules were recognized that could be good candidates for progression in CRC. The outcomes showed that one module was decreased during progression, and was associated with a good prognosis. In contrast, the other module was increased during progression and was involved in angiogenesis and metastasis pathways. Also, further analysis showed that each module was correlated with drug resistance and sensitivity. In doing so, we demonstrated that three groups of genes could take part in the progression of CRC, and each of them could be appropriate candidates for diagnosis, prognosis, and suitable drug selection in CRC.
C1 [Akbari, Fatemeh; Peymani, Maryam; Ghaedi, Kamran] Islamic Azad Univ, Fac Basic Sci, Dept Biol, Shahrekord Branch, Shahrekord, Iran.
   [Salehzadeh, Ali] Islamic Azad Univ, Dept Biol, Rasht Branch, Rasht, Iran.
   [Ghaedi, Kamran] Univ Isfahan, Fac Biol Sci & Technol, Dept Cell & Mol Biol & Microbiol, Esfahan, Iran.
C3 Islamic Azad University; Islamic Azad University; University of Isfahan
RP Peymani, M (corresponding author), Islamic Azad Univ, Fac Basic Sci, Dept Biol, Shahrekord Branch, Shahrekord, Iran.; Salehzadeh, A (corresponding author), Islamic Azad Univ, Dept Biol, Rasht Branch, Rasht, Iran.
EM m.peymani@iaushk.ac.ir; salehzadeh@iaurasht.ac.ir
RI Ghaedi, Kamran/X-9824-2018; Salehzadeh, Ali/AAO-4547-2021
OI Peymani, Maryam/0000-0001-5075-5661
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NR 40
TC 1
Z9 1
U1 0
U2 0
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
EI 2452-0144
J9 GENE REP
JI Gene Rep.
PD DEC
PY 2021
VL 25
AR 101403
DI 10.1016/j.genrep.2021.101403
EA OCT 2021
PG 8
WC Genetics & Heredity
WE Emerging Sources Citation Index (ESCI)
SC Genetics & Heredity
GA WY7NI
UT WOS:000719464800003
DA 2025-01-04
ER

PT J
AU Verkuijl, SJ
   Jonker, JE
   Trzpis, M
   Burgerhof, JGM
   Broens, PMA
   Furnée, EJB
AF Verkuijl, Sanne J.
   Jonker, Jara E.
   Trzpis, Monika
   Burgerhof, Johannes G. M.
   Broens, Paul M. A.
   Furnee, Edgar J. B.
TI Functional outcomes of surgery for colon cancer: A systematic review and
   meta-analysis
SO EJSO
LA English
DT Review
DE Colon cancer; Bowel dysfunction; Postoperative; Follow-up; Meta-analysis
ID LOW ANTERIOR RESECTION; QUALITY-OF-LIFE; INFLUENCING BOWEL FUNCTION;
   RECTAL-CANCER; AUTONOMIC DENERVATION; PLEXUS TRANSECTION;
   CLINICAL-TRIALS; ANASTOMOSIS; COLECTOMY; MOTILITY
AB Introduction: As survival rates of colon cancer increase, knowledge about functional outcomes is becoming ever more important. The primary aim of this systematic review and meta-analysis was to quantify functional outcomes after surgery for colon cancer. Secondly, we aimed to determine the effect of time to follow-up and type of colectomy on postoperative functional outcomes.
   Materials and methods: A systematic literature search was performed to identify studies reporting bowel function following surgery for colon cancer. Outcome parameters were bowel function scores and/or prevalence of bowel symptoms. Additionally, the effect of time to follow-up and type of resection was analyzed.
   Results: In total 26 studies were included, describing bowel function between 3 to 178 months following right hemicolectomy (n = 4207), left hemicolectomy/sigmoid colon resection (n = 4211), and subtotal/ total colectomy (n = 161). In 16 studies (61.5%) a bowel function score was used. Pooled prevalence for liquid and solid stool incontinence was 24.1% and 6.9%, respectively. The most prevalent constipation-associated symptoms were incomplete evacuation and obstructive, difficult emptying (33.3% and 31.4%, respectively). Major Low Anterior Resection Syndrome was present in 21.1%. No differences between time to follow-up or type of colectomy were found.
   Conclusion: Bowel function problems following surgery for colon cancer are common, show no improvement over time and do not depend on the type of colectomy. Apart from fecal incontinence, constipation-associated symptoms are also highly prevalent. Therefore, more attention should be paid to all possible aspects of bowel dysfunction following surgery for colon cancer and targeted treatment should commence promptly. (C) 2020 The Authors. Published by Elsevier Ltd.
C1 [Verkuijl, Sanne J.; Jonker, Jara E.; Trzpis, Monika; Broens, Paul M. A.] Univ Groningen, Univ Med Ctr Groningen, Anorectal Physiol Lab, Dept Surg, Hanzepl 1,POB 30 001, NL-9700 RB Groningen, Netherlands.
   [Burgerhof, Johannes G. M.] Univ Groningen, Univ Med Ctr Groningen, Dept Epidemiol, Groningen, Netherlands.
   [Broens, Paul M. A.] Univ Groningen, Univ Med Ctr Groningen, Div Pediat Surg, Dept Surg, Groningen, Netherlands.
   [Furnee, Edgar J. B.] Univ Groningen, Univ Med Ctr Groningen, Div Abdominal Surg, Dept Surg, Groningen, Netherlands.
C3 University of Groningen; University of Groningen; University of
   Groningen; University of Groningen
RP Verkuijl, SJ (corresponding author), Univ Groningen, Univ Med Ctr Groningen, Anorectal Physiol Lab, Dept Surg, Hanzepl 1,POB 30 001, NL-9700 RB Groningen, Netherlands.
EM s.j.verkuijl@umcg.nl
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NR 63
TC 28
Z9 32
U1 3
U2 9
PU ELSEVIER SCI LTD
PI London
PA 125 London Wall, London, ENGLAND
SN 0748-7983
EI 1532-2157
J9 EJSO-EUR J SURG ONC
JI EJSO
PD MAY
PY 2021
VL 47
IS 5
BP 960
EP 969
DI 10.1016/j.ejso.2020.11.136
EA MAY 2021
PG 10
WC Oncology; Surgery
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Surgery
GA SA1RF
UT WOS:000649074700006
PM 33277056
OA Green Submitted, hybrid
DA 2025-01-04
ER

PT J
AU Dehghan, F
   Boozarpour, S
   Torabizadeh, Z
   Alijanpour, S
AF Dehghan, Farnaz
   Boozarpour, Sohrab
   Torabizadeh, Zhila
   Alijanpour, Sakineh
TI miR-21: a promising biomarker for the early detection of colon cancer
SO ONCOTARGETS AND THERAPY
LA English
DT Article
DE colon cancer; pathological stages; miR-21; gene expression; biomarker;
   early diagnosis
ID COLORECTAL-CANCER; MICRORNA-21; EXPRESSION; PROMOTES; STAGE; INHIBITION;
   MODULATION; GENDER; RISK
AB Purpose: The aim of this study was to compare the expression of miR-21 gene in stages HIV of formalin-fixed paraffin-embedded (FFPE) tissue in patients with colon cancer and introduce miR-21 as a potential molecular marker for detection of colon cancer in the early stages.
   Introduction: Currently, identification of key molecules involved in the pathogenesis of cancer is one of the areas under consideration. miRNAs, are small RNAs which have been identified in many cancers. In this study, we investigated the expression of miR-21 in three pathologic stages in patients with colon cancer in the north of Iran.
   Patients and methods: A total of 40 FFPE samples were obtained from patients with stages II, III, and IV from hospitals in Mazandaran and Golestan provinces. After extraction of RNA, treatment with DNase I and cDNA synthesis was performed and miR-21 expression was assessed by qPCR. Then, the data were analyzed using statistical software R (3.4.3).
   Results: The expression of miR-21 in stage II was significantly different from stage IV. However, no significant difference was observed between the other stages. In stage II, the level of miR-21 expression was higher in men than women. Moreover, in the second pathological stage, miR-21 expression was reduced in patients with adjacent lymphoid tissue engagement. In addition, the expression of miR-21 in grade I was significantly higher than grade II.
   Conclusion: The results of this study suggest that miR-21 can be a diagnostic marker for early stages of colon cancer, especially in men. It can also be considered as a good candidate for targeted treatment of colon cancer in the early stages of the disease. Furthermore, for the first time, we suggested that miR-21 can be a good molecular marker for classification of the stages of colon cancer.
C1 [Dehghan, Farnaz; Boozarpour, Sohrab; Alijanpour, Sakineh] Gonbad Kavous Univ, Fac Basic Sci, Dept Biol, Gonbad Kavous, Golestan, Iran.
   [Torabizadeh, Zhila] Sari Univ Med Sci, Fac Med, Dept Med Pathol, Sari, Mazandaran, Iran.
RP Boozarpour, S (corresponding author), Gonbad Kavous Univ, Basirat BLV, Shahid Fallahy St, Gonbad Kavous 4971799151, Golestan, Iran.
EM so.boozarpour@gonbad.ac.ir
RI Alijanpour, SAkineh/AAA-3416-2021; Boozarpour, Sohrab/A-6858-2019
OI torabizade, jila/0000-0002-7065-8225; Alijanpour,
   Sakineh/0000-0002-0235-9776; Boozarpour, Sohrab/0000-0003-0873-7499
CR [Anonymous], TEHRAN U MED J
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NR 46
TC 18
Z9 18
U1 1
U2 7
PU DOVE MEDICAL PRESS LTD
PI ALBANY
PA PO BOX 300-008, ALBANY, AUCKLAND 0752, NEW ZEALAND
SN 1178-6930
J9 ONCOTARGETS THER
JI OncoTargets Ther.
PY 2019
VL 12
BP 5601
EP 5607
DI 10.2147/OTT.S199508
PG 7
WC Biotechnology & Applied Microbiology; Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biotechnology & Applied Microbiology; Oncology
GA IK7TZ
UT WOS:000476796400003
PM 31371997
OA Green Published, gold, Green Submitted
DA 2025-01-04
ER

PT J
AU Zhao, YH
   Wang, CX
   Goel, A
AF Zhao, Yinghui
   Wang, Chuanxin
   Goel, Ajay
TI A combined treatment with melatonin and andrographis promotes autophagy
   and anticancer activity in colorectal cancer
SO CARCINOGENESIS
LA English
DT Article
ID NATURAL-PRODUCTS; LC3 LIPIDATION; CURCUMIN; CELLS; SUPPRESSION;
   APOPTOSIS; EFFICACY; THERAPY
AB We systematically used multiple in vitroand in vivomodels to demonstrate melatonin and andrographis exhibit pronounced synergistic activity in CRC inhibition, mediated in part by autophagy-associated pathways induced apoptotic activation, highlighting the combinatorial therapeutic potential of these two natural products in patients with CRC.
   Colorectal cancer (CRC) is one of the most frequent malignancies worldwide and remains one of the leading causes of cancer-related deaths in the USA. The high degree of morbidity and mortality associated with this disease is largely due to the inadequate efficacy of current treatments as well the development of chemoresistance. In recent years, several pharmaceutical agents screened from natural products have shown the promise to offer a safe, inexpensive and synergistically multi-targeted treatment option in various cancers. Given the growing evidence of anti-carcinogenic properties of two natural compounds, melatonin (MLT) and andrographis (Andro), we aimed to evaluate their synergistic anticancer effects in CRC. We demonstrate that indeed these two compounds possessed a synergistic anticancer effect in terms of their ability to inhibit cell viability, suppression of colony-formation and induction of apoptosis (P < 0.05). In line with our in vitro findings, we were able to validate this combinatorial anticancer activity in xenograft animal models (P < 0.001) as well as tumor-derived 3D organoids (P < 0.01). RNA-sequencing analysis revealed candidate pathways and genes that mediated antitumor efficacy of MLT and Andro in CRC, among which autophagy pathway and related genes, including NR4A1, CTSL and Atg12, were found to be primarily responsible for the increased anticancer effect by the two natural products. In conclusion, our data reveal a potent and synergistic therapeutic effect of MLT and Andro in the treatment of CRC and provides a rationale for suppressing autophagy in cancer cells as a potential therapeutic strategy for CRC.
C1 [Zhao, Yinghui; Goel, Ajay] City Hope Natl Med Ctr, Biomed Res Ctr, Dept Mol Diagnost & Expt Therapeut, Beckman Res Inst, Monrovia, CA 91016 USA.
   [Zhao, Yinghui; Wang, Chuanxin] Shandong Univ, Hosp 2, Cheeloo Coll Med, Dept Clin Lab, Jinan, Peoples R China.
   [Wang, Chuanxin] Shandong Engn & Technol Res Ctr Tumor Marker Dete, Jinan, Peoples R China.
   [Wang, Chuanxin] Shandong Prov Clin Med Res Ctr, Clin Lab, Jinan, Peoples R China.
   [Goel, Ajay] City Hope Natl Med Ctr, Comprehens Canc Ctr, Duarte, CA USA.
C3 Shandong University; City of Hope
RP Goel, A (corresponding author), City Hope Natl Med Ctr, Comprehens Canc Ctr, 1218 S Fifth Ave, Monrovia, CA 91016 USA.
EM ajgoel@coh.org
RI Goel, Ajay/ADO-9623-2022
OI Zhao, Yinghui/0000-0003-1105-8980; Goel, Ajay/0000-0003-1396-6341
FU National Cancer Institute, National Institutes of Health [CA184792,
   CA187956, CA227602, CA072851, CA202797]
FX This work was supported by CA184792, CA187956, CA227602, CA072851 and
   CA202797 grants from the National Cancer Institute, National Institutes
   of Health.
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NR 61
TC 19
Z9 20
U1 1
U2 12
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0143-3334
EI 1460-2180
J9 CARCINOGENESIS
JI Carcinogenesis
PD MAR 11
PY 2022
VL 43
IS 3
BP 217
EP 230
DI 10.1093/carcin/bgac008
EA MAR 2022
PG 14
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 1L3YO
UT WOS:000768373200001
PM 35089340
OA Green Published
DA 2025-01-04
ER

PT J
AU Li, Y
   Duo, YH
   Bi, JG
   Zeng, XW
   Mei, L
   Bao, SY
   He, LS
   Shan, AJ
   Zhang, Y
   Yu, XF
AF Li, Yang
   Duo, Yanhong
   Bi, Jiangang
   Zeng, Xiaowei
   Mei, Lin
   Bao, Shiyun
   He, Lisheng
   Shan, Aijun
   Zhang, Yue
   Yu, Xiaofang
TI Targeted delivery of anti-miR-155 by functionalized mesoporous silica
   nanoparticles for colorectal cancer therapy
SO INTERNATIONAL JOURNAL OF NANOMEDICINE
LA English
DT Article
DE miR-155; mesoporous silica nanoparticles; AS1411 aptamer; NF-kappa B;
   5-fluorouracil
ID BREAST-CANCER; SURFACE MODIFICATION; DRUG-RESISTANCE; APTAMER AS1411;
   MOUSE MODEL; IN-VITRO; MIRNA; MIR-155; CHEMORESISTANCE; PROLIFERATION
AB Introduction: MicroRNA-155 (miR-155) is an oncogenic microRNA, which is upregulated in many human cancers including colorectal cancer (CRC). Overexpression of miR-155 has been found to regulate several cancer-related pathways, and therefore, targeting miR-155 may be an effective strategy for cancer therapy. However, effective and safe delivery of anti-miR-155 to tumors remains challenging for the clinical applications of anti-miR-155-based therapeutics.
   Methods: In this study, we explored the expression of miR-155 and the transcription factor nuclear factor kappa B (NF-kappa B) in CRC tissues and cell lines, and the possible relationship between miR-155 and NF-kappa B. We further report on anti-miR-155-loaded mesoporous silica nanoparticles (MSNs) modified with polymerized dopamine (PDA) and AS1411 aptamer (MSNs-anti-miR-155@PDA-Apt) for the targeted treatment of CRC.
   Results: Results showed that miR-155 is overexpressed in CRC tissues and cell lines, and there is a positive feedback loop between NF-kappa B and miR-155. Compared to the control groups, MSNs-anti-miR-155@PDA-Apt could efficiently downregulate miR-155 expression in SW480 cells and achieve significantly high targeting efficiency and enhanced therapeutic effects in both in vivo and in vitro experiments. Furthermore, inhibition of miR-155 by MSNs-anti-miR-155@PDA-Apt can enhance the sensitivity of SW480 to 5-fluorouracil chemotherapy.
   Conclusion: Thus, our results suggested that MSNs-anti-miR-155@PDA-Apt is a promising nanoformulation for CRC treatment.
C1 [Li, Yang; Duo, Yanhong; Bi, Jiangang; Bao, Shiyun; Zhang, Yue; Yu, Xiaofang] Jinan Univ, Shenzhen Peoples Hosp, Clin Med Coll 2, Dept Hepatobiliary & Pancreas Surg, 1017 Dongmen North Rd, Shenzhen 518020, Peoples R China.
   [Li, Yang; Shan, Aijun] Jinan Univ, Shenzhen Peoples Hosp, Clin Med Coll 2, Dept Emergency, Shenzhen 518020, Peoples R China.
   [Duo, Yanhong] Lanzhou Univ, Sch Life Sci, Minist Educ, Key Lab Plant Cell Activ & Stress Adaptat, Lanzhou 730000, Gansu, Peoples R China.
   [Zeng, Xiaowei; Mei, Lin] Tsinghua Univ, Grad Sch Shenzhen, Div Life & Hlth Sci, Shenzhen 518020, Peoples R China.
   [He, Lisheng] Jinan Univ, Shenzhen Peoples Hosp, Clin Med Coll 2, Dept Pathol, Shenzhen 518020, Peoples R China.
C3 Jinan University; Jinan University; Lanzhou University; Tsinghua
   University; Tsinghua Shenzhen International Graduate School; Jinan
   University
RP Zhang, Y; Yu, XF (corresponding author), Jinan Univ, Shenzhen Peoples Hosp, Clin Med Coll 2, Dept Hepatobiliary & Pancreas Surg, 1017 Dongmen North Rd, Shenzhen 518020, Peoples R China.
EM szrmyy@126.com; yuxfshui@hotmail.com
RI Shan, Aijun/AHB-5123-2022; Zeng, Xiaowei/AFH-5246-2022; Li,
   Yang/AAM-5383-2020; Mei, Lin/ABD-5937-2021
OI Shan, Aijun/0000-0002-2698-711X; Mei, Lin/0000-0001-6503-5149
FU Science, Technology & Innovation Commission of Shenzhen Municipality
   [JCYJ20160422170206664]
FX This work was supported by the Science, Technology & Innovation
   Commission of Shenzhen Municipality (No JCYJ20160422170206664).
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NR 57
TC 97
Z9 99
U1 3
U2 54
PU DOVE MEDICAL PRESS LTD
PI ALBANY
PA PO BOX 300-008, ALBANY, AUCKLAND 0752, NEW ZEALAND
SN 1178-2013
J9 INT J NANOMED
JI Int. J. Nanomed.
PY 2018
VL 13
BP 1241
EP 1256
DI 10.2147/IJN.S158290
PG 16
WC Nanoscience & Nanotechnology; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Science & Technology - Other Topics; Pharmacology & Pharmacy
GA FX9ZN
UT WOS:000426469800001
PM 29535520
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Wang, XW
   Luo, X
   Tian, YP
   Wu, T
   Weng, J
   Li, Z
   Ye, F
   Huang, XF
AF Wang, Xianwu
   Luo, Xi
   Tian, Yunpeng
   Wu, Ting
   Weng, Jian
   Li, Zhu
   Ye, Feng
   Huang, Xuefei
TI Equipping Natural Killer Cells with Cetuximab through Metabolic
   Glycoengineering and Bioorthogonal Reaction for Targeted Treatment of
   KRAS Mutant Colorectal Cancer
SO ACS CHEMICAL BIOLOGY
LA English
DT Article
ID LINE NK-92; IMMUNOTHERAPY; NK
AB While Cetuximab can be used to treat KRAS wild-type colon cancer cells by targeting EGFR and inhibiting the activation of downstream signaling pathways, it exhibits little therapeutic effect on KRAS mutant colon cancer cells. Natural killer (NK) cells are a class of powerful immune cells with anticancer activities. However, NK cells typically lack inherent tumor targeting abilities. Here, a new method is established to bestow NK-92 cells with tumor targeting abilities by installing cetuximab on the cell surface. Through metabolic glycoengineering, azide groups were introduced onto the surface of NK-92 cells. Bioorthogonal strain promoted the azide-alkyne cycloaddition click reaction of engineered NK-92 cells with alkyne modified cetuximab functionalized NK cells with the antibody. The resulting NK-92 cells were significantly more effective than the parent NK-92 cells in protecting against tumor development in a KRAS mutant mouse tumor model resistant to cetuximab treatment. Thus, NK cell functionalization with antibodies enabled by metabolic glycoengineering is a promising strategy to enhance anticancer immune therapy.
C1 [Wang, Xianwu; Weng, Jian] Xiamen Univ, Coll Mat, Dept Biomat, Key Lab Biomed Engn Fujian Prov, Xiamen 361005, Peoples R China.
   [Luo, Xi; Ye, Feng] Xiamen Univ, Dept Med Oncol, Affiliated Hosp 1, Xiamen 361003, Peoples R China.
   [Luo, Xi; Ye, Feng] Xiamen Univ, Xiamen Key Lab Antitumor Drug Transformat Res, Affiliated Hosp 1, Xiamen 361003, Peoples R China.
   [Tian, Yunpeng; Li, Zhu] Xiamen Nuokangde Biol Technol Co Ltd, Xiamen 361006, Peoples R China.
   [Wu, Ting] Xiamen Univ, Sch Med, Dept Basic Med, Xiamen 361005, Peoples R China.
   [Huang, Xuefei] Michigan State Univ, Inst Quantitat Hlth Sci & Engn, Dept Chem & Biomed Engn, E Lansing, MI 48824 USA.
C3 Xiamen University; Xiamen University; Xiamen University; Xiamen
   University; Michigan State University
RP Ye, F (corresponding author), Xiamen Univ, Dept Med Oncol, Affiliated Hosp 1, Xiamen 361003, Peoples R China.; Ye, F (corresponding author), Xiamen Univ, Xiamen Key Lab Antitumor Drug Transformat Res, Affiliated Hosp 1, Xiamen 361003, Peoples R China.; Li, Z (corresponding author), Xiamen Nuokangde Biol Technol Co Ltd, Xiamen 361006, Peoples R China.; Huang, XF (corresponding author), Michigan State Univ, Inst Quantitat Hlth Sci & Engn, Dept Chem & Biomed Engn, E Lansing, MI 48824 USA.
EM lizhu@nkdbio.com; yefengdoctor@xmu.edu.cn; huangxu2@msu.edu
OI weng, jian/0000-0002-5813-6061
FU  [2019NKD0002]
FX Xiamen Nuokangde Biological Technology Co., Ltd. is the initiator and
   funding provider of this work (2019NKD0002).
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NR 33
TC 17
Z9 21
U1 4
U2 37
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 1554-8929
EI 1554-8937
J9 ACS CHEM BIOL
JI ACS Chem. Biol.
PD APR 16
PY 2021
VL 16
IS 4
BP 724
EP 730
DI 10.1021/acschembio.1c00022
EA APR 2021
PG 7
WC Biochemistry & Molecular Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology
GA RO8SG
UT WOS:000641310300017
PM 33829754
DA 2025-01-04
ER

PT J
AU Huang, KCY
   Chiang, SF
   Chang, HY
   Chen, WTL
   Yang, PC
   Chen, TW
   Liang, JA
   Shiau, A
   Ke, TW
   Chao, KSC
AF Huang, Kevin Chih-Yang
   Chiang, Shu-Fen
   Chang, Hsin-Yu
   Chen, William Tzu-Liang
   Yang, Pei-Chen
   Chen, Tsung-Wei
   Liang, Ji-An
   Shiau, An-Cheng
   Ke, Tao-Wei
   Clifford Chao, K. S.
TI Engineered sTRAIL-armed MSCs overcome STING deficiency to enhance the
   therapeutic efficacy of radiotherapy for immune checkpoint blockade
SO CELL DEATH & DISEASE
LA English
DT Article
ID MESENCHYMAL STEM-CELLS; TUMOR MICROENVIRONMENT; TRAIL EXPRESSION;
   CANCER; MECHANISM; DEATH
AB Radiotherapy (RT) mainly elicits antitumor immunity via the cGAS/STING axis for type I interferon (IFN) production. However, dysregulation of cGAS/STING constrains radiotherapy-induced antitumor immunity and type I IFN-dependent cell death and is associated with shorter survival of patients with colorectal cancer (CRC). Due to their tumor tropism, mesenchymal stem cells (MSCs) have shown the potential to deliver therapeutic genes for cancer therapy. Here, we showed that MSCs enhance the sensitivity to RT by inducing TRAIL-dependent cell death and remodel the tumor microenvironment by recruiting CD8(+) immune cells to upregulate PD-L1 in the tumor. By engineering MSCs to express CRC-specific soluble TRAIL via adenovirus-associated virus 2 (AAV2), we found that the therapeutic activity of MSC-sTRAIL was superior to that of MSCs alone when combined with RT. Combined treatment with MSC-sTRAIL and RT significantly reduced cell viability and increased apoptosis by inducing TRAIL-dependent cell death in STING-deficient colorectal cancer cells. MSC-sTRAIL directly triggered TRAIL-dependent cell death to overcome the deficiency of the cGAS/STING axis. Moreover, these combination treatments of MSC-sTRAIL and RT significantly remodeled the tumor microenvironment, which was more suitable for anti-PD-L1 immunotherapy. Taken together, this therapeutic strategy represents a novel targeted treatment option for patients with colorectal cancer, especially cGAS/STING-deficient patients.
C1 [Huang, Kevin Chih-Yang; Liang, Ji-An] China Med Univ, Dept Biomed Imaging & Radiol Sci, Taichung 40402, Taiwan.
   [Huang, Kevin Chih-Yang; Chang, Hsin-Yu] China Med Univ, China Med Univ Hosp, Translat Res Core, Taichung 40402, Taiwan.
   [Chiang, Shu-Fen] Minist Hlth & Welf, Feng Yuan Hosp, Lab Precis Med, Taichung 42055, Taiwan.
   [Chang, Hsin-Yu; Yang, Pei-Chen; Clifford Chao, K. S.] China Med Univ, China Med Univ Hosp, Proton Therapy & Sci Ctr, Taichung 40402, Taiwan.
   [Chen, William Tzu-Liang] China Med Univ, HsinChu Hosp, Dept Colorectal Surg, Hsinchu 302, Taiwan.
   [Chen, William Tzu-Liang; Ke, Tao-Wei] China Med Univ, China Med Univ Hosp, Dept Colorectal Surg, Taichung 40402, Taiwan.
   [Chen, William Tzu-Liang] China Med Univ, Sch Med, Dept Surg, Taichung 40402, Taiwan.
   [Chen, Tsung-Wei; Clifford Chao, K. S.] China Med Univ, Grad Inst Biomed Sci, Taichung 40402, Taiwan.
   [Chen, Tsung-Wei] Asia Univ, Asia Univ Hosp, Dept Pathol, Taichung 41354, Taiwan.
   [Liang, Ji-An; Shiau, An-Cheng; Clifford Chao, K. S.] China Med Univ, China Med Univ Hosp, Dept Radiat Oncol, Taichung, Taiwan.
   [Liang, Ji-An; Clifford Chao, K. S.] China Med Univ, Sch Med, Dept Radiotherapy, Taichung 40402, Taiwan.
   [Ke, Tao-Wei] China Med Univ, Sch Chinese Med, Taichung 40402, Taiwan.
   [Ke, Tao-Wei; Clifford Chao, K. S.] China Med Univ, Grad Inst Chinese Med, Taichung 40402, Taiwan.
C3 China Medical University Taiwan; China Medical University Taiwan; China
   Medical University Hospital - Taiwan; China Medical University Taiwan;
   China Medical University Hospital - Taiwan; China Medical University
   Taiwan; China Medical University Taiwan; China Medical University
   Hospital - Taiwan; China Medical University Taiwan; China Medical
   University Taiwan; Asia University Taiwan; China Medical University
   Taiwan; China Medical University Hospital - Taiwan; China Medical
   University Taiwan; China Medical University Taiwan; China Medical
   University Taiwan
RP Huang, KCY (corresponding author), China Med Univ, Dept Biomed Imaging & Radiol Sci, Taichung 40402, Taiwan.; Huang, KCY (corresponding author), China Med Univ, China Med Univ Hosp, Translat Res Core, Taichung 40402, Taiwan.; Chao, KSC (corresponding author), China Med Univ, China Med Univ Hosp, Proton Therapy & Sci Ctr, Taichung 40402, Taiwan.; Chao, KSC (corresponding author), China Med Univ, Grad Inst Biomed Sci, Taichung 40402, Taiwan.; Chao, KSC (corresponding author), China Med Univ, China Med Univ Hosp, Dept Radiat Oncol, Taichung, Taiwan.; Chao, KSC (corresponding author), China Med Univ, Sch Med, Dept Radiotherapy, Taichung 40402, Taiwan.; Chao, KSC (corresponding author), China Med Univ, Grad Inst Chinese Med, Taichung 40402, Taiwan.
EM chihyang0425@mail.cmu.edu.tw; d94032@mail.cmuh.org.tw
RI Huang, Kevin Chih-Yang/Q-4862-2016; liang, jian/HNI-8846-2023; Hu,
   Luna/KOC-2661-2024; Huang, Kevin Chih-Yang/O-5170-2015
OI Huang, Kevin Chih-Yang/0000-0002-0266-3233
FU China Medical University Hospital [DMR-110-130, DMR-CELL-2103,
   DMR-CELL-2102]; Ministry of Science and Technology (Taiwan)
   [MOST110-2628-B-039-005, MOST110-2314-B-039-032]; Ministry of Health and
   Welfare [MOHW111-18]; Health and welfare surcharge on tobacco products,
   China Medical University Hospital Cancer Research Center of Excellence
   [MOHW110-TDU-B-212-144024]
FX We thank the National RNAi Core Facility at Academia Sinica in Taiwan
   for providing shRNA reagents and related services. This study was
   partially based on data from the China Medical University Hospital
   cancer registry. This study was supported in part by China Medical
   University Hospital (DMR-110-130, DMR-CELL-2103, and DMR-CELL-2102),
   Ministry of Science and Technology (MOST110-2628-B-039-005 and
   MOST110-2314-B-039-032, Taiwan), Ministry of Health and Welfare
   (MOHW111-18) and the Health and welfare surcharge on tobacco products,
   China Medical University Hospital Cancer Research Center of Excellence
   (MOHW110-TDU-B-212-144024). Experiments and data analysis were performed
   in part through the use of the Medical Research Core Facilities Center,
   Office of Research and Development at China Medical University,
   Taichung, Taiwan, R.O.C.
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NR 61
TC 17
Z9 17
U1 3
U2 17
PU SPRINGERNATURE
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON, N1 9XW, ENGLAND
SN 2041-4889
J9 CELL DEATH DIS
JI Cell Death Dis.
PD JUL 14
PY 2022
VL 13
IS 7
AR 610
DI 10.1038/s41419-022-05069-0
PG 12
WC Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology
GA 2X8DQ
UT WOS:000825429900001
PM 35835756
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Yu, Z
   Li, XD
   Duan, JH
   Yang, XD
AF Yu, Zhen
   Li, Xundou
   Duan, Jinhong
   Yang, Xian-Da
TI Targeted Treatment of Colon Cancer with Aptamer-Guided Albumin
   Nanoparticles Loaded with Docetaxel
SO INTERNATIONAL JOURNAL OF NANOMEDICINE
LA English
DT Article
DE aptamer; nanoparticles; colon cancer; targeted drug delivery system
ID DRUG-DELIVERY; ENHANCED PERMEABILITY; SOLID TUMORS; IN-VITRO;
   DOXORUBICIN; CHEMOTHERAPY; RETENTION; BLOCKADE; PROTEIN; ROLES
AB Purpose: Chemotherapy of colon cancer needs improvement to mitigate the severe adverse effects (AEs) associated with the cytotoxic drugs. The aim of this study is to develop a novel targeted drug delivery system (TDDS) with practical application potential for colon cancer treatment.
   Methods: The TDDS was built by loading docetaxel (DTX) in albumin nanoparticles (NPs) that were functionalized with nucleolin-targeted aptamers (AS1411).
   Results: The TDDS (Apt-NPs-DTX) had an average size of 62 nm and was negatively charged with a zeta potential of -31.2 mV. DTX was released from the albumin NP with a typical sustained release profile. Aptamer-guided NPs were preferentially ingested by nucleolin-expressing CT26 colon cancer cells vs the control cells. In vitro cytotoxicity study showed that Apt-NPs-DTX significantly enhanced the killing of CT26 colon cancer cells. Importantly, compared with non-targeted drug delivery, Apt-NPs-DTX treatment significantly improved antitumor efficacy and prolonged the survival of CT26-bearing mice, without raising systemic toxicity.
   Conclusion: The results suggest that Apt-NPs-DTX has potential in the targeted treatment of colon cancer.
C1 [Yu, Zhen; Li, Xundou; Duan, Jinhong; Yang, Xian-Da] Chinese Acad Med Sci & Peking Union Med Coll, Inst Basic Med Sci, Beijing, Peoples R China.
C3 Chinese Academy of Medical Sciences - Peking Union Medical College;
   Peking Union Medical College
RP Yang, XD (corresponding author), Chinese Acad Med Sci & Peking Union Med Coll, Inst Basic Med Sci, Beijing, Peoples R China.
EM ayangmd@hotmail.com
RI Yang, Xianda/G-5132-2018
FU CAMS Innovation Fund for Medical Sciences [CIFMS 2016-I2M-3-004];
   Ministry of Science and Technology [2017YFA0205504]
FX This work was supported by the CAMS Innovation Fund for Medical Sciences
   (CIFMS 2016-I2M-3-004) and the Ministry of Science and Technology
   (2017YFA0205504).
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NR 56
TC 49
Z9 49
U1 2
U2 30
PU DOVE MEDICAL PRESS LTD
PI ALBANY
PA PO BOX 300-008, ALBANY, AUCKLAND 0752, NEW ZEALAND
SN 1178-2013
J9 INT J NANOMED
JI Int. J. Nanomed.
PY 2020
VL 15
BP 6737
EP 6748
DI 10.2147/IJN.S267177
PG 12
WC Nanoscience & Nanotechnology; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Science & Technology - Other Topics; Pharmacology & Pharmacy
GA NO4CI
UT WOS:000569432700005
PM 32982230
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Sartore-Bianchi, A
   Amatu, A
   Porcu, L
   Ghezzi, S
   Lonardi, S
   Leone, F
   Bergamo, F
   Fenocchio, E
   Martinelli, E
   Borelli, B
   Tosi, F
   Racca, P
   Valtorta, E
   Bonoldi, E
   Martino, C
   Vaghi, C
   Marrapese, G
   Ciardiello, F
   Zagonel, V
   Bardelli, A
   Trusolino, L
   Torri, V
   Marsoni, S
   Siena, S
AF Sartore-Bianchi, Andrea
   Amatu, Alessio
   Porcu, Luca
   Ghezzi, Silvia
   Lonardi, Sara
   Leone, Francesco
   Bergamo, Francesca
   Fenocchio, Elisabetta
   Martinelli, Erika
   Borelli, Beatrice
   Tosi, Federica
   Racca, Patrizia
   Valtorta, Emanuele
   Bonoldi, Emanuela
   Martino, Cosimo
   Vaghi, Caterina
   Marrapese, Giovanna
   Ciardiello, Fortunato
   Zagonel, Vittorina
   Bardelli, Alberto
   Trusolino, Livio
   Torri, Valter
   Marsoni, Silvia
   Siena, Salvatore
TI HER2 Positivity Predicts Unresponsiveness to EGFR-Targeted Treatment in
   Metastatic Colorectal Cancer
SO ONCOLOGIST
LA English
DT Article
DE Colorectal cancer; HER2; ERBB2; Anti-EGFR monoclonal antibodies
ID COLON
AB Background HER2 amplification is detected in 3% of patients with colorectal cancer (CRC), making tumors in the metastatic setting vulnerable to double pharmacological HER2 blockade. Preclinical findings show that it also might impair response to anti-epidermal growth factor receptor (EGFR) treatment. Subjects and Methods Patients with KRAS exon 2 wild-type metastatic CRC underwent molecular screening of HER2 positivity by HERACLES criteria (immunohistochemistry 3+ or 2+ in >= 50% of cells, confirmed by fluorescence in situ hybridization). A sample of consecutive HER2-negative patients was selected as control. A regression modeling strategy was applied to identify predictors explaining the bulk of HER2 positivity and the association with response to previous anti-EGFR treatment. Results From August 2012 to April 2018, a total of 100 HER2-positive metastatic CRC tumors were detected out of 1,485 KRAS exon 2 wild-type screened patients (6.7%). HER2-positive patients show more frequently lung metastases (odds ratio [OR], 2.04; 95% confidence interval [CI], 1.15-3.61; p = .014) and higher tumor burden (OR, 1.48; 95% CI, 1.10-2.01; p = .011), and tumors were more likely to be left sided (OR, 0.50; 95% CI, 0.22-1.11; p = .088). HER2-positive patients who received treatment with anti-EGFR agents (n = 79) showed poorer outcome (objective response rate, 31.2% vs. 46.9%, p = .031; progression-free survival, 5.7 months vs. 7 months, p = .087). Conclusion Testing for HER2 should be offered to all patients with metastatic CRC because the occurrence of this biomarker is unlikely to be predicted based on main clinicopathological features. Patients with HER2-amplified metastatic CRC are less likely to respond to anti-EGFR therapy. Implications for Practice Patients with HER2-amplified/overexpressed metastatic colorectal cancer (mCRC) harbor a driver actionable molecular alteration that has been shown in preclinical models to hamper efficacy of the anti-epidermal growth factor receptor (EGFR) targeted therapies. The present study confirmed that this molecular feature was associated with worse objective tumor response and shorter progression-free survival in response to previous anti-EGFR therapies. Moreover, it was found that the occurrence of this biomarker is unlikely to be predicted based on main clinicopathological features. Therefore, HER2 status assessment should be included in the molecular diagnostic workup of all mCRC for speedy referral to clinical trials encompassing HER2-targeted double blockade independently of previous anti-EGFR treatment.
C1 [Sartore-Bianchi, Andrea; Amatu, Alessio; Ghezzi, Silvia; Tosi, Federica; Valtorta, Emanuele; Bonoldi, Emanuela; Vaghi, Caterina; Marrapese, Giovanna; Marsoni, Silvia; Siena, Salvatore] Grande Osped Metropolitano Niguarda, Niguarda Canc Ctr, Milan, Italy.
   [Sartore-Bianchi, Andrea; Tosi, Federica; Vaghi, Caterina; Siena, Salvatore] Univ Milan, Dipartimento Oncol & EmatoOncol, Piazza Osped Maggiore 3, I-20162 Milan, Italy.
   [Porcu, Luca; Torri, Valter] IRCCS, Ist Ric Farmacol Mario Negri, Clin Res Methodol Lab, Milan, Italy.
   [Lonardi, Sara; Bergamo, Francesca; Zagonel, Vittorina] IRCCS, Ist Oncol Veneto, Dept Clin & Expt Oncol, Unit Med Oncol 1, Padua, Italy.
   [Leone, Francesco; Fenocchio, Elisabetta; Martino, Cosimo; Bardelli, Alberto; Trusolino, Livio] IRCCS, Candiolo Canc Inst FPO, I-10060 Turin, Italy.
   [Leone, Francesco; Fenocchio, Elisabetta; Bardelli, Alberto; Trusolino, Livio] Univ Torino, Dept Oncol, I-10060 Turin, Italy.
   [Martinelli, Erika; Ciardiello, Fortunato] Univ Campania Luigi Vanvitelli, Div Med Oncol, Dept Precis Med, Sch Med, Naples, Italy.
   [Borelli, Beatrice] Univ Hosp Pisa, Unit Med Oncol 2, Pisa, Italy.
   [Racca, Patrizia] Azienda Osped Univ AOU Citta Salute & Sci Torino, Dept Med Oncol, Colorectal Unit, Turin, Italy.
   [Marsoni, Silvia] Inst Mol Oncol IFOM, FIRC, Milan, Italy.
C3 University of Milan; Istituto di Ricerche Farmacologiche Mario Negri
   IRCCS; IRCCS Istituto Oncologico Veneto (IOV); IRCCS Fondazione del
   Piemonte per l'Oncologia; University of Turin; Universita della Campania
   Vanvitelli; University of Pisa; Azienda Ospedaliero Universitaria
   Pisana; A.O.U. Citta della Salute e della Scienza di Torino; IFOM - FIRC
   Institute of Molecular Oncology
RP Siena, S (corresponding author), Univ Milan, Dipartimento Oncol & EmatoOncol, Piazza Osped Maggiore 3, I-20162 Milan, Italy.
EM salvatore.siena@unimi.it
RI Torri, Valter/H-7550-2015; SIENA, SALVATORE/AAC-5806-2019; Leone,
   Francesco/AAB-2355-2022; Sartore-Bianchi, Andrea/AAB-9848-2019; TOSI,
   FEDERICA MARIA/AIA-1174-2022; Amatu, Alessio/K-2669-2018; Porcu,
   Luca/AAD-8322-2019; Trusolino, Livio/A-3896-2011; Bergamo,
   Francesca/AAB-9010-2019; Borelli, B/AAJ-8829-2021; BARDELLI,
   Alberto/J-9721-2018; zagonel, vittorina/F-4226-2014; LEONE,
   Francesco/R-3248-2016; Lonardi, Sara/F-4228-2014
OI BARDELLI, Alberto/0000-0003-1647-5070; zagonel,
   vittorina/0000-0002-0829-2525; TOSI, FEDERICA MARIA/0000-0001-6146-7411;
   Martino, Cosimo/0000-0002-7286-9755; Fenocchio,
   Elisabetta/0000-0001-6679-0955; SIENA, SALVATORE/0000-0002-2681-2846;
   Amatu, Alessio/0000-0001-5396-3378; vaghi, caterina/0000-0001-5023-3521;
   Torri, Valter/0000-0001-9541-9354; Marsoni, Silvia/0000-0002-5361-7122;
   LEONE, Francesco/0000-0001-5422-9706; Sartore-Bianchi,
   Andrea/0000-0003-0780-0409; Lonardi, Sara/0000-0002-7593-8138;
   Trusolino, Livio/0000-0002-6379-3365; VALTORTA,
   EMANUELE/0000-0002-5087-6233; Porcu, Luca/0000-0002-0911-9775
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NR 24
TC 98
Z9 100
U1 2
U2 11
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 1083-7159
EI 1549-490X
J9 ONCOLOGIST
JI Oncologist
PD OCT
PY 2019
VL 24
IS 10
BP 1395
EP 1402
DI 10.1634/theoncologist.2018-0785
PG 8
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA JE0FR
UT WOS:000490365300018
PM 30952821
OA Green Published, Bronze
DA 2025-01-04
ER

PT J
AU Zhang, YR
   Zhao, YY
   Li, Q
   Wang, Y
AF Zhang, Yingru
   Zhao, Yiyang
   Li, Qi
   Wang, Yan
TI Macrophages, as a Promising Strategy to Targeted Treatment for
   Colorectal Cancer Metastasis in Tumor Immune Microenvironment
SO FRONTIERS IN IMMUNOLOGY
LA English
DT Review
DE colorectal cancer; metastasis; macrophages; targeted treatment;
   signaling pathways
ID POOR-PROGNOSIS; KAPPA-B; SUPPRESSOR-CELLS; LIVER METASTASIS; M2
   POLARIZATION; IFN-GAMMA; T-CELLS; EXPRESSION; ACTIVATION; MIGRATION
AB The tumor immune microenvironment plays a vital role in the metastasis of colorectal cancer. As one of the most important immune cells, macrophages act as phagocytes, patrol the surroundings of tissues, and remove invading pathogens and cell debris to maintain tissue homeostasis. Significantly, macrophages have a characteristic of high plasticity and can be classified into different subtypes according to the different functions, which can undergo reciprocal phenotypic switching induced by different types of molecules and signaling pathways. Macrophages regulate the development and metastatic potential of colorectal cancer by changing the tumor immune microenvironment. In tumor tissues, the tumor-associated macrophages usually play a tumor-promoting role in the tumor immune microenvironment, and they are also associated with poor prognosis. This paper reviews the mechanisms and stimulating factors of macrophages in the process of colorectal cancer metastasis and intends to indicate that targeting macrophages may be a promising strategy in colorectal cancer treatment.
C1 [Zhang, Yingru; Zhao, Yiyang; Li, Qi; Wang, Yan] Shanghai Univ Tradit Chinese Med, Shuguang Hosp, Dept Med Oncol, Shanghai, Peoples R China.
   [Li, Qi] Shanghai Univ Tradit Chinese Med, Acad Integrat Med, Shanghai, Peoples R China.
C3 Shanghai University of Traditional Chinese Medicine; Shanghai University
   of Traditional Chinese Medicine
RP Li, Q; Wang, Y (corresponding author), Shanghai Univ Tradit Chinese Med, Shuguang Hosp, Dept Med Oncol, Shanghai, Peoples R China.; Li, Q (corresponding author), Shanghai Univ Tradit Chinese Med, Acad Integrat Med, Shanghai, Peoples R China.
EM qili@shutcm.edu.cn; yanwang@shutcm.edu.cn
FU National Natural Science Foundation of China [81774095, 82074232,
   82030118]
FX This work was supported by the National Natural Science Foundation of
   China (81774095, 82074232, 82030118).
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NR 185
TC 26
Z9 26
U1 1
U2 34
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 1664-3224
J9 FRONT IMMUNOL
JI Front. Immunol.
PD JUL 13
PY 2021
VL 12
AR 685978
DI 10.3389/fimmu.2021.685978
PG 15
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA TT8CL
UT WOS:000680570900001
PM 34326840
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Wang, X
   Mao, M
   Xu, GJ
   Lin, F
   Sun, P
   Baklaushev, VP
   Chekhonin, VP
   Peltzer, K
   Zhang, J
   Zhang, C
AF Wang, Xin
   Mao, Min
   Xu, Guijun
   Lin, Feng
   Sun, Peng
   Baklaushev, Vladimir P.
   Chekhonin, Vladimir P.
   Peltzer, Karl
   Zhang, Jin
   Zhang, Chao
TI The incidence, associated factors, and predictive nomogram for early
   death in stage IV colorectal cancer
SO INTERNATIONAL JOURNAL OF COLORECTAL DISEASE
LA English
DT Article
DE Colorectal cancer; Stage IV; SEER; Early death; Nomogram
ID PROGNOSTIC-FACTORS; COLON; SURVIVAL; HAZARD
AB PurposeThe purpose of the present study was to investigate the incidence and associated factors for early death in stage IV colorectal cancer (CRC) and to construct the predictive nomogram.MethodsPatients with stage IV CRC, who had been diagnosed between 2010 and 2014 in the Surveillance, Epidemiology, and End Results datasets, were eligible for this retrospective cohort study. The univariable and multivariable logistic regression models were conducted to determine the associated factors for early death (survival time 3months). The predictive nomogram was constructed and the internal validation was performed.ResultsTen thousand two hundred sixty-three out of 36,461 (28.1%) eligible patients resulted in all causes of early death (25.8% for cancer-specific early death and 2.3% for non-cancer early death). Advanced age, marital status, right colon, poor differentiation, higher N stage, and bone metastasis were positively associated with all causes of early death, cancer-specific early death, and non-cancer early death, while higher T stage, positive carcinoembryonic antigen, and distant metastases (bone, lung, liver, and brain) were only positively associated with all causes of early death and cancer-specific early death. The calibration curve for all causes of early death, cancer-specific early death, and non-cancer early death showed the prediction curve closely approximated at the 45 degrees line and the areas under the curve were 75.7% (95% CI, 74.9-76.4%), 75.9% (95% CI, 75.1-76.6%), and 76.9% (95% CI, 76.3-77.6%), respectively.ConclusionsThe nomogram was calibrated to predict all causes of early death development, cancer-specific early death development, and non-cancer early death development. These findings can be utilized in early screening and to tailor targeted treatment regimens for stage IV CRC patients.
C1 [Wang, Xin] Army Med Univ, Dept Epidemiol & Biostat, Affiliated Hosp 1, Chongqing, Peoples R China.
   [Mao, Min] Army Med Univ, Dept Pathol, Affiliated Hosp 1, Chongqing, Peoples R China.
   [Mao, Min] Army Med Univ, Southwest Canc Ctr, Affiliated Hosp 1, Chongqing, Peoples R China.
   [Xu, Guijun; Lin, Feng; Zhang, Jin; Zhang, Chao] Tianjin Med Univ Canc Inst & Hosp, Dept Bone & Soft Tissue Tumors, Tianjins Clin Res Ctr Canc, Natl Clin Res Ctr Canc,Key Lab Canc Prevent & The, Huanhu Xi Rd, Tianjin 300060, Peoples R China.
   [Sun, Peng] Harbin Med Univ, Affiliated Hosp 2, Dept Gen Surg, Harbin, Heilongjiang, Peoples R China.
   [Sun, Peng] Chinese Acad Med Sci, Dept Colorectal Surg, Peking Union Med Coll, Natl Canc Ctr, Beijing, Peoples R China.
   [Baklaushev, Vladimir P.] Fed Biomed Agcy Russian Federat, Fed Res & Clin Ctr Specialized Med Care & Med Tec, Moscow, Russia.
   [Chekhonin, Vladimir P.] Fed Med Res Ctr Psychiat & Narcol, Dept Basic & Appl Neurobiol, Moscow, Russia.
   [Peltzer, Karl] Univ Limpopo, Dept Res & Innovat, Turfloop, Mankweng, South Africa.
C3 Army Medical University; Army Medical University; Army Medical
   University; Tianjin Medical University; Harbin Medical University;
   Chinese Academy of Medical Sciences - Peking Union Medical College;
   Peking Union Medical College; University of Limpopo
RP Zhang, J; Zhang, C (corresponding author), Tianjin Med Univ Canc Inst & Hosp, Dept Bone & Soft Tissue Tumors, Tianjins Clin Res Ctr Canc, Natl Clin Res Ctr Canc,Key Lab Canc Prevent & The, Huanhu Xi Rd, Tianjin 300060, Peoples R China.
EM dczhangj@163.com; drzhangchao@tmu.edu.cn
RI Peltzer, Karl/Q-7334-2019; Mao, Min/IAQ-2666-2023; Baklaushev,
   Vladimir/U-7877-2019; Chekhonin, Vladimir/T-4511-2018; Sun,
   Peng/KDO-4243-2024; Wang, Xin/N-8865-2018
OI Wang, Xin/0000-0001-9325-3194; Baklaushev, Vladimir/0000-0003-1039-4245;
   Chekhonin, Vladimir P./0000-0003-4386-7897
FU Natural Science Foundation of China [81702161, 81801781, 81802508];
   Natural Science Foundation of the Tianjin Science and Technology
   Committee of China [17JCQNJC11000]; Natural Science Foundation of
   Tianjin Medical University [2016KYZQ10]; Doctor Start-up Grant of
   Tianjin Medical University Cancer Institute and Hospital [B1711]; Top
   talent training program of the first affiliated hospital of PLA Army
   Medical University [SWH2018BJKJ-12]
FX Natural Science Foundation of China (81702161, 81801781, and 81802508);
   Natural Science Foundation of the Tianjin Science and Technology
   Committee of China (17JCQNJC11000); Natural Science Foundation of
   Tianjin Medical University (2016KYZQ10); Doctor Start-up Grant of
   Tianjin Medical University Cancer Institute and Hospital (B1711); Top
   talent training program of the first affiliated hospital of PLA Army
   Medical University (SWH2018BJKJ-12).
CR [Anonymous], FRONT IMMUNOL
   [Anonymous], ADV EXP MED BIOL
   [Anonymous], ANN ONCOL S
   [Anonymous], CANC MANAG RES
   [Anonymous], WORLD J SURG
   Arnold D, 2017, ANN ONCOL, V28, P1713, DOI 10.1093/annonc/mdx175
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NR 31
TC 41
Z9 42
U1 1
U2 18
PU SPRINGER
PI NEW YORK
PA ONE NEW YORK PLAZA, SUITE 4600, NEW YORK, NY, UNITED STATES
SN 0179-1958
EI 1432-1262
J9 INT J COLORECTAL DIS
JI Int. J. Colorectal Dis.
PD JUL
PY 2019
VL 34
IS 7
BP 1189
EP 1201
DI 10.1007/s00384-019-03306-1
PG 13
WC Gastroenterology & Hepatology; Surgery
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology; Surgery
GA ID3YM
UT WOS:000471613000004
PM 31089875
DA 2025-01-04
ER

PT J
AU Xiao, RS
   Zheng, F
   Kang, K
   Xiao, L
   Bi, AY
   Chen, YT
   Zhou, Q
   Feng, XP
   Chen, ZK
   Yin, H
   Wang, W
   Chen, ZH
   Cheng, XM
   Zeng, WB
AF Xiao, Runsha
   Zheng, Fan
   Kang, Kuo
   Xiao, Lei
   Bi, Anyao
   Chen, Yiting
   Zhou, Qi
   Feng, Xueping
   Chen, Zhikang
   Yin, Hao
   Wang, Wei
   Chen, Zihua
   Cheng, Xiaomiao
   Zeng, Wenbin
TI Precise visualization and ROS-dependent photodynamic therapy of
   colorectal cancer with a novel mitochondrial viscosity photosensitive
   fluorescent probe
SO BIOMATERIALS RESEARCH
LA English
DT Article
DE Colorectal cancer; Fluorescent probe; Precise visualization; Viscosity;
   Mitochondrion-specific photosensitizer; Photodynamic therapy;
   Theranostics
ID DIAGNOSIS; NANOPARTICLES; AGENTS
AB BackgroundColorectal cancer (CRC) is a prominent global cancer with high mortality rates among human beings. Efficient diagnosis and treatment have always been a challenge for CRC management. Fluorescence guided cancer therapy, which combines diagnosis with therapy into one platform, has brought a new chance for achieving precise cancer theranostics. Among this, photosensitizers, applied in photodynamic therapy (PDT), given the integration of real-time imaging capacity and efficacious treatment feasibility, show great potential to serve as remarkable tools. Although much effort has been put into constructing photosensitizers for locating and destroying CRC cells, it is still in high need to develop novel photosensitizers to attain specific detection and fulfil effective therapy.MethodsProbe HTI was rational synthesized for the diagnosis and treatment of CRC. Spectrometric determination was carried out first, followed by the 1O2 generation ability test. Then, HTI was displayed in distinguishing CRC cells from normal cells Further, the PDT effect of the photosensitizer was studied in vitro. Additionally, HTI was used in CRC BALB/c nude mice model to validate its viscosity labelling and tumor suppression characteristics.ResultsWe successfully fabricated a mitochondrial targeting probe, HTI, together with remarkable viscosity sensitivity, ultralow background interference, and excellent 1O2 generation capacity. HTI was favorably applied to the viscosity detection, displaying a 11-fold fluorescent intensity enhancement in solvents from 1.57 cp to 2043 cp. Then, it was demonstrated that HTI could distinguish CRC cells from normal cells upon the difference in mitochondrial viscosity. Moreover, HTI was qualified for producing 1O2 with high efficiency in cells, supported by the sparkling signals of DCFH after incubation with HTI under light irradiation. More importantly, the viscosity labelling and tumor suppression performance in CRC CDX model was determined, enriching the multifunctional validation of HTI in vivo.ConclusionsIn this study, HTI was demonstrated to show a sensitive response to mitochondrial viscosity and possess a high 1O2 generation capacity. Both in vitro cell imaging and in vivo tumor treatment trials proved that HTI was effectively served as a robust scaffold for tumor labeling and CRC cells clearance. This breakthrough discovery held immense potential for advancing the early diagnosis and management of CRC through PDT. By leveraging HTI's properties, medical professionals could benefit from improved diagnostic accuracy and targeted treatment in CRC management, ultimately leading to enhanced patient outcomes.
C1 [Xiao, Runsha; Kang, Kuo; Xiao, Lei; Feng, Xueping; Chen, Zhikang; Chen, Zihua] Cent South Univ, Xiangya Hosp, Dept Gen Surg, Changsha 410013, Peoples R China.
   [Xiao, Runsha; Kang, Kuo; Chen, Zhikang; Chen, Zihua] Cent South Univ, Xiangya Hosp, Hunan Key Lab Precise Diag & Treatment Gastrointes, Changsha 410013, Peoples R China.
   [Xiao, Runsha; Kang, Kuo; Chen, Zhikang; Chen, Zihua] Cent South Univ, Xiangya Hosp, Natl Clin Res Ctr Geriatr Disorders, Changsha 410013, Peoples R China.
   [Zheng, Fan; Bi, Anyao; Zeng, Wenbin] Cent South Univ, Xiangya Sch Pharmaceut Sci, Changsha 410013, Peoples R China.
   [Zheng, Fan; Bi, Anyao; Zeng, Wenbin] Cent South Univ, Hunan Key Lab Diagnost & Therapeut Drug Res Chron, Changsha 410013, Peoples R China.
   [Xiao, Lei] Cent South Univ, Dept Colorectal Surg, Affiliated Canc Hosp, Xiangya Sch Med, Changsha 410013, Peoples R China.
   [Chen, Yiting] Cent South Univ, Xiangya Hosp, Dept Crit Care Med, Changsha 410013, Peoples R China.
   [Zhou, Qi; Feng, Xueping] Cent South Univ, Xiangya Hosp, Inst Med Sci, Changsha 410013, Peoples R China.
   [Yin, Hao] Shanghai Changzheng Hosp, Organ Transplant Ctr, Shanghai 200003, Peoples R China.
   [Wang, Wei] Cent South Univ, Xiang Ya Hosp 3, Cell Transplantat & Gene Therapy Inst, Changsha 410013, Peoples R China.
   [Wang, Wei] Engn & Technol Res Ctr Xenotransplantat Hunan Prov, Changsha 410013, Peoples R China.
   [Cheng, Xiaomiao] Cent South Univ, Xiangya Hosp, Dept Nephrol, Changsha 410013, Peoples R China.
   [Cheng, Xiaomiao] Xiangya Changde Hosp, Dept Nephrol, Changde 415000, Peoples R China.
C3 Central South University; Central South University; Central South
   University; Central South University; Central South University; Central
   South University; Central South University; Central South University;
   Naval Medical University; Central South University; Central South
   University
RP Chen, ZH (corresponding author), Cent South Univ, Xiangya Hosp, Dept Gen Surg, Changsha 410013, Peoples R China.; Chen, ZH (corresponding author), Cent South Univ, Xiangya Hosp, Hunan Key Lab Precise Diag & Treatment Gastrointes, Changsha 410013, Peoples R China.; Chen, ZH (corresponding author), Cent South Univ, Xiangya Hosp, Natl Clin Res Ctr Geriatr Disorders, Changsha 410013, Peoples R China.; Zeng, WB (corresponding author), Cent South Univ, Xiangya Sch Pharmaceut Sci, Changsha 410013, Peoples R China.; Zeng, WB (corresponding author), Cent South Univ, Hunan Key Lab Diagnost & Therapeut Drug Res Chron, Changsha 410013, Peoples R China.; Cheng, XM (corresponding author), Cent South Univ, Xiangya Hosp, Dept Nephrol, Changsha 410013, Peoples R China.; Cheng, XM (corresponding author), Xiangya Changde Hosp, Dept Nephrol, Changde 415000, Peoples R China.
EM zihuac@outlook.com; cxm131@126.com; wbzeng@hotmail.com
RI Zeng, Wenbin/F-4466-2010; Wang, Wei/N-9423-2019
OI wang, wei/0000-0001-6853-7785
FU We gratefully acknowledge the financial supports from the National
   Natural Science Foundation of China and the Open Sharing Fund for the
   Large-scale Instruments and Equipments of Central South University.;
   National Natural Science Foundation of China; Open Sharing Fund for the
   Large-scale Instruments and Equipments of Central South University
FX We gratefully acknowledge the financial supports from the National
   Natural Science Foundation of China and the Open Sharing Fund for the
   Large-scale Instruments and Equipments of Central South University.
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NR 69
TC 5
Z9 5
U1 12
U2 56
PU AMER ASSOC ADVANCEMENT SCIENCE
PI WASHINGTON
PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 USA
SN 1226-4601
EI 2055-7124
J9 BIOMATER RES
JI Biomater. Res.
PD NOV 8
PY 2023
VL 27
IS 1
AR 112
DI 10.1186/s40824-023-00450-2
PG 12
WC Engineering, Biomedical; Materials Science, Biomaterials
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Engineering; Materials Science
GA X3GF3
UT WOS:001097363300001
PM 37941059
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Lv, WH
   Zhao, Y
   Li, XD
   Zhang, MQ
AF Lv, W. -H.
   Zhao, Y.
   Li, X. -D.
   Zhang, M. -Q.
TI Clinical effects of bevacizumab targeted treatment on advanced
   colorectal cancer with liver metastasis
SO EUROPEAN REVIEW FOR MEDICAL AND PHARMACOLOGICAL SCIENCES
LA English
DT Article
DE Bevacizumab; Targeted treatment; Advanced colorectal cancer; Liver
   metastasis; FOLFOX and CEUS
ID CONTRAST-ENHANCED ULTRASONOGRAPHY; 1ST-LINE TREATMENT; OXALIPLATIN;
   FOLFOX4
AB OBJECTIVE: In this study, the clinical effect of bevacizumab targeted treatment on advanced colorectal cancer with liver metastasis were studied.
   PATIENTS AND METHODS: We consecutively selected 86 cases of patients with advanced colorectal cancer with liver metastasis, and divided them into the control group and observation group (n = 43 each). The FOLFOX chemotherapy scheme (oxaliplatin + fluorouracil + leucovorin) was given to the control group, FOLFOX plus bevacizumab treatment was given to the observation group.
   RESULTS: It was found that the progression-free survival period and median survival period was significantly prolonged in the observation group, the survival rate was increased within 1 year and 2 years (p < 0.05), also the comparison of 3-year survival rates was not statistically significant (p > 0.05). Moreover, the overall effective rates in the observation group were significantly higher that the control group (p < 0.05). In terms of the complication occurrence rates, the difference was not statistically significant. However, the rise time (RT) and mean transit time (mTT) in the observation group significantly increased with the time (p < 0.05). The RT and mTT were unchanged (p > 0.05) in the control group; the RT and mTT at each time point of the observation group were significantly higher than the control group (p < 0.05).
   CONCLUSIONS: The bevacizumab targeted treatment of advanced colorectal cancer with liver metastasis can improve the survival rate, prolong the survival period and cannot increase the complications, the CEUS quantitative indicator rise time and mean transit time were significantly changed, which can be used as an important indicator to predict responses.
C1 [Lv, W. -H.; Zhao, Y.; Li, X. -D.; Zhang, M. -Q.] Cangzhou Cent Hosp, Dept Radiotherapy, Cangzhou City, Peoples R China.
RP Lv, WH (corresponding author), Cangzhou Cent Hosp, Dept Radiotherapy, Cangzhou City, Peoples R China.
EM luweihua179623@163.com
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NR 17
TC 4
Z9 5
U1 0
U2 3
PU VERDUCI PUBLISHER
PI ROME
PA VIA GREGORIO VII, ROME, 186-00165, ITALY
SN 1128-3602
J9 EUR REV MED PHARMACO
JI Eur. Rev. Med. Pharmacol. Sci.
PD JUN
PY 2016
VL 20
IS 11
BP 2249
EP 2255
PG 7
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA DU8JR
UT WOS:000382459700011
PM 27338048
DA 2025-01-04
ER

PT J
AU Zhang, QX
   Zhang, FZ
   Li, SS
   Liu, RF
   Jin, TT
   Dou, Y
   Zhou, ZH
   Zhang, JX
AF Zhang, Qixiong
   Zhang, Fuzhong
   Li, Shanshan
   Liu, Renfeng
   Jin, Taotao
   Dou, Yin
   Zhou, Zhenhua
   Zhang, Jianxiang
TI A Multifunctional Nanotherapy for Targeted Treatment of Colon Cancer by
   Simultaneously Regulating Tumor Microenvironment
SO THERANOSTICS
LA English
DT Article
DE colitis-associated colon cancer; anti-inflammation; reactive oxygen
   species; nanoparticle; camptothecin-11; site-specific therapy
ID INFLAMMATORY-BOWEL-DISEASE; COLORECTAL-CANCER; DRUG-DELIVERY; COATED
   NANOPARTICLES; CAMPTOTHECIN; IRINOTECAN; THERAPY; COLITIS; CYCLODEXTRIN;
   APOPTOSIS
AB Colitis-associated colon cancer (CAC) is a widely recognized cancer, while treatment with the existing chemotherapeutic drugs affords limited clinical benefits. Herein we proposed a site-specific, combination nanotherapy strategy for targeted treatment of CAC by the oral route.
   Methods: A reactive oxygen species (ROS)-responsive and hydrogen peroxide-eliminating material OCD was synthesized, which was further produced into a functional nanoparticle (OCD NP). The antioxidative stress and anti-inflammatory effects of OCD NP were examined by in vitro and in vivo experiments. By packaging an anticancer drug camptothecin-11 (CPT-11) into OCD NP, a ROS-responsive nanotherapy CPT-11/OCD NP was obtained, and its antitumor activity was evaluated by both in vitro and in vivo studies. Preliminary safety studies were also performed for CPT-11/OCD NP in mice.
   Results: OCD NP significantly attenuated oxidative stress and inhibited inflammatory response in different cells and mice with induced colitis. CPT-11/OCD NP could selectively release drug molecules under intestinal pH conditions and at high levels of ROS. In C26 murine colon carcinoma cells, this nanotherapy showed significantly higher antitumor activity compared to free CPT-11 and a non-responsive CPT-11 nanotherapy. Correspondingly, oral delivery of CPT-11/OCD NP notably inhibited tumorigenesis and tumor growth in mice with induced CAC. By combination therapy with the nanovehicle OCD NP in the inflammatory phase, more desirable therapeutic effects were achieved. Furthermore, CPT-11/OCD NP displayed excellent safety profile for oral administration at a dose that is 87.3-fold higher than that employed in therapeutic studies.
   Conclusions: Anticancer nanotherapies derived from intrinsic anti-inflammatory nanocarriers are promising for targeted combination treatment of inflammation-associated tumors by simultaneously shaping pro-inflammatory microenvironment toward a relatively normal niche sensitive to chemotherapy.
C1 [Zhang, Qixiong; Zhang, Fuzhong; Liu, Renfeng; Jin, Taotao; Dou, Yin; Zhang, Jianxiang] Third Mil Med Univ, Coll Pharm, Dept Pharmaceut, Chongqing 400038, Peoples R China.
   [Li, Shanshan] Southwest Univ, Coll Pharmaceut Sci, Dept Pharmaceut Engn, Chongqing 400715, Peoples R China.
   [Liu, Renfeng; Jin, Taotao; Zhou, Zhenhua] Third Mil Med Univ, Southwest Hosp, Dept Neurol, 30 Gaotanyan Main St, Chongqing 400038, Peoples R China.
C3 Army Medical University; Southwest University - China; Army Medical
   University
RP Zhou, ZH (corresponding author), Third Mil Med Univ, Southwest Hosp, Dept Neurol, 30 Gaotanyan Main St, Chongqing 400038, Peoples R China.; Zhang, JX (corresponding author), Third Mil Med Univ, Dept Pharmaceut, 30 Gaotanyan Main St, Chongqing 400038, Peoples R China.
EM exploiter001@126.com; jxzhang1980@gmail.com
RI Li, Shanshan/HLH-7747-2023; Zhang, Jianxiang/A-6626-2009; Zhang,
   Qixiong/AAY-2557-2021; Zhou, Zhenhua/AID-6326-2022
FU National Natural Science Foundation of China [81701832, 81471774];
   Graduate Student Research Innovation Project of Chongqing; Program for
   Distinguished Young Scholars of TMMU
FX This study was supported by the National Natural Science Foundation of
   China (Nos. 81701832 and 81471774), the Graduate Student Research
   Innovation Project of Chongqing, and the Program for Distinguished Young
   Scholars of TMMU.
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NR 80
TC 50
Z9 52
U1 1
U2 67
PU IVYSPRING INT PUBL
PI LAKE HAVEN
PA PO BOX 4546, LAKE HAVEN, NSW 2263, AUSTRALIA
SN 1838-7640
J9 THERANOSTICS
JI Theranostics
PY 2019
VL 9
IS 13
BP 3732
EP 3753
DI 10.7150/thno.34377
PG 22
WC Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine
GA IB0MZ
UT WOS:000469954200005
PM 31281510
OA Green Submitted, Green Published, gold
DA 2025-01-04
ER

PT J
AU Morovati, S
   Mohammadi, A
   Masoudi, R
   Heidari, AA
   Sangabi, MA
AF Morovati, Solmaz
   Mohammadi, Ali
   Masoudi, Ramin
   Heidari, Amir Ali
   Sangabi, Mehdi Asad
TI The power of mumps virus: Matrix protein activates apoptotic pathways in
   human colorectal cell lines
SO PLOS ONE
LA English
DT Article
ID NEWCASTLE-DISEASE VIRUS; VACCINE-STRAIN MEASLES; BCL-2 HOMOLOG;
   MITOCHONDRIAL-MEMBRANE; BH3-ONLY PROTEINS; SPLICED VARIANT; TUMOR-CELLS;
   BH3 DOMAIN; BAX; CANCER
AB New therapeutic approaches can significantly impact the control of colorectal cancer (CRC), which is increasing worldwide. In this study, we investigated the potential of targeting viral proteins to combat cancer cells. Specifically, we examined the anticancer potential of the matrix (M) protein of the mumps virus Hoshino strain in SW480 CRC cell lines. To begin, we individually transfected SW480 cells with pcDNA3 plasmids containing the mumps virus M gene. We then investigated the percentage of cell death, caspase activity, and the expression levels of genes involved in apoptosis pathways. Following this, we performed bioinformatics analysis on the M protein to identify any similarities with Bcl-2 family members and their viral homologs. Our diagnostic methods showed that treatment with the mumps M protein induced apoptosis and upregulated the expression and activity of pro-apoptotic proteins in SW480 CRC cells compared to the control and vector groups. Based on our bioinformatics studies, we proposed that the BH3 motif in the M protein may trigger apoptosis in CRC cells by interacting with cellular Bax. Overall, our study showed for the first time that the mumps virus M protein could be considered as a targeted treatment for CRC by inducing apoptotic pathways.
C1 [Morovati, Solmaz; Masoudi, Ramin] Shiraz Univ, Sch Vet Med, Dept Pathobiol, Div Biotechnol, Shiraz, Iran.
   [Mohammadi, Ali; Sangabi, Mehdi Asad] Shiraz Univ, Sch Vet Med, Dept Pathobiol, Div Virol, Shiraz, Iran.
   [Heidari, Amir Ali] Shiraz Univ, Sch Vet Med, Dept Clin Sci, Div Aquat Anim Hlth & Dis, Shiraz, Iran.
C3 Shiraz University; Shiraz University; Shiraz University
RP Mohammadi, A (corresponding author), Shiraz Univ, Sch Vet Med, Dept Pathobiol, Div Virol, Shiraz, Iran.
EM mohammad@shirazu.ac.ir
RI Mohammadi, Ali/ABI-6158-2020; Masoudi, Ramin/A-3445-2015; Morovati,
   Solmaz/JNE-4220-2023
OI Mohammadi, Ali/0000-0002-5651-3329; Morovati, Solmaz/0000-0002-6269-1228
FU School of Veterinary Science, Shiraz University; Veterinary medicine
   faculty of Shiraz University
FX The authors wish to express their gratitude to the staff and technicians
   of the Veterinary medicine faculty of Shiraz University for their
   support.
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NR 70
TC 3
Z9 3
U1 0
U2 1
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD DEC 13
PY 2023
VL 18
IS 12
AR e0295819
DI 10.1371/journal.pone.0295819
PG 20
WC Multidisciplinary Sciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Science & Technology - Other Topics
GA CP5A6
UT WOS:001126450500033
PM 38091318
OA gold
DA 2025-01-04
ER

PT J
AU Bignucolo, A
   De Mattia, E
   Cecchin, E
   Roncato, R
   Toffoli, G
AF Bignucolo, Alessia
   De Mattia, Elena
   Cecchin, Erika
   Roncato, Rossana
   Toffoli, Giuseppe
TI Pharmacogenomics of Targeted Agents for Personalization of Colorectal
   Cancer Treatment
SO INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
LA English
DT Review
DE targeted agents; anti-EGFR agents; antiangiogenic molecules; Vascular
   Endothelial Growth Factor (VEGF); pharmacogenomics; somatic mutation;
   Rat Sarcoma Oncogene (RAS); inflammation; metastatic colorectal cancer
ID EGFR ANTIBODY MIXTURE; RANDOMIZED PHASE-II; 1ST-LINE TREATMENT;
   SUPPORTIVE CARE; DOUBLE-BLIND; WILD-TYPE; ACQUIRED-RESISTANCE; KRAS
   MUTATIONS; RAS MUTATIONS; MONOCLONAL-ANTIBODIES
AB The use of targeted agents in the treatment of metastatic colorectal cancer (CRC) has improved patient outcomes. Anti-epidermal growth factor receptor (anti-EGFR) agents (cetuximab and panitumumab) and antiangiogenic molecules (bevacizumab, regorafeninb, ramucirumab, and aflibercept) have been successfully integrated into clinical practice. Other drugs have been designed to target additional deregulated pathways in CRC, such as MAPK (mitogen-activated protein kinase)/PI3K-AKT (phosphatidylinositol-3-kinase-AKT serine/threonine kinase)/mTOR (mammalian target of rapamycin), HER-2 and 3 (human epidermal growth factor receptor-2 and -3), and BRAF. A major issue with targeted treatment is early identification of patients with primary or secondary drug resistance. Pharmacogenomic research has demonstrated its value in this field, highlighting some tumor mutations that could discriminate responders from non-responders. The tumor genetic profile of the RAS/RAF pathway is needed before treatment with anti-EGFR agents; mutations in EGFR pathway genes have also been explored in relation to antiangiogenic molecules although further data are required prior to their integration into clinical practice. The introduction of immunotherapy has paved the way for a new generation of predictive markers, including genome-wide assessment of the tumor landscape. Furthermore, the development of next generation sequencing technology and non-invasive approaches to analyze circulating tumor DNA will make real-time monitoring of the tumor pharmacogenomic markers possible in the clinical routine, rendering precision medicine available to every patient.
C1 [Bignucolo, Alessia; De Mattia, Elena; Cecchin, Erika; Roncato, Rossana; Toffoli, Giuseppe] CRO Natl Canc Inst, Clin & Expt Pharmacol, Via Franco Gallini 2, I-33081 Aviano, PN, Italy.
C3 IRCCS Aviano (CRO)
RP De Mattia, E (corresponding author), CRO Natl Canc Inst, Clin & Expt Pharmacol, Via Franco Gallini 2, I-33081 Aviano, PN, Italy.
EM alessia.bignucolo@cro.it; edemattia@cro.it; ececchin@cro.it;
   rroncato@cro.it; gtoffoli@cro.it
RI Toffoli, Giuseppe/F-6642-2018; RONCATO, ROSSANA/AAB-6786-2019; De
   Mattia, Elena/F-6593-2018; Bignucolo, Alessia/AAZ-5587-2020; Cecchin,
   Erika/K-2448-2018
OI Toffoli, Giuseppe/0000-0002-5323-4762; RONCATO,
   ROSSANA/0000-0002-4219-6182; De Mattia, Elena/0000-0003-4948-8767;
   Bignucolo, Alessia/0000-0003-4379-291X; Cecchin,
   Erika/0000-0001-7517-7490
FU "Associazione Italiana per la Ricerca sul Cancro" (AIRC) [12214]
FX This work was supported by the "Associazione Italiana per la Ricerca sul
   Cancro" (AIRC; Special Program Molecular Clinical Oncology, 5x1000 [No.
   12214]).
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NR 99
TC 20
Z9 23
U1 0
U2 6
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
SN 1661-6596
EI 1422-0067
J9 INT J MOL SCI
JI Int. J. Mol. Sci.
PD JUL
PY 2017
VL 18
IS 7
AR 1522
DI 10.3390/ijms18071522
PG 26
WC Biochemistry & Molecular Biology; Chemistry, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Chemistry
GA FF2SJ
UT WOS:000408746800191
PM 28708103
OA Green Submitted, Green Published, gold
DA 2025-01-04
ER

PT J
AU Xu, HJ
   Xia, HW
   Zhou, S
   Tang, QL
   Bi, F
AF Xu, Huanji
   Xia, Hongwei
   Zhou, Sheng
   Tang, Qiulin
   Bi, Feng
TI Cholesterol activates the Wnt/PCP-YAP signaling in SOAT1-targeted
   treatment of colon cancer
SO CELL DEATH DISCOVERY
LA English
DT Article
AB Intracellular free cholesterol can be converted to cholesteryl ester and stored as lipid droplets through SOAT1-mediated esterification. Compelling evidence implicate targeting SOAT1 as a promising therapeutic strategy for cancer management. Herein, we demonstrate how targeting SOAT1 promotes YAP expression by elevating cellular cholesterol content in colon cancer cells. Results revealed that cholesterol alleviates the inhibitory effect of LRP6 on the Wnt/PCP pathway by impeding the interaction of LRP6 with FZD7. Subsequently, FZD7-mediated PCP signaling directly elevated YAP expression by activating RhoA. Nystatin-mediated cholesterol sequestration significantly inhibited YAP expression under SOAT1 inhibition. Moreover, nystatin synergized with the SOAT1 inhibitor avasimibe in suppressing the viability of colon cancer cells in vitro and in vivo. The present study provides new mechanistic insights into the functions of cholesterol metabolism on growth signaling pathways and implicates a novel strategy for cholesterol metabolic-targeted treatment of colon cancers.
C1 [Xu, Huanji; Xia, Hongwei; Zhou, Sheng; Tang, Qiulin; Bi, Feng] Sichuan Univ, West China Hosp, Ctr Canc, Dept Med Oncol, Chengdu 610041, Sichuan, Peoples R China.
   [Xu, Huanji; Xia, Hongwei; Zhou, Sheng; Tang, Qiulin; Bi, Feng] Sichuan Univ, West China Hosp, Lab Mol Targeted Therapy Oncol, Chengdu 610041, Sichuan, Peoples R China.
C3 Sichuan University; Sichuan University
RP Bi, F (corresponding author), Sichuan Univ, West China Hosp, Ctr Canc, Dept Med Oncol, Chengdu 610041, Sichuan, Peoples R China.; Bi, F (corresponding author), Sichuan Univ, West China Hosp, Lab Mol Targeted Therapy Oncol, Chengdu 610041, Sichuan, Peoples R China.
EM bifeng@scu.edu.cn
RI Xu, Huanji/HZJ-6972-2023; Bi, Feng/J-7459-2015
OI Xu, Huanji/0000-0003-0314-5646
FU 1.3.5 project for disciplines of excellence, West China Hospital,
   Sichuan University; National Natural Science Foundation of China
   [82073059]; Science Fund for Creative Research Groups of the National
   Natural Science Foundation of China [81621003]
FX The authors thank Dr. Weidong Zhu (Tongji University School of Medicine,
   China) for the gifts of LRP6 and deletion mutants vectors. This research
   was supported by 1.3.5 project for disciplines of excellence, West China
   Hospital, Sichuan University; the National Natural Science Foundation of
   China (82073059); and Science Fund for Creative Research Groups of the
   National Natural Science Foundation of China (81621003).
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NR 50
TC 22
Z9 22
U1 1
U2 9
PU SPRINGERNATURE
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON, N1 9XW, ENGLAND
EI 2058-7716
J9 CELL DEATH DISCOV
JI Cell Death Discov.
PD FEB 26
PY 2021
VL 7
IS 1
AR 38
DI 10.1038/s41420-021-00421-3
PG 13
WC Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology
GA QQ6NP
UT WOS:000624640100001
PM 33637695
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Al-Mosawi, AKM
   Bahrami, AR
   Nekooei, S
   Saljooghi, AS
   Matin, MM
AF Kamil Mohammad Al-Mosawi, Aseel
   Bahrami, Ahmad Reza
   Nekooei, Sirous
   Saljooghi, Amir Sh.
   Matin, Maryam M.
TI Using magnetic mesoporous silica nanoparticles armed with EpCAM aptamer
   as an efficient platform for specific delivery of 5-fluorouracil to
   colorectal cancer cells
SO FRONTIERS IN BIOENGINEERING AND BIOTECHNOLOGY
LA English
DT Article
DE colorectal cancer; mesoporous silica nanoparticles; superparamagnetic
   iron oxide; 5-fluorouracil; epithelial cell adhesion molecule
ID ADHESION MOLECULE; TARGETED DELIVERY; CELLULAR UPTAKE; FOLIC-ACID;
   THERAPY; CARRIER; SIZE
AB Background: Theranostic nanoparticles with both imaging and therapeutic capacities are highly promising in successful diagnosis and treatment of advanced cancers.Methods: Here, we developed magnetic mesoporous silica nanoparticles (MSNs) loaded with 5-fluorouracil (5-FU) and surface-decorated with polyethylene glycol (PEG), and epithelial cell adhesion molecule (EpCAM) aptamer (Apt) for controlled release of 5-FU and targeted treatment of colorectal cancer (CRC) both in vitro and in vivo. In this system, Au NPs are conjugated onto the exterior surface of MSNs as a gatekeeper for intelligent release of the anti-cancer drug at acidic conditions.Results: Nanocarriers were prepared with a final size diameter of 78 nm, the surface area and pore size of SPION-MSNs were calculated as 636 m(2)g(-1), and 3 nm based on the BET analysis. The release of 5-FU from nanocarriers was pH-dependent, with an initial rapid release (within 6 h) followed by a sustained release for 96 h at pH 5.4. Tracking the cellular uptake by flow cytometry technique illustrated more efficient and higher uptake of targeted nanocarriers in HT-29 cells compared with non-targeted formula. In vitro results demonstrated that nanocarriers inhibited the growth of cancer cells via apoptosis induction. Furthermore, the targeted NPs could significantly reduce tumor growth in immunocompromised C57BL/6 mice bearing HT-29 tumors, similar to those injected with free 5-FU, while inducing less side effects.Conclusion: These findings suggest that application of Apt-PEG-Au-NPs@5-FU represents a promising theranostic platform for EpCAM-positive CRC cells, although further experiments are required before it can be practiced in the clinic.
C1 [Kamil Mohammad Al-Mosawi, Aseel; Bahrami, Ahmad Reza; Matin, Maryam M.] Ferdowsi Univ Mashhad, Fac Sci, Dept Biol, Mashhad, Iran.
   [Bahrami, Ahmad Reza] Ferdowsi Univ Mashhad, Inst Biotechnol, Ind Biotechnol Res Grp, Mashhad, Iran.
   [Nekooei, Sirous] Mashhad Univ Med Sci, Qaem Hosp, Dept Radiol, Mashhad, Iran.
   [Saljooghi, Amir Sh.] Ferdowsi Univ Mashhad, Fac Sci, Dept Chem, Mashhad, Iran.
   [Saljooghi, Amir Sh.; Matin, Maryam M.] Ferdowsi Univ Mashhad, Inst Biotechnol, Novel Diagnost & Therapeut Res Grp, Mashhad, Iran.
   [Matin, Maryam M.] Acad Ctr Educ Culture & Res ACECR, Stem Cells & Regenerat Med Res Grp, Mashhad, Iran.
C3 Ferdowsi University Mashhad; Ferdowsi University Mashhad; Mashhad
   University of Medical Sciences; Ferdowsi University Mashhad; Ferdowsi
   University Mashhad; Academic Center for Education, Culture & Research
   (ACECR)
RP Matin, MM (corresponding author), Ferdowsi Univ Mashhad, Fac Sci, Dept Biol, Mashhad, Iran.; Saljooghi, AS (corresponding author), Ferdowsi Univ Mashhad, Fac Sci, Dept Chem, Mashhad, Iran.; Saljooghi, AS; Matin, MM (corresponding author), Ferdowsi Univ Mashhad, Inst Biotechnol, Novel Diagnost & Therapeut Res Grp, Mashhad, Iran.; Matin, MM (corresponding author), Acad Ctr Educ Culture & Res ACECR, Stem Cells & Regenerat Med Res Grp, Mashhad, Iran.
EM matin@um.ac.ir; saljooghi@um.ac.ir
RI ALmosawi, Aseel/ABE-5757-2021; M. Matin, Maryam/W-1884-2017
OI M. Matin, Maryam/0000-0002-7949-7712; Sh. Saljooghi,
   Amir/0000-0001-5764-469X; Kamil, Aseel/0000-0001-9714-805X
FU Ferdowsi University of Mashhad [51720]
FX Funding This work was supported by Ferdowsi University of Mashhad, Grant
   Number: 51720.
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NR 50
TC 14
Z9 14
U1 4
U2 22
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 2296-4185
J9 FRONT BIOENG BIOTECH
JI Front. Bioeng. Biotechnol.
PD JAN 6
PY 2023
VL 10
AR 1095837
DI 10.3389/fbioe.2022.1095837
PG 18
WC Biotechnology & Applied Microbiology; Engineering, Biomedical
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biotechnology & Applied Microbiology; Engineering
GA 8A4TA
UT WOS:000916231800001
PM 36686226
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Czauderna, C
   Luley, K
   von Bubnoff, N
   Marquardt, JU
AF Czauderna, Carolin
   Luley, Kim
   von Bubnoff, Nikolas
   Marquardt, Jens U.
TI Tailored Systemic Therapy for Colorectal Cancer Liver Metastases
SO INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
LA English
DT Review
DE colorectal cancer; molecular biomarkers; prognosis; prediction
ID TRANS-ARTERIAL CHEMOEMBOLIZATION; FOLFIRI PLUS BEVACIZUMAB; PHASE-II
   TRIAL; WILD-TYPE; 1ST-LINE TREATMENT; RAS MUTATIONS; OPEN-LABEL;
   MICROSATELLITE INSTABILITY; NEOADJUVANT CHEMOTHERAPY; SUBGROUP ANALYSES
AB Liver metastases are the most common site of metastatic spread in colorectal cancer. Current treatment approaches involve effective systemic therapies in combination with surgical and/or interventional strategies. Multimodal strategies greatly improved clinical outcomes of patients with metastatic colorectal cancer over the last decades. Identification of predictive and prognostic biomarkers helped to comprehensively refine individual targeted treatment approaches and resulted in median overall survival rates of 30 months or longer. Current guidelines, thus, recommend treatment selection according to patients' performance status, tumor localization and stage as well as the tumor's molecular and genetic status. Here, we outline the latest developments in molecular decision-making for patients with upfront resectable, potentially or initially unresectable and non/never-resectable colorectal cancer liver metastases.
C1 [Czauderna, Carolin; Marquardt, Jens U.] Univ Med Ctr Schleswig Holstein, Dept Med 1, Campus Lubeck, D-23558 Lubeck, Germany.
   [Luley, Kim; von Bubnoff, Nikolas] Univ Med Ctr Schleswig Holstein, Dept Hematooncol, Campus Lubeck, D-23558 Lubeck, Germany.
C3 University of Kiel; Schleswig Holstein University Hospital; University
   of Kiel; Schleswig Holstein University Hospital
RP Marquardt, JU (corresponding author), Univ Med Ctr Schleswig Holstein, Dept Med 1, Campus Lubeck, D-23558 Lubeck, Germany.
EM carolin.czauderna@uni-luebeck.de; Kim.Luley@uksh.de;
   Nikolas.vonBubnoff@uksh.de; Jens.Marquardt@uksh.de
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NR 84
TC 7
Z9 8
U1 1
U2 13
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
SN 1661-6596
EI 1422-0067
J9 INT J MOL SCI
JI Int. J. Mol. Sci.
PD NOV
PY 2021
VL 22
IS 21
AR 11780
DI 10.3390/ijms222111780
PG 14
WC Biochemistry & Molecular Biology; Chemistry, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Chemistry
GA WX6AP
UT WOS:000718676800001
PM 34769209
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Sveen, A
   Bruun, J
   Eide, PW
   Eilertsen, IA
   Ramirez, L
   Murumägi, A
   Arjama, M
   Danielsen, SA
   Kryeziu, K
   Elez, E
   Tabernero, J
   Guinney, J
   Palmer, HG
   Nesbakken, A
   Kallioniemi, O
   Dienstmann, R
   Lothe, RA
AF Sveen, Anita
   Bruun, Jarle
   Eide, Peter W.
   Eilertsen, Ina A.
   Ramirez, Lorena
   Murumagi, Astrid
   Arjama, Mariliina
   Danielsen, Stine A.
   Kryeziu, Kushtrim
   Elez, Elena
   Tabernero, Josep
   Guinney, Justin
   Palmer, Hector G.
   Nesbakken, Arild
   Kallioniemi, Olli
   Dienstmann, Rodrigo
   Lothe, Ragnhild A.
TI Colorectal Cancer Consensus Molecular Subtypes Translated to Preclinical
   Models Uncover Potentially Targetable Cancer Cell Dependencies
SO CLINICAL CANCER RESEARCH
LA English
DT Article
ID COLON-CANCER; MICROSATELLITE INSTABILITY; HETEROGENEITY; LINES; THERAPY;
   PROGNOSIS; PATTERNS; CLASSIFICATION; SENSITIVITY; INHIBITORS
AB Purpose: Response to standard oncologic treatment is limited in colorectal cancer. The gene expression-based consensus molecular subtypes (CMS) provide a new paradigm for stratified treatment and drug repurposing; however, drug discovery is currently limited by the lack of translation of CMS to preclinical models.
   Experimental Design: We analyzed CMS in primary colorectal cancers, cell lines, and patient-derived xenografts (PDX). For classification of preclinical models, we developed an optimized classifier enriched for cancer cell-intrinsic gene expression signals, and performed high-throughput in vitro drug screening (n = 459 drugs) to analyze subtype-specific drug sensitivities.
   Results: The distinct molecular and clinicopathologic characteristics of each CMS group were validated in a single-hospital series of 409 primary colorectal cancers. The new, cancer cell-adapted classifier was found to perform well in primary tumors, and applied to a panel of 148 cell lines and 32 PDXs, these colorectal cancer models were shown to recapitulate the biology of the CMS groups. Drug screening of 33 cell lines demonstrated subtype-dependent response profiles, confirming strong response to EGFR and HER2 inhibitors in the CMS2 epithelial/canonical group, and revealing strong sensitivity to HSP90 inhibitors in cells with the CMS1 microsatellite instability/immune and CMS4 mesenchymal phenotypes. This association was validated in vitro in additional CMS-predicted cell lines. Combination treatment with 5-fluorouracil and luminespib showed potential to alleviate chemoresistance in a CMS4 PDX model, an effect not seen in a chemosensitive CMS2 PDX model.
   Conclusions: We provide translation of CMS classification to preclinical models and uncover a potential for targeted treatment repurposing in the chemoresistant CMS4 group. (C) 2017 AACR.
C1 [Sveen, Anita; Bruun, Jarle; Eide, Peter W.; Eilertsen, Ina A.; Danielsen, Stine A.; Kryeziu, Kushtrim; Lothe, Ragnhild A.] Oslo Univ Hosp, Inst Canc Res, Dept Mol Oncol, POB 4953 Nydalen, NO-0424 Oslo, Norway.
   [Sveen, Anita; Bruun, Jarle; Eide, Peter W.; Eilertsen, Ina A.; Danielsen, Stine A.; Kryeziu, Kushtrim; Nesbakken, Arild; Lothe, Ragnhild A.] Oslo Univ Hosp, KG Jebsen Colorectal Canc Res Ctr, Oslo, Norway.
   [Bruun, Jarle; Murumagi, Astrid; Arjama, Mariliina; Kallioniemi, Olli] Univ Helsinki, FIMM, Helsinki, Finland.
   [Ramirez, Lorena; Elez, Elena; Tabernero, Josep; Palmer, Hector G.; Dienstmann, Rodrigo] Univ Autonoma Barcelona, CIBERONC, Vall dHebron Univ Hosp, Barcelona, Spain.
   [Ramirez, Lorena; Elez, Elena; Tabernero, Josep; Palmer, Hector G.; Dienstmann, Rodrigo] Univ Autonoma Barcelona, CIBERONC, Inst Oncol VHIO, Barcelona, Spain.
   [Guinney, Justin; Dienstmann, Rodrigo] Fred Hutchinson Canc Res Ctr, SAGE Bionetworks, 1124 Columbia St, Seattle, WA 98104 USA.
   [Nesbakken, Arild] Oslo Univ Hosp, Dept Gastrointestinal Surg, Oslo, Norway.
   [Nesbakken, Arild; Lothe, Ragnhild A.] Univ Oslo, Inst Clin Med, Oslo, Norway.
C3 University of Oslo; University of Oslo; University of Helsinki; CIBER -
   Centro de Investigacion Biomedica en Red; CIBERONC; Hospital
   Universitari Vall d'Hebron; Autonomous University of Barcelona; Vall
   d'Hebron Institut d'Oncologia (VHIO); CIBER - Centro de Investigacion
   Biomedica en Red; CIBERONC; Autonomous University of Barcelona; Fred
   Hutchinson Cancer Center; University of Oslo; University of Oslo
RP Lothe, RA (corresponding author), Oslo Univ Hosp, Inst Canc Res, Dept Mol Oncol, POB 4953 Nydalen, NO-0424 Oslo, Norway.
EM rlothe@rr-research.no
RI Kallioniemi, Olli/H-5111-2011; Kryeziu, Kushtrim/AAR-4845-2020;
   Tabernero, Josep/AAG-5026-2019; Élez, Elena/AAH-2945-2019; Palmer,
   Héctor/AAG-8332-2019; Kallioniemi, Olli/H-4738-2012
OI Kallioniemi, Olli/0000-0002-3231-0332; Guinney, Justin
   H/0000-0003-1477-1888; Palmer, Hector/0000-0002-9823-5638; Tabernero,
   Josep/0000-0002-2495-8139; Murumagi, Astrid/0000-0002-7797-188X; Sveen,
   Anita/0000-0001-8219-6251; Lothe, Ragnhild A./0000-0002-1693-1032;
   Ramirez Corpas, Lorena/0000-0003-1792-7390; Kryeziu,
   Kushtrim/0000-0002-6633-4818; Elez, Elena/0000-0002-4653-6324
FU Norwegian Cancer Society [6824048-2016, 182759-2016]; Southern and
   Eastern Norway Regional Health Authority; foundation Stiftelsen Kristian
   Gerhard Jebsen; Research Council of Norway (FRIPRO Toppforsk) [250993];
   European Union (Seventh Framework Programme (FP7-PEOPLE-COFUND)
   [609020]; Merck KGaA, Darmstadt, Germany
FX This study was supported by the Norwegian Cancer Society (project number
   6824048-2016 to A. Sveen and project number 182759-2016 to R.A. Lothe),
   the Southern and Eastern Norway Regional Health Authority (to R. A.
   Lothe), the foundation Stiftelsen Kristian Gerhard Jebsen (to R.A.
   Lothe), the Research Council of Norway (FRIPRO Toppforsk, project number
   250993; and grants to the Norwegian Cancer Genomics Consortium, both to
   R. A. Lothe), the European Union Seventh Framework Programme
   (FP7-PEOPLE-2013-COFUND, grant agreement number 609020 Scientia Fellows
   to R. A. Lothe), and Merck KGaA, Darmstadt, Germany (Grant for Oncology
   Innovation 2015, "Next generation of clinical trials with matched
   targeted therapies in colorectal cancer" to R. Dienstmann and J.
   Guinney).
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NR 50
TC 171
Z9 187
U1 0
U2 27
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1078-0432
EI 1557-3265
J9 CLIN CANCER RES
JI Clin. Cancer Res.
PD FEB 15
PY 2018
VL 24
IS 4
BP 794
EP 806
DI 10.1158/1078-0432.CCR-17-1234
PG 13
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA FW3FF
UT WOS:000425191300009
PM 29242316
OA Green Submitted, Green Published, Bronze
DA 2025-01-04
ER

PT J
AU Madunic, K
   Mayboroda, OA
   Zhang, T
   Weber, J
   Boons, GJ
   Morreau, H
   van Vlierberghe, R
   van Wezel, T
   Lageveen-Kammeijer, GSM
   Wuhrer, M
AF Madunic, Katarina
   Mayboroda, Oleg A.
   Zhang, Tao
   Weber, Julia
   Boons, Geert-Jan
   Morreau, Hans
   van Vlierberghe, Ronald
   van Wezel, Tom
   Lageveen-Kammeijer, Guinevere S. M.
   Wuhrer, Manfred
TI Specific (sialyl-)Lewis core 2 <i>O</i>-glycans differentiate colorectal
   cancer from healthy colon epithelium
SO THERANOSTICS
LA English
DT Article
DE Tumor associated carbohydrate antigens (TACAs); mass spectrometry;
   glycomics; therapeutic target
ID SIALYL-LEWIS-X; BLOOD-GROUP-H; SELECTIN-LIGAND; SIALOSYL-TN;
   STRUCTURAL-CHARACTERIZATION; MONOCLONAL-ANTIBODY; POOR-PROGNOSIS;
   EXPRESSION; CARCINOMA; GLYCOSYLATION
AB Cells are covered with a dense layer of carbohydrates, some of which are solely present on neoplastic cells. The so-called tumor-associated carbohydrate antigens (TACAs) are increasingly recognized as promising targets for immunotherapy. These carbohydrates differ from those of the surrounding non-cancerous tissues and contribute to the malignant phenotype of the cancer cells by promoting proliferation, metastasis, and immunosuppression. However, due to tumor tissue heterogeneity and technological limitations, TACAs are insufficiently explored.
   Methods: A workflow was established to decode the colorectal cancer (CRC)-associated O-linked glycans from approximately 20,000 cell extracts. Extracts were obtained through laser capture microdissection of formalin fixed paraffin embedded tissues of both primary tumors and metastatic sites, and compared to healthy colon mucosa from the same patients. The released O-glycans were analyzed by porous graphitized carbon liquid chromatography-tandem mass spectrometry in negative ion mode.
   Results: Distinctive O-glycosylation features were found in cancerous, stromal and normal colon mucosal regions. Over 100 O-linked glycans were detected in cancerous regions with absence in normal mucosa. From those, six core 2 O-glycans were exclusively found in more than 33% of the cancers, carrying the terminal (sialyl-)Lewis(X/A) antigen. Moreover, two O-glycans were present in 72% of the analyzed cancers and 94% of the investigated cancers expressed at least one of these two O-glycans. In contrast, normal colon mucosa predominantly expressed core 3 O-glycans, carrying alpha 2-6-linked sialylation, (sulfo-)Lewis(X/A) and Sda antigens.
   Conclusion: In this study, we present a novel panel of highly specific TACAs, based upon differences in the glycomic profiles between CRC and healthy colon mucosa. These TACAs are promising new targets for development of innovative cancer immune target therapies and lay the foundation for the targeted treatment of CRC.
C1 [Madunic, Katarina; Mayboroda, Oleg A.; Zhang, Tao; Lageveen-Kammeijer, Guinevere S. M.; Wuhrer, Manfred] Leiden Univ, Ctr Prote & Metabol, Med Ctr, Postbus 9600, NL-2300 RC Leiden, Netherlands.
   [van Vlierberghe, Ronald] Leiden Univ, Dept Surg, Med Ctr, Postbus 9600, NL-2300 RC Leiden, Netherlands.
   [Morreau, Hans; van Wezel, Tom] Leiden Univ, Dept Pathol, Med Ctr, Postbus 9600, NL-2300 RC Leiden, Netherlands.
   [Weber, Julia; Boons, Geert-Jan] Univ Utrecht, Dept Chem Biol & Drug Discovery, Univ Weg 99, NL-3584 CG Utrecht, Netherlands.
C3 Leiden University - Excl LUMC; Leiden University; Leiden University
   Medical Center (LUMC); Leiden University; Leiden University Medical
   Center (LUMC); Leiden University - Excl LUMC; Leiden University; Leiden
   University Medical Center (LUMC); Leiden University - Excl LUMC; Utrecht
   University
RP Wuhrer, M (corresponding author), Leiden Univ, Ctr Prote & Metabol, Med Ctr, Postbus 9600, NL-2300 RC Leiden, Netherlands.
EM m.wuhrer@lumc.nl
RI Madunic, Katarina/AAF-1173-2021; Wuhrer, Manfred/ABE-9168-2020;
   Mayboroda, Oleg/N-4850-2019; van Wezel, Tom/AAL-5626-2021; Zhang,
   Tao/ABB-3362-2021; Kammeijer, Guinevere/KHU-1226-2024; Boons,
   Geert-Jan/J-3211-2016
OI Lageveen-Kammeijer, Guinevere/0000-0001-7670-1151; Zhang,
   Tao/0000-0003-0427-9953; Boons, Geert-Jan/0000-0003-3111-5954; van
   Wezel, Tom/0000-0001-5773-7730
FU European Commission [676421]
FX This work was supported by the European Commission's Horizon 2020
   programme "GlyCoCan" project, grant number 676421.
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NR 77
TC 24
Z9 24
U1 2
U2 24
PU IVYSPRING INT PUBL
PI LAKE HAVEN
PA PO BOX 4546, LAKE HAVEN, NSW 2263, AUSTRALIA
SN 1838-7640
J9 THERANOSTICS
JI Theranostics
PY 2022
VL 12
IS 10
BP 4498
EP 4512
DI 10.7150/thno.72818
PG 15
WC Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine
GA 1X4ZW
UT WOS:000807464800002
PM 35832079
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Gelej, M
   Zajac, P
   Dabrowska, M
   Drejws-Watrobska, A
   Galinska, B
   Galus, L
   Gwózdz-Cieslik, A
   Hetman, K
   Kawecki, M
   Malik, M
   Streb, J
   Wierzbicka, K
   Wiosek, P
   Radecka, B
AF Gelej, Marek
   Zajac, Patryk
   Dabrowska, Maria
   Drejws-Watrobska, Anna
   Galinska, Bogumila
   Galus, Lukasz
   Gwozdz-Cieslik, Agnieszka
   Hetman, Katarzyna
   Kawecki, Maciej
   Malik, Mateusz
   Streb, Joanna
   Wierzbicka, Katarzyna
   Wiosek, Piotr
   Radecka, Barbara
TI Encorafenib plus cetuximab in patients with BRAFV600E-mutated metastatic
   colorectal cancer - Polish multicenter experience
SO ONCOLOGY IN CLINICAL PRACTICE
LA English
DT Article
DE colorectal cancer; BRAFV600E mutation; encorafenib; cetuximab
ID CLINICAL-PRACTICE; BRAF; GUIDELINE
AB Introduction. The BRAF mutation occurs in 8-12% of patients with colorectal cancer. This is associated with unfavorable prognosis - in metastatic disease, median survival does not exceed one year. Molecularly targeted treatment - encorafenib with cetuximab - is the standard of care in cases of chemotherapy failure. Material and methods. Medical data of 18 patients treated with encorafenib and cetuximab in 2021-2023 in 10 oncology centers in Poland were assessed. We analyzed clinical, pathomorphological, and molecular factors, as well as the effectiveness and safety of treatment. Results. The median age in the group was 63 years. Patients with metastases limited to one location predominated (78%). Treatment with encorafenib and cetuximab was used not only in the third (in 50% of patients) or fourth (in 28%) lines of treatment but also in the second (in 22%). The objective response rate was 29.4%, and the disease control rate was 76.4%. The median progression-free survival was 7.1 months. Four patients (22%) had a response lasting over 12 months. Conclusions. The results of the analysis confirmed the efficacy and safety of targeted treatment with encorafenib and cetuximab in patients with metastatic colorectal cancer with the BRAFV600E mutation, known from other studies.
C1 [Gelej, Marek; Malik, Mateusz; Streb, Joanna; Wierzbicka, Katarzyna; Wiosek, Piotr; Radecka, Barbara] Univ Opole, Inst Med Sci, Dept Oncol, Opole, Poland.
   [Gelej, Marek; Zajac, Patryk; Wierzbicka, Katarzyna; Radecka, Barbara] Opole Oncol Ctr Prof Tadeusz Koszarowski, Oncol Clin Daily Ward, Opole, Poland.
   [Zajac, Patryk; Wiosek, Piotr] Univ Opole, Dept Clin Biochem & Lab Diagnost, Fac Med, PL-45052 Opole, Poland.
   [Dabrowska, Maria] Prov Specialist Hosp 4 Bytom, Dept Clin Oncol, Bytom, Poland.
   [Drejws-Watrobska, Anna; Hetman, Katarzyna] West Pomeranian Oncol Ctr, Dept Clin Oncol, Szczecin, Poland.
   [Galinska, Bogumila] Pomeranian Med Univ, Independent Publ Clin Hosp Prof Tadeusz Sokolowski, Szczecin, Poland.
   [Galus, Lukasz] Med Univ Poznan, Inst Oncol, Dept Clin & Expt Oncol, Poznan, Poland.
   [Gwozdz-Cieslik, Agnieszka] Swietokrzyskie Ctr Onkol, Dept Clin Oncol, Kielce, Poland.
   [Kawecki, Maciej] Natl Inst Oncol Mar Sklodowska Curie, Natl Res Inst, Dept Oncol & Radiotherapy, Warsaw, Poland.
   [Malik, Mateusz] Lower Silesian Oncol Pulmonol & Hematol Ctr, Dept Clin Oncol, Wroclaw, Poland.
   [Streb, Joanna] Jagiellonian Univ, Dept Oncol, Krakow, Poland.
   [Wierzbicka, Katarzyna] Univ Clin Ctr, Dept Oncol & Radiotherapy, Gdansk, Poland.
   [Wiosek, Piotr] Prov Hosp, Oncol Dept, Elblag, Poland.
   [Gelej, Marek] Opole Oncol Ctr Prof Tadeusz Koszarowski Opole, Oncol Clin Daily Ward, Ul Katowicka, PL-45061 Opole, Poland.
C3 University of Opole; University of Opole; Pomeranian Medical University;
   Poznan University of Medical Sciences; Jagiellonian University;
   Collegium Medicum Jagiellonian University
RP Gelej, M (corresponding author), Opole Oncol Ctr Prof Tadeusz Koszarowski Opole, Oncol Clin Daily Ward, Ul Katowicka, PL-45061 Opole, Poland.
EM mgelej@gmail.com
RI Dąbrowska, Maria/AAN-7177-2020
OI RADECKA, BARBARA/0000-0001-7979-7523; Zajac, Patryk/0000-0002-9474-6983
FU Pierre-Fabre
FX Funding The study was made possible thanks to a research grant from
   Pierre-Fabre.
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NR 16
TC 0
Z9 0
U1 0
U2 0
PU VIA MEDICA
PI GDANSK
PA UL SWIETOKRZYSKA 73, 80-180 GDANSK, POLAND
SN 2450-1654
EI 2450-6478
J9 ONCOL CLIN PRACT
JI Oncol. Clin. Pract.
PY 2024
VL 20
IS 4
BP 264
EP 269
DI 10.5603/ocp.98519
EA DEC 2023
PG 6
WC Oncology
WE Emerging Sources Citation Index (ESCI)
SC Oncology
GA E2R0H
UT WOS:001195782500001
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Li, YJ
   Wu, T
   Saeed, MM
   Cui, XA
AF Li, Yujun
   Wu, Tong
   Saeed, Muhammad Muddasar
   Cui, Xiaonan
TI Bevacizumab for the treatment of metastatic colorectal cancer
   complicated by abdominal aortic aneurysm and mural thrombus: a case
   report
SO FRONTIERS IN ONCOLOGY
LA English
DT Article
DE abdominal aortic aneurysm; bevacizumab; colorectal cancer; molecular
   targeting treatment; case report
AB Bevacizumab, a humanized monoclonal antibody targeting vascular endothelial growth factor (VEGF), was the first anti-angiogenic agent incorporated into metastatic colorectal cancer treatment strategies and demonstrated broad-spectrum anti-tumor efficacy. Commonly reported adverse events include hypertension, proteinuria, gastrointestinal perforation, bleeding, and thromboembolism. However, there are only a few reports on abdominal aortic aneurysms (AAA) as a complication of bevacizumab therapy. Given the high risk of fatal rupture with AAA, we present a case of bevacizumab-associated AAA to raise clinician awareness of this possible, rare, and serious adverse reaction.
C1 [Li, Yujun; Wu, Tong; Saeed, Muhammad Muddasar; Cui, Xiaonan] Dalian Med Univ, Affiliated Hosp 1, Dept Oncol, Dalian, Peoples R China.
C3 Dalian Medical University
RP Cui, XA (corresponding author), Dalian Med Univ, Affiliated Hosp 1, Dept Oncol, Dalian, Peoples R China.
EM cxn23@sina.com
CR Aragon-Ching JB, 2008, ACTA ONCOL, V47, P1600, DOI 10.1080/02841860801978905
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NR 16
TC 0
Z9 0
U1 1
U2 1
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 2234-943X
J9 FRONT ONCOL
JI Front. Oncol.
PD NOV 18
PY 2024
VL 14
AR 1416349
DI 10.3389/fonc.2024.1416349
PG 4
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA N9G2R
UT WOS:001367328900001
PM 39624630
OA gold
DA 2025-01-04
ER

PT J
AU Lin, YL
   Pan, XX
   Chen, ZH
   Lin, SY
   Shen, ZL
   Chen, SQ
AF Lin, Yilin
   Pan, Xiaoxian
   Chen, Zhihua
   Lin, Suyong
   Shen, Zhanlong
   Chen, Shaoqin
TI Prognostic value and immune infiltration of novel signatures in colon
   cancer microenvironment
SO CANCER CELL INTERNATIONAL
LA English
DT Article
DE Colon cancer; Tumor microenvironment; Noncoding RNA; H19; Immune
   infiltration; Survival
ID CELL; RNA
AB Background Growing evidence has shown that the prognosis for colon cancer depends on changes in microenvironment. The purpose of this study was to elucidate the prognostic value of long noncoding RNAs (lncRNAs) related to immune microenvironment (IM) in colon cancer. Methods Single sample gene set enrichment analysis (ssGSEA) was used to identify the subtypes of colon cancer based on the immune genomes of 29 immune signatures. Cox regression analysis identified a lncRNA signatures associated with immune infiltration. The Tumor Immune Estimation Resource database was used to analyze immune cell content. Results Colon cancer samples were divided into three subtypes by unsupervised cluster analysis. Cox regression analysis identified an immune infiltration-related 5-lncRNA signature. This signature combined with clinical factors can effectively improve the predictive ability for the overall survival (OS) of colon cancer. At the same time, we found that the expression of H19 affects the content of B cells and macrophages in the microenvironment of colon cancer and affects the prognosis of colon cancer. Finally, we constructed the H19 regulatory network and further analyzed the possible mechanisms. We found that knocking down the expression of H19 can significantly inhibit the expression of CCND1 and VEGFA. At the same time, the immunohistochemical assay found that the expression of CCND1 and VEGFA protein was significantly positively correlated with the infiltration of M2 type macrophages. Conclusion The findings may help to formulate clinical strategies and understand the underlying mechanisms of H19 regulation. H19 may be a biomarker for targeted treatment of colon cancer.
C1 [Chen, Zhihua; Lin, Suyong; Chen, Shaoqin] Fujian Med Univ, Dept Surg Gastroenterol, Affiliated Hosp 1, 20 Chazhong Rd, Fuzhou, Fujian, Peoples R China.
   [Lin, Yilin; Shen, Zhanlong] Peking Univ Peoples Hosp, Dept Surg Gastroenterol, 11 Xizhimen South St, Beijing, Peoples R China.
   [Pan, Xiaoxian] Fujian Med Univ, Dept Radiotherapy, Affiliated Hosp 1, Fuzhou, Fujian, Peoples R China.
C3 Fujian Medical University; Fujian Medical University
RP Chen, SQ (corresponding author), Fujian Med Univ, Dept Surg Gastroenterol, Affiliated Hosp 1, 20 Chazhong Rd, Fuzhou, Fujian, Peoples R China.; Shen, ZL (corresponding author), Peking Univ Peoples Hosp, Dept Surg Gastroenterol, 11 Xizhimen South St, Beijing, Peoples R China.
EM shenzhanlong@pkuph.edu.cn; chenshaoqln1613@163.com
RI Shen, Zhanlong/ABH-8734-2020
FU Natural Science Foundation of Fujian Province of China [2019J01448];
   National Natural Science Foundation of China [81972240]
FX This work was supported by the Natural Science Foundation of Fujian
   Province of China [Grant Number 2019J01448]. This work was also
   supported by the National Natural Science Foundation of China (Grant No.
   81972240).
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NR 54
TC 4
Z9 4
U1 0
U2 11
PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
EI 1475-2867
J9 CANCER CELL INT
JI Cancer Cell Int.
PD DEC 18
PY 2021
VL 21
IS 1
AR 679
DI 10.1186/s12935-021-02342-8
PG 19
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA XQ2RN
UT WOS:000731397800002
PM 34922547
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU de la Fouchardière, C
AF de la Fouchardiere, Christelle
TI Regorafenib in the treatment of metastatic colorectal cancer
SO FUTURE ONCOLOGY
LA English
DT Article
DE adherence to oral treatment; anti-angiogenic treatment; late lines of
   treatment; metastatic colorectal cancer; regorafenib; regorafenib
   adverse events; targeted treatment; tyrosine-kinase inhibitor
ID INDUCED HYPOTHYROIDISM; KINASE INHIBITORS; BAY 73-4506; START LOW;
   MULTICENTER; PLUS; METABOLITES; STRATEGIES; MANAGEMENT; SORAFENIB
AB Regorafenib is an orally available multikinase inhibitor, currently approved in metastatic chemorefractory colorectal cancer patients. The results of two large randomized Phase III trials are available, providing significant results in overall and progression-free survival in this situation. Its use requires a special attention regarding patient selection, dosing schedule and management of adverse events. Identifying patients who will tolerate and have benefit from regorafenib is a challenge for clinicians. Therapeutic monitoring (especially cfDNA), predictive biomarkers and specific perfusion-based imaging techniques will may be result in optimizing regorafenib treatment.
C1 [de la Fouchardiere, Christelle] Univ Lyon 1, Ctr Leon Berard, Med Oncol Dept, Lyon, France.
C3 UNICANCER; Centre Leon Berard; Universite Claude Bernard Lyon 1
RP de la Fouchardière, C (corresponding author), Univ Lyon 1, Ctr Leon Berard, Med Oncol Dept, Lyon, France.
EM christelle.delafouchardiere@lyon.unicancer.fr
RI de la Fouchardiere, Christelle/AAW-7887-2021
OI DE LA FOUCHARDIERE, CHRISTELLE/0000-0003-2291-5693
FU Bayer
FX C de la Fouchardiere has received grants from Bayer. The author has no
   other relevant affiliations or financial involvement with any
   organization or entity with a financial interest in or financial
   conflict with the subject matter or materials discussed in the
   manuscript apart from those disclosed.
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NR 45
TC 16
Z9 17
U1 0
U2 8
PU FUTURE MEDICINE LTD
PI LONDON
PA UNITEC HOUSE, 3RD FLOOR, 2 ALBERT PLACE, FINCHLEY CENTRAL, LONDON, N3
   1QB, ENGLAND
SN 1479-6694
EI 1744-8301
J9 FUTURE ONCOL
JI Future Oncol.
PD SEP
PY 2018
VL 14
IS 22
BP 2239
EP 2246
DI 10.2217/fon-2017-0512
PG 8
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA GZ0DW
UT WOS:000449031000004
PM 29569472
DA 2025-01-04
ER

PT J
AU Tang, HB
   Zhou, TY
   Jin, WL
   Zong, SM
   Mamtimin, T
   Salama, E
   Jeon, BH
   Liu, P
   Han, HW
   Li, XK
AF Tang, Haibo
   Zhou, Tuoyu
   Jin, Weilin
   Zong, Simin
   Mamtimin, Tursunay
   Salama, El-Sayed
   Jeon, Byong-Hun
   Liu, Pu
   Han, Huawen
   Li, Xiangkai
TI Tumor-targeting engineered probiotic Escherichia coli Nissle 1917
   inhibits colorectal tumorigenesis and modulates gut microbiota
   homeostasis in mice
SO LIFE SCIENCES
LA English
DT Article
DE Engineered probiotic; Escherichia coli Nissle 1917; AOM; DSS model;
   Tumor-targeting treatment; Gut microbiota
ID CANCER; CELLS; ALIGNMENT; ADHESION; AZURIN; EXPRESSION; APOPTOSIS;
   PROTEIN; MODEL
AB Aims: Preliminary studies have identified the use of probiotics as a potential treatment strategy against colorectal cancer (CRC). However, natural probiotics lack direct tumor-targeting and tumor-killing activity in the intestine. This study aimed to construct a tumor-targeting engineered probiotic to combat CRC.Main methods: Standard adhesion assay was performed to analyze the adherence ability of tumor-binding protein HlpA to CT26 cells. CCK-8 assay, Hoechst 33258 staining and flow cytometry analysis were used for examining cytotoxicity of tumoricidal protein azurin toward CT26 cells. An engineered probiotic Ep-AH harboring azurin and hlpA genes was developed using Escherichia coli Nissle 1917 (EcN) chassis. Antitumor effects of Ep-AH were evaluated in the azoxymethane (AOM) and dextran sodium sulfate salt (DSS)-induced CRC mice. Moreover, analysis of gut microbiota was conducted via fecal 16S rRNA gene sequencing and shotgun metagenomic sequencing.Key findings: Azurin caused a dose-dependent increase of apoptosis in CT26 cells. Ep-AH treatment reversed weight loss (p < 0.001), fecal occult blood (p < 0.01), and shortening of colon length (p < 0.001) than model group, as well as reducing tumorigenesis by 36 % (p < 0.001). Both Ep-H and Ep-A (EcN expressing HlpA or azurin) were less effective than Ep-AH. Furthermore, Ep-AH enriched the members of beneficial bacteria (e.g., Blautia and Bifidobacterium) and reversed abnormal changes of genes associated with several metabolic pathways (e.g., lipopolysaccharide biosynthesis).Significance: These results demonstrated that Ep-AH had excellent therapeutic benefits on cancer remission and gut microbiota modulation. Our study provides an effective strategy for anti-CRC treatment.
C1 [Tang, Haibo; Zhou, Tuoyu; Zong, Simin; Mamtimin, Tursunay; Liu, Pu; Han, Huawen; Li, Xiangkai] Lanzhou Univ, Sch Life Sci, Key Lab Cell Act & Stress Adaptat, Minist Educ, Lanzhou, Peoples R China.
   [Han, Huawen] Lanzhou Univ, Ctr Grassland Microbiome, State Key Lab Grassland Agroecosyst, Lanzhou, Peoples R China.
   [Jin, Weilin] Lanzhou Univ, Hosp 1, Clin Med Coll 1, Med Frontier Innovat Res Ctr,Inst Canc Neurosci, Lanzhou, Peoples R China.
   [Salama, El-Sayed] Lanzhou Univ, Sch Publ Hlth, Dept Occupat & Environm Hlth, Lanzhou, Peoples R China.
   [Jeon, Byong-Hun] Hanyang Univ, Dept Earth Resources & Environm Engn, Seoul, South Korea.
C3 Lanzhou University; Lanzhou University; Lanzhou University; Lanzhou
   University; Hanyang University
RP Han, HW; Li, XK (corresponding author), Lanzhou Univ, Sch Life Sci, Key Lab Cell Act & Stress Adaptat, Minist Educ, Lanzhou, Peoples R China.; Han, HW (corresponding author), Lanzhou Univ, Ctr Grassland Microbiome, State Key Lab Grassland Agroecosyst, Lanzhou, Peoples R China.
EM hanhuawen@lzu.edu.cn; xkli@lzu.edu.cn
RI Jeon, Byong-Hun/AAF-4352-2020; Jin, Wei-Lin/A-8355-2013; Salama,
   El-Sayed/AAI-7179-2020; Li, Xiangkai/HDN-9439-2022
OI Salama, El-Sayed/0000-0002-8446-0033; Jin, Wei-Lin/0000-0001-8011-2405;
   Jeon, Byong-Hun/0000-0002-5478-765X
FU National Natural Science Foundation of China [32070117, 32200080];
   International Science and Technology Cooperation Project of Gansu
   Province [2021-0204-GHC- 0019]; Gansu Association for Science and
   Technology Innovation- Driven Boosting Project [GKX20210506-16-5]
FX This work was supported by the National Natural Science Foundation of
   China (No. 32070117, 32200080) , International Science and Technology
   Cooperation Project of Gansu Province (No. 2021-0204-GHC- 0019) and
   Gansu Association for Science and Technology Innovation- Driven Boosting
   Project (No. GKX20210506-16-5) . The authors appreciate the Central Lab
   of College of Life Science, Lanzhou University for providing instruments
   and equipment, as well as the Majorbio and Personalbio (Shanghai, China)
   for providing sequencing service. The authors also appreciate the
   contributions of Yanyi Chen, Wenxue Wang, Zemin Wang and Kunyue Zhang in
   sample collection. The raw sequencing reads from 16S rRNA gene
   sequencing and metagenomic sequencing have been deposited separately in
   the NCBI Sequence Read Archive database (accession numbers: PRJNA907521
   and PRJNA907967) . Additional data supporting this study are available
   from the corresponding authors on reasonable request.
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NR 75
TC 10
Z9 10
U1 3
U2 28
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0024-3205
EI 1879-0631
J9 LIFE SCI
JI Life Sci.
PD JUL 1
PY 2023
VL 324
AR 121709
DI 10.1016/j.lfs.2023.121709
EA APR 2023
PG 13
WC Medicine, Research & Experimental; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine; Pharmacology & Pharmacy
GA G7HB1
UT WOS:000990814100001
PM 37100380
DA 2025-01-04
ER

PT J
AU Wachsmannova, L
   Mego, M
   Stevurkova, V
   Zajac, V
   Ciernikova, S
AF Wachsmannova, L.
   Mego, M.
   Stevurkova, V.
   Zajac, V.
   Ciernikova, S.
TI Novel strategies for comprehensive mutation screening of the APC gene
SO NEOPLASMA
LA English
DT Article
DE colorectal cancer; familial adenomatous polyposis; large deletions;
   noncoding mutations; molecular diagnostic algorithms
ID FAMILIAL ADENOMATOUS POLYPOSIS; PROMOTER 1B DELETION; GERMLINE
   MUTATIONS; CANCER; EXPRESSION; LEADS; HYPERMETHYLATION; TUMORS; P53
AB Colorectal cancer is the 4th most common cause of cancer related deaths worldwide and new possibilities in accurate diagnosis and targeted treatment are highly required. Mutations in adenomatous polyposis coli (APC) gene play a pivotal role in adenoma-carcinoma pathway of colorectal tumorigenesis. The quarter century from its' first cloning, APC became one of the most frequently mutated, known driver genes in colorectal cancer. Intensive routine molecular testing of APC has brought the benefits for patients with family history of polyposis or colorectal cancer. Nevertheless, multiple mutational disease-causing mechanisms make the genetic testing still challenging. This minireview is focused on implementation of novel APC mutation screening diagnostic strategies for polyposis families according to the current findings. A further understanding and improved algorithms may help to increase the mutation detection rate. APC germline mutations achieve close to 100% penetrance, so more comprehensive approach followed by preventive and therapeutic strategies might reflect in decrease in burden of colorectal cancer.
C1 [Wachsmannova, L.; Stevurkova, V.; Zajac, V.; Ciernikova, S.] Slovak Acad Sci, Canc Res Inst BMC, Dept Genet, Bratislava, Slovakia.
   [Mego, M.] Comenius Univ, Dept Med Oncol, Fac Med, Bratislava, Slovakia.
   [Mego, M.] Natl Canc Inst, Bratislava, Slovakia.
C3 Slovak Academy of Sciences; Comenius University Bratislava; National
   Institute of Oncology (NOU)
RP Wachsmannova, L (corresponding author), Slovak Acad Sci, Canc Res Inst BMC, Dept Genet, Bratislava, Slovakia.
EM exonlmat@savba.sk
RI Ciernikova, Sona/ABB-3569-2021
OI Ciernikova, Sona/0000-0002-8139-6945
FU  [VEGA 2/0170/13];  [VEGA 2/0029/15];  [VEGA 2/0099/17]
FX This article and our experiments mentioned in this minireview were
   performed with the kind support provided by the grants VEGA 2/0170/13,
   VEGA 2/0029/15 and VEGA 2/0099/17.
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NR 49
TC 13
Z9 14
U1 0
U2 6
PU AEPRESS SRO
PI BRATISLAVA
PA BAJZOVA 7, BRATISLAVA, 821 08, SLOVAKIA
SN 0028-2685
EI 1338-4317
J9 NEOPLASMA
JI Neoplasma
PY 2017
VL 64
IS 3
BP 338
EP 343
DI 10.4149/neo_2017_303
PG 6
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA EV9HA
UT WOS:000402095500003
PM 28253712
OA Bronze
DA 2025-01-04
ER

PT J
AU Markt, SC
   Booker, BD
   Bensken, W
   Schiltz, NK
   Schumacher, FR
   Rose, J
   Cooper, G
   Selfridge, JE
   Koroukian, SM
AF Markt, Sarah C.
   Booker, Benjamin D.
   Bensken, Wyatt
   Schiltz, Nicholas K.
   Schumacher, Fredrick R.
   Rose, Johnie
   Cooper, Greg
   Selfridge, J. Eva
   Koroukian, Siran M.
TI Sociodemographic and clinical factors associated with receipt of
   biomarker testing in patients with metastatic colorectal cancer
SO CANCER MEDICINE
LA English
DT Article
DE biomarker; disparities; metastatic colorectal cancer
ID CELL LUNG-CANCER; COST-EFFECTIVENESS; BREAST-CANCER; COLON-CANCER;
   DISPARITIES; HEALTH; IMPACT; TRIALS; RACE; AGE
AB Background Standard clinical practice and national guidelines dictate somatic testing of metastatic colorectal cancer (mCRC) tumors to guide appropriate therapy; however, previous studies suggest that not all patients are tested. The objective of this study was to investigate potential differences in testing for mCRC by demographic and clinical factors. Methods We performed a retrospective review of de-identified patient data derived from electronic health records (EHRs) of 25,469 patients diagnosed with mCRC between the years 2013 and 2020. Our outcome was a receipt of the following tests: (a) biomarker testing (BRAF, KRAS, NRAS, MMR/MSI) and (b) next-generation sequencing (NGS). We interrogated our data using the machine-learning algorithm Classification and Regression Tree (CART), a unique approach to identifying combinations of, rather than individual demographic and clinical characteristics associated with receipt of testing. Results A total of 25,469 patients were identified with mCRC. Of these, 21,133 (83%) received either biomarker testing only (n = 12,485) or any testing (biomarker + NGS) (n = 8648). The proportion of patients who received any testing increased over calendar time for all age, race, and sex categories. Receipt of any testing was highest (90%) among younger and patients with better performance status, and there was no difference in receipt of any testing by race. The highest percentage of NGS testing was among those with better performance status, <70 years old, commercial or other governmental program payers, and low comorbidity burden; however, those who were Black or Hispanic had a lower prevalence of NGS testing than those who were White. Conclusions and Relevance Considerable variations exist in somatic biomarker testing across subgroups of the population. Identification of genomic alterations can aid in determining targeted treatment and improving clinical outcomes; therefore, equitable use of these testing strategies, particularly NGS, is necessary.
C1 [Markt, Sarah C.; Booker, Benjamin D.; Bensken, Wyatt; Schiltz, Nicholas K.; Schumacher, Fredrick R.; Rose, Johnie; Cooper, Greg; Koroukian, Siran M.] Case Western Reserve Univ, Sch Med, Dept Populat & Quantitat Hlth Sci, Robbins Bldg 210E 2210 Circle Dr, Cleveland, OH 44106 USA.
   [Markt, Sarah C.; Schumacher, Fredrick R.; Rose, Johnie; Cooper, Greg; Selfridge, J. Eva; Koroukian, Siran M.] Case Western Reserve Univ, Sch Med, Case Comprehens Canc Ctr, Cleveland, OH 44106 USA.
   [Schiltz, Nicholas K.] Case Western Reserve Univ, Francis Payne Bolton Sch Nursing, Cleveland, OH 44106 USA.
   [Rose, Johnie; Cooper, Greg] Univ Hosp Cleveland, Med Ctr, Dept Internal Med, Cleveland, OH 44106 USA.
   [Selfridge, J. Eva] Univ Hosp Cleveland, Med Ctr, Div Solid Tumor Oncol, Cleveland, OH 44106 USA.
C3 University System of Ohio; Case Western Reserve University; University
   System of Ohio; Case Western Reserve University; University System of
   Ohio; Case Western Reserve University; University System of Ohio; Case
   Western Reserve University; Case Western Reserve University Hospital;
   University Hospitals of Cleveland; University System of Ohio; Case
   Western Reserve University; Case Western Reserve University Hospital;
   University Hospitals of Cleveland
RP Markt, SC (corresponding author), Case Western Reserve Univ, Sch Med, Dept Populat & Quantitat Hlth Sci, Robbins Bldg 210E 2210 Circle Dr, Cleveland, OH 44106 USA.
EM sarah.markt@case.edu
RI Bensken, Wyatt/AAI-1146-2019; Koroukian, Siran/S-9127-2019; Markt,
   Sarah/O-7554-2019
OI Markt, Sarah/0000-0003-2873-0358
FU American Cancer Society [WIA-20-111-01-RWIA]
FX American Cancer Society, Grant/Award Number: WIA-20-111-01-RWIA
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NR 33
TC 3
Z9 3
U1 0
U2 2
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 2045-7634
J9 CANCER MED-US
JI Cancer Med.
PD JAN
PY 2023
VL 12
IS 2
BP 1850
EP 1859
DI 10.1002/cam4.4995
EA JUL 2022
PG 10
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 8E9PB
UT WOS:000825255400001
PM 35837788
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Hao, YB
   Zhang, JH
   Shan, GY
   Zhang, N
   Jin, WW
   Nan, KJ
AF Hao, Yibin
   Zhang, Jianhua
   Shan, Guoyong
   Zhang, Ning
   Jin, Wenwen
   Nan, Kejun
TI Establishment of optimal regulatory network of colorectal cancer based
   on p42.3 protein
SO SAUDI JOURNAL OF BIOLOGICAL SCIENCES
LA English
DT Article
DE p42.3; Colorectal cancer; Gene markers; Protein similarity algorithm;
   Bayesian theory
ID MOLECULAR-STRUCTURES; GENETIC-MARKERS; WWOX GENE; CELL; PROGRESSION;
   EXPRESSION; DRUGS; P53
AB Objective: to establish regulatory network of colorectal cancer involving p42.3 protein and to provide theoretical evidence for deep functional exploration of p42.3 protein in the onset and development of colorectal cancer. Methods: with protein similarity algorithm, reference protein set of p42.3 cell apoptosis was built according to structural features of p42.3. GO and KEGG databases were used to establish regulatory network of tumor cell apoptosis involving p42.3; meanwhile, the largest possible working pathway that involves p42.3 protein was screened out based on Bayesian network theory. Besides, GO and KEGG were used to build regulatory network on early diagnosis gene markers for colorectal cancer including WWOX, K-ras, COX-2, p53, APC, DCC and PTEN, at the same time, a regulatory network of colorectal cancer cell apoptosis which involves p42.3 was established. Results: cell apoptotic regulatory network that p42.3 participates in primarily consists of Bcl-2 family genes and the largest possible pathway is p42.3 -> FKBP -> Bcl-2 centered as FKBP protein. Combined with colorectal cancer regulatory network that involves early diagnosis gene markers, it can be predicted that p42.3 is most likely to regulate the colorectal cancer cell apoptosis through FKBP -> Bcl-2 -> Bax -> caspase-9 -> caspase-3 pathway. Conclusion: the colorectal cancer apoptosis network based on p42.3 established in the study provides theoretical evidence for deep exploration of p42.3 regulatory mechanism and molecular targeting treatment of colorectal cancer. (C) 2017 Production and hosting by Elsevier B.V.on behalf of King Saud University.
C1 [Hao, Yibin; Nan, Kejun] Xi An Jiao Tong Univ, Affiliated Hosp 1, Dept Oncol, Xian 710077, Shaanxi, Peoples R China.
   [Hao, Yibin; Shan, Guoyong] Peoples Hosp Zhengzhou, Dept Oncol Radiotherapy, Zhengzhou 450003, Henan, Peoples R China.
   [Zhang, Jianhua; Zhang, Ning; Jin, Wenwen] Zhengzhou Univ, Med Engn Technol & Data Min Inst, Zhengzhou 450001, Henan, Peoples R China.
C3 Xi'an Jiaotong University; Zhengzhou University
RP Nan, KJ (corresponding author), Xi An Jiao Tong Univ, Affiliated Hosp 1, Dept Oncol, Xian 710077, Shaanxi, Peoples R China.
EM nankejun2013@yeah.net
RI zhang, ying/HJB-1230-2022; Zhang, Ning/A-3217-2016
FU Natural Science Foundation of Henan Province [162300410290]; National
   Key R&D Program of China [2016YFC1303200]
FX The Natural Science Foundation of Henan Province. No. 162300410290;
   National Key R&D Program of China, Grant No. 2016YFC1303200.
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NR 24
TC 6
Z9 6
U1 0
U2 12
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 1319-562X
J9 SAUDI J BIOL SCI
JI Saudi J. Biol. Sci.
PD DEC
PY 2017
VL 24
IS 8
BP 1781
EP 1786
DI 10.1016/j.sjbs.2017.11.012
PG 6
WC Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Life Sciences & Biomedicine - Other Topics
GA FR2KE
UT WOS:000418895100008
PM 29551923
OA Green Published, hybrid
DA 2025-01-04
ER

PT J
AU Shen, KX
   Li, D
   Guan, JJ
   Ding, JX
   Wang, ZT
   Gu, JK
   Liu, TJ
   Chen, XS
AF Shen, Kexin
   Li, Di
   Guan, Jingjing
   Ding, Jianxun
   Wang, Zhongtang
   Gu, Jingkai
   Liu, Tongjun
   Chen, Xuesi
TI Targeted sustained delivery of antineoplastic agent with multicomponent
   polylactide stereocomplex micelle
SO NANOMEDICINE-NANOTECHNOLOGY BIOLOGY AND MEDICINE
LA English
DT Article
DE Polylactide; Stereocomplex interaction; Multicomponent micelle;
   Targetability; Chemotherapy
ID DRUG-DELIVERY; COLORECTAL-CANCER; POLYMERIC MICELLES; BLOCK-COPOLYMER;
   NANOCARRIERS; CHEMOTHERAPY; THERAPY; NANOPARTICLES; NANOMEDICINE;
   STATISTICS
AB A c(RGDfC)-decorated polylactide stereocomplex micelle (cRGD-SCM) was prepared through the stereocomplex and hydrophobic interactions among 4-arm poly(ethylene glycol)-block-poly(D-lactide) (4-arm PEG-b-PDLA), methoxy poly(ethylene glycol)-block-poly(Llactide) (mPEG-b-PLLA), and c(RGDfC)-poly(ethylene glycol)-block-poly(L-lactide) (cRGD-PEG-b-PLLA) for targeted treatment of a(v)beta(3) integrin-positive C26 colon cancer. Doxorubicin (DOX), a model antitumor drug, was loaded into cRGD-SCM with a diameter of approximately 100 nm, and the drug loading efficiency was 45.9 wt.%. cRGD-SCM/DOX with a sustained release pattern exhibited prolonged circulation time, upregulated accumulation in tumor, enhanced tumor inhibition, and decreased side effects compared with free DOX and non-targeting SCM/DOX in vivo. More interestingly, the targeting ligand in the terminal of PEG can be easily replaced with other targeting groups according to the different types of malignancies. Therefore, the cRGD-decorated platform might be a promising targeted drug delivery system for personal chemotherapy clinically. (C) 2017 Elsevier Inc. All rights reserved.
C1 [Shen, Kexin; Guan, Jingjing; Gu, Jingkai; Liu, Tongjun] Jilin Univ, Changchun, Peoples R China.
   [Shen, Kexin; Li, Di; Ding, Jianxun; Chen, Xuesi] Chinese Acad Sci, Changchun Inst Appl Chem, Key Lab Polymer Ecomat, Changchun, Peoples R China.
   [Wang, Zhongtang] Shandong Univ, Shandong Acad Med Sci, Shandong Canc Hosp, Dept Radiat Oncol, Jinan, Peoples R China.
C3 Jilin University; Chinese Academy of Sciences; Changchun Institute of
   Applied Chemistry, CAS; University of Jinan; Shandong University;
   Shandong First Medical University & Shandong Academy of Medical Sciences
RP Liu, TJ (corresponding author), Jilin Univ, Changchun, Peoples R China.; Ding, JX (corresponding author), Chinese Acad Sci, Changchun Inst Appl Chem, Key Lab Polymer Ecomat, Changchun, Peoples R China.; Wang, ZT (corresponding author), Shandong Univ, Shandong Acad Med Sci, Shandong Canc Hosp, Dept Radiat Oncol, Jinan, Peoples R China.
EM jxding@ciac.ac.cn; zhongtangw@163.com; tongjunliu@163.com
RI Li, Di/ADN-4545-2022; Chen, Xuesi/ABB-5039-2020; Ding,
   Jianxun/A-6155-2013
FU National Natural Science Foundation of China [51673190, 51303174,
   51603204, 51673187, 51473165, 81430087]
FX This research was financially supported by the National Natural Science
   Foundation of China (Nos. 51673190, 51303174, 51603204, 51673187,
   51473165, and 81430087).
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NR 45
TC 23
Z9 24
U1 0
U2 77
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 1549-9634
EI 1549-9642
J9 NANOMED-NANOTECHNOL
JI Nanomed.-Nanotechnol. Biol. Med.
PD APR
PY 2017
VL 13
IS 3
BP 1279
EP 1288
DI 10.1016/j.nano.2016.12.022
PG 10
WC Nanoscience & Nanotechnology; Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Science & Technology - Other Topics; Research & Experimental Medicine
GA EU5QX
UT WOS:000401089100048
PM 28064009
DA 2025-01-04
ER

PT J
AU Shi, JY
   Ma, ZW
   Pan, H
   Liu, Y
   Chu, YQ
   Wang, JL
   Chen, LJ
AF Shi, Jinyan
   Ma, Zhiwei
   Pan, Hao
   Liu, Yang
   Chu, Yuqi
   Wang, Jinglei
   Chen, Lijiang
TI Biofilm-encapsulated nano drug delivery system for the treatment of
   colon cancer
SO JOURNAL OF MICROENCAPSULATION
LA English
DT Article
DE Composite carrier; Escherichia coli's outer membrane vesicles;
   mesoporous silica; oral administration; colon cancer therapy
ID MESOPOROUS SILICA NANOPARTICLES; OUTER-MEMBRANE VESICLES; MESENCHYMAL
   STEM-CELLS; CARRIER
AB Aim In this study, 5-fluorouracil (5-FU) is delivered to target colon without the interference of mononuclear phagocyte system (MPS). Methods Outer membrane vesicles (OMVs) were used as the biological shield to disguise mesoporous silica (MSN) and 5-FU. OMVs-MSN-5-FU were prepared by high pressure co-extrusion, and characterised on the basis of size, drug loading, transmission electron microscope, infra-red spectroscopy, differential scanning calorimetry, thermal gravity analysis, %in vitrorelease, MTT assay, cell uptake andin vivoimaging. Results OMVs-MSN-5-FU with -18.22 +/- 0.17 mV zeta potential and 90.4 +/- 9.1 nm size were used for oral treatment of colon cancer. Drug loading of the drug was 50.22%+/- 0.17 (w/w). The cumulative release of OMVs-MSN-5-FU reached 75.07%+/- 0.94 in tumour microenvironment. The percentage of cell viability of OMVs-MSN-5-FU was 33.75%+/- 2.73.In vivoexperiments results confirmed that OMVs-MSN-5-FU could be taken up by colon cancer cells. Conclusions The study provided a promising nano platform for the targeting treatment of colon cancer.
C1 [Shi, Jinyan; Ma, Zhiwei; Pan, Hao; Liu, Yang; Chu, Yuqi; Wang, Jinglei; Chen, Lijiang] Liaoning Univ, Sch Pharmaceut Sci, 66 Chongshan Mid Rd, Shenyang 110036, Peoples R China.
C3 Liaoning University
RP Chen, LJ (corresponding author), Liaoning Univ, Sch Pharmaceut Sci, 66 Chongshan Mid Rd, Shenyang 110036, Peoples R China.
EM chlj16@163.com
RI Ma, Zhiwei/GPX-5773-2022; shi, jin/KDO-7906-2024
FU Shenyang Science and Technology Program of China [F16-205-1-44,
   Z17-5-078]; Liaoning Provincial Department of education innovative
   talents support project [LR2017065]
FX This work was supported by the Shenyang Science and Technology Program
   of China under Grant [numbers F16-205-1-44 and Z17-5-078] and Liaoning
   Provincial Department of education innovative talents support project
   under Grant [number LR2017065].
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NR 42
TC 32
Z9 33
U1 3
U2 54
PU TAYLOR & FRANCIS LTD
PI ABINGDON
PA 2-4 PARK SQUARE, MILTON PARK, ABINGDON OR14 4RN, OXON, ENGLAND
SN 0265-2048
EI 1464-5246
J9 J MICROENCAPSUL
JI J. Microencapsul.
PD OCT 2
PY 2020
VL 37
IS 7
BP 481
EP 491
DI 10.1080/02652048.2020.1797914
EA JUL 2020
PG 11
WC Chemistry, Applied; Engineering, Chemical; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Chemistry; Engineering; Pharmacology & Pharmacy
GA NV2UL
UT WOS:000555121000001
PM 32700606
DA 2025-01-04
ER

PT J
AU Cruz-Nova, P
   Gibbens-Bandala, B
   Ancira-Cortez, A
   Ramírez-Nava, G
   Santos-Cuevas, C
   Luna-Gutiérrez, M
   Ocampo-García, B
AF Cruz-Nova, Pedro
   Gibbens-Bandala, Brenda
   Ancira-Cortez, Alejandra
   Ramirez-Nava, Gerardo
   Santos-Cuevas, Clara
   Luna-Gutierrez, Myrna
   Ocampo-Garcia, Blanca
TI Chemo-radiotherapy with <SUP>177</SUP>Lu-PLGA(RGF)-CXCR4L for the
   targeted treatment of colorectal cancer
SO FRONTIERS IN MEDICINE
LA English
DT Article
DE colorectal cancer; Regorafenib; PLGA nanoparticles; CXCR4L; Lu-177;
   chemoradiotherapy
ID PLGA-BASED NANOPARTICLES; DRUG-DELIVERY; REGORAFENIB; CXCR4; THERAPY;
   AGENTS
AB IntroductionMore than 1.9 million new cases of colorectal cancer and 935,000 deaths were estimated to have occurred worldwide in 2020. Therapies for metastatic colorectal cancer include cytotoxic chemotherapy and targeted therapies in multiple lines of treatment. Nevertheless, the optimal use of these agents has not yet been resolved. Regorafenib (RGF) is an Food and Drug Administration (FDA)-authorized multikinase inhibitor indicated for patients with metastatic colorectal cancer, non-responding to priority lines of chemotherapy and immunotherapy. Nanoparticles have been used in specific applications, such as site-specific drug delivery systems, cancer therapy, and clinical bioanalytical diagnostics. C-X-C Chemokine receptor type 4 (CXCR4) is the most widely-expressed chemokine receptor in more than 23 human cancer types, including colorectal cancer. This research aimed to synthesize and preclinically evaluate a targeted nanosystem for colorectal cancer chemo-radiotherapy using RGF encapsulated in Poly(D,L-lactic-co-glycolic acid) (PLGA) nanoparticles coated with a CXCR4 ligand (CXCR4L) and Lu-177 as a therapeutic & beta;-emitter. MethodsEmpty PLGA and PLGA(RGF) nanoparticles were prepared using the microfluidic method, followed by the DOTA and CXCR4L functionalization and nanoparticle radiolabeling with Lu-177. The final nanosystem gave a particle size of 280 nm with a polydispersity index of 0.347. In vitro and in vivo toxicity effects were assessed using the HCT116 colorectal cancer cell line. Results(177)Lu-PLGA(RGF)-CXCR4L nanoparticles decreased cell viability and proliferation by inhibiting Erk and Akt phosphorylation and promoting apoptosis. Moreover, in vivo administration of Lu-177-PLGA(RGF)-CXCR4L significantly reduced tumor growth in an HCT116 colorectal cancer xenograft model. The biokinetic profile showed hepatic and renal elimination. DiscussionData obtained in this research justify additional preclinical safety trials and the clinical evaluation of Lu-177-PLGA(RGF)-CXCR4L as a potential combined treatment of colorectal cancer.
C1 [Cruz-Nova, Pedro; Gibbens-Bandala, Brenda; Ancira-Cortez, Alejandra; Santos-Cuevas, Clara; Luna-Gutierrez, Myrna; Ocampo-Garcia, Blanca] Inst Nacl Invest Nucl, Dept Mat Radiact, Ocoyoacac, Mexico State, Mexico.
   [Ramirez-Nava, Gerardo] Tecnol Monterrey, Inst Adv Mat Sustainable Mfg, Mexico City, Mexico.
C3 Tecnologico de Monterrey
RP Gibbens-Bandala, B; Ocampo-García, B (corresponding author), Inst Nacl Invest Nucl, Dept Mat Radiact, Ocoyoacac, Mexico State, Mexico.
EM brenda.g.servicios@inin.gob.mx
RI Cruz-Nova, Pedro/AAQ-7981-2021; Ancira-Cortez, Alejandra/AAQ-8494-2021;
   CUEVAS, CLARA/A-2968-2015
OI Cruz-Nova, Pedro/0000-0001-5719-7324; Gibbens-Bandala,
   Brenda/0000-0003-2419-0307
FU Consejo Mexiquense de Ciencia y Tecnologa del Estado de Mxico (COMECyT)
   [CAT2021-0036]
FX Funding This study was supported by the Consejo Nacional de Ciencia y
   Tecnologia (CONACyT, A1-S-38087) and was carried out as part of the
   activities of the "Laboratorio Nacional de Investigacion y Desarrollo de
   Radiofarmacos, ININ."
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NR 49
TC 2
Z9 3
U1 3
U2 10
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
EI 2296-858X
J9 FRONT MED-LAUSANNE
JI Front. Med.
PD JUN 12
PY 2023
VL 10
AR 1191315
DI 10.3389/fmed.2023.1191315
PG 19
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA J9SZ5
UT WOS:001012965200001
PM 37378300
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Lin, S
   Chen, WY
   Chen, ZZ
   Liang, JQ
   Zhong, L
   Jiang, M
AF Lin, Sen
   Chen, Weiyi
   Chen, Zhuangzhong
   Liang, Jiaqi
   Zhong, Ling
   Jiang, Mei
TI Efficacy of sintilimab and fruquintinib combination treatment in the
   management of microsatellite-stable metastatic colorectal cancer: a case
   report
SO ANNALS OF TRANSLATIONAL MEDICINE
LA English
DT Article
DE Programmed death-1 inhibitor (PD-1 inhibitor); vascular endothelial
   growth factor receptor inhibitor (VEGFR inhibitor); tumor mutation
   burden (TMB); microsatellite-stable (MSS); case report
ID TUMOR MUTATIONAL BURDEN; MISMATCH REPAIR-DEFICIENT; OPEN-LABEL;
   SINGLE-ARM; IMMUNOTHERAPY; ATEZOLIZUMAB; MULTICENTER; BEVACIZUMAB;
   CARCINOMA; PREDICTOR
AB Background: The immune microenvironment of deficient mismatch repair or microsatellite instability high (dMMR/MSI-H) colorectal cancer exhibits better immune activity, and patients with dMMR/MSI-H colorectal cancer benefit from immunotherapy with programmed death-1 (PD-1)/PD-1 ligand (PD-L1) inhibitors and cytotoxic T-lymphocyte associated protein 4 (CTLA-4) inhibitors as a first-line treatment. However, for microsatellite-stable (MSS) colorectal cancer, which accounts for the majority of the cases of colorectal cancer, immunotherapy has yielded little success, especially in cases of patients with advanced colorectal cancer in whom multiple lines of chemotherapy have failed. Hence, safe and effective targeted treatment strategies are urgently needed to achieve greater survival benefits. Case Description: We report a case in which next-generation sequencing (NGS) and immunohistochemistry (IHC) showed that that the patient's molecular characteristics were as follows: MSS, low expression of PD-L1, and high tumor mutation burden (TMB-H). Due to the failure of multiple lines of chemotherapy and severe chemotherapeutic adverse effects, a combined targeted immunotherapy regimen was utilized. After 6 months of treatment, imaging suggested near-complete clinical remission, and at the 18-month follow-up, the patient had a good quality of life and imaging showed no tumor recurrence. Conclusions: This case suggests that a good response to a combined targeted immunotherapy regimen can be achieved in patients with MSS metastatic colorectal cancer, in addition, it also suggests that TMB-H is a predictive biomarker for clinical benefit from immunotherapy in MSS metastatic colorectal cancer.
C1 [Lin, Sen; Chen, Weiyi; Liang, Jiaqi] Guangzhou Univ Chinese Med, Clin Med Coll 1, Dept Oncol, Guangzhou, Peoples R China.
   [Chen, Zhuangzhong; Jiang, Mei] Guangzhou Univ Chinese Med, Affiliated Hosp 1, Dept Oncol, Guangzhou, Peoples R China.
   [Zhong, Ling] Guangdong Prov Hosp Tradit Chinese Med, Zhuhai Branch, Intervent Div, Zhuhai, Peoples R China.
C3 Guangzhou University of Chinese Medicine; Guangzhou University of
   Chinese Medicine; Guangzhou University of Chinese Medicine
RP Jiang, M (corresponding author), Guangzhou Univ Chinese Med, Affiliated Hosp 1, Dept Oncol, Guangzhou, Peoples R China.
EM jiangmei619611@163.com
RI chen, zhaoyang/GRS-1470-2022
OI Lin, Sen/0000-0002-6371-3927; Jiang, Mei/0009-0007-4762-2041
FU Teaching Reform Project of the Department of Education of Guangdong
   Province of China [2020138]
FX The authors thank the 3D Medicines Inc. for providing the
   next-generation sequencing (NGS) , and Hemangi Palav (HMP) employed in
   the Transystom Editing and Translation Services for assistance in
   editing the manuscripts. We would also like to acknowledge the
   cooperation and contribution of the patient and her family. Funding:
   This work was supported by the Teaching Reform Project of the Department
   of Education of Guangdong Province of China (No. 2020138) .
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NR 30
TC 3
Z9 3
U1 0
U2 7
PU AME PUBL CO
PI SHATIN
PA FLAT-RM C 16F, KINGS WING PLAZA 1, NO 3 KWAN ST, SHATIN, HONG KONG
   00000, PEOPLES R CHINA
SN 2305-5839
EI 2305-5847
J9 ANN TRANSL MED
JI ANN. TRANSL. MED.
PD MAR
PY 2022
VL 10
IS 6
DI 10.21037/atm-22-359
EA MAR 2022
PG 9
WC Oncology; Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Research & Experimental Medicine
GA 0R8BY
UT WOS:000777966300001
PM 35433988
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Raskov, H
   Soby, JH
   Troelsen, J
   Bojesen, RD
   Gögenur, I
AF Raskov, Hans
   Soby, Jacob H.
   Troelsen, Jesper
   Bojesen, Rasmus D.
   Gogenur, Ismail
TI Driver Gene Mutations and Epigenetics in Colorectal Cancer
SO ANNALS OF SURGERY
LA English
DT Review
DE colorectal cancer; driver gene mutations; epigenetics
ID EPITHELIAL-MESENCHYMAL TRANSITION; INTRACELLULAR BACTERIA; LANDSCAPE;
   CDX2; MECHANISMS; PROGNOSIS; MORTALITY; UPDATE; GENOME; LUNG
AB Objective: The majority of patients with colorectal cancer are diagnosed with locally advanced and/or disseminated disease, and treatment options include surgery in combination with cytotoxic chemotherapy regimens, biologics, and/or radiotherapy. Thus, colorectal cancer remains a heavy burden on society and health care systems. Mounting evidence show that driver gene mutations play only part of the role in carcinogenesis. Epigenetics are strongly implicated in initiation and progression of colorectal cancer along with major players such as intestinal microbiotic dysbiosis and chronic mucosal inflammation. To assess phenotypic changes in proteins and gene expression, multigene expression signatures based on sequencing techniques have been developed to hopefully improve predictors of the tumor profile, immune response, and therapeutic outcomes. Our objective was to review current advances in the field and to update surgeons and academics on driver gene mutations and epigenetics in colorectal cancer. Background and methods: This is a narrative review studying relevant research published in the PUBMED database from 2012-2018. Results and conclusion: Increased understanding of the molecular biology will improve options to characterize colorectal cancer with regard to mutations and molecular pathways, including microsatellite instability, epigenetics, microbiota, and microenvironment. Research will inevitably improve risk group stratification and targeted treatment approaches. Epigenetic profiling and epigenetic modulating drugs will increase risk stratification, increase accessibility for DNA targeting chemotherapeutics and reduce cytotoxic drug resistance. New generation antibiotics such as biofilm inhibitors and quorum sensing inhibitors are being developed to target the carcinogenetic impact of colonic dysbiosis and inflammation.
C1 [Raskov, Hans; Soby, Jacob H.; Bojesen, Rasmus D.; Gogenur, Ismail] Zealand Univ Hosp, Ctr Surg Sci, Koge, Denmark.
   [Soby, Jacob H.; Gogenur, Ismail] Zealand Univ Hosp, Dept Surg, Koge, Denmark.
   [Troelsen, Jesper] Roskilde Univ, Dept Sci & Environm, Roskilde, Denmark.
   [Bojesen, Rasmus D.] Zealand Univ Hosp, Slagelse Hosp, Dept Surg, Koge, Denmark.
C3 Roskilde University
RP Raskov, H (corresponding author), Zealand Univ Hosp, Ctr Surg Sci, Koge, Denmark.
EM raskov@mail.dk
RI Troelsen, Jesper Thorvald/B-6264-2013
OI Troelsen, Jesper Thorvald/0000-0002-4177-3267; Bojesen, Rasmus
   Dahlin/0000-0003-3998-1160; Soby, Jacob Hartmann/0000-0003-1493-5600;
   Gogenur, Ismail/0000-0002-3753-268X
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TC 62
Z9 65
U1 5
U2 33
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 0003-4932
EI 1528-1140
J9 ANN SURG
JI Ann. Surg.
PD JAN
PY 2020
VL 271
IS 1
BP 75
EP 85
DI 10.1097/SLA.0000000000003393
PG 11
WC Surgery
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Surgery
GA LC0JF
UT WOS:000525016300017
PM 31188207
DA 2025-01-04
ER

PT J
AU Shen, JJ
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AF Shen, Jia-Jie
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TI Synthesis, characterization, and efficacy evaluation of a PH-responsive
   Fe-MOF@GO composite drug delivery system for the treating colorectal
   cancer
SO HELIYON
LA English
DT Article
DE Metal -organic framework; Graphene oxide; Luteolin; Matrine; Responsive
   release of acidic pH; Anti -colorectal cancer
ID METAL-ORGANIC FRAMEWORKS; NANOPARTICLES; PERFORMANCE; MIL-100(FE);
   METASTASIS; EXPRESSION; THERAPY; FE3O4
AB Luteolin is a potent anti-colorectal cancer chemical. However, its effectiveness is hindered by its poor solubility in water and fat, and it is easy to degrade by gastrointestinal enzymes. In this study, a nano-composite carrier, NH2-MIL-101(Fe)@GO (MG), based on aminated MIL-101(Fe) and graphene oxide (GO) was developed and evaluated. This carrier co-delivered luteolin and matrine, while marine was used to balance the pH for the nano-preparation. The loading capacities for luteolin and matrine were approximately 9.8% and 14.1%, respectively. Luteolin's release at pH = 5 was significantly higher than at pH = 7.4, indicating it had an acidic pH response release characteristic. Compared to MOF and GO alone, MG and NH2-MIL-101(Fe) @GO@Drugs (MGD) enhanced anti-cancer activity by inhibiting tumor cell migration, increasing ROS generation, and upregulating the expression of Caspase-3 and Caspase-9. In conclusion, this study contributes new ideas and methods to the treatment strategy of multicomponent anti-colorectal cancer therapy. It also advances drug delivery systems and supports the development of more effective and targeted treatment approaches for colorectal cancer.
C1 [Shen, Jia-Jie; Mei, Zhang-Hao; Li, Ting -Ting; Li, Hui -Fen; Zhuang, Xue-Fei; Pan, Lin-Mei] Nanjing Univ Chinese Med, Plant Med Deep Proc Engn Ctr, Nanjing 210023, Peoples R China.
   [Xue, Shi-Jiao] Qidong Hosp Tradit Chinese Med, Nantong 226200, Peoples R China.
C3 Nanjing University of Chinese Medicine
RP Pan, LM (corresponding author), Nanjing Univ Chinese Med, Plant Med Deep Proc Engn Ctr, Nanjing 210023, Peoples R China.
EM linmeipan@njucm.edu.cn
FU National key research and development program of China [2017YFC1700602]
FX This research was supported by the national key research and development
   program of China (2017YFC1700602) .
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NR 45
TC 9
Z9 9
U1 11
U2 25
PU CELL PRESS
PI CAMBRIDGE
PA 50 HAMPSHIRE ST, FLOOR 5, CAMBRIDGE, MA 02139 USA
EI 2405-8440
J9 HELIYON
JI Heliyon
PD MAR 30
PY 2024
VL 10
IS 6
AR e28066
DI 10.1016/j.heliyon.2024.e28066
EA MAR 2024
PG 10
WC Multidisciplinary Sciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Science & Technology - Other Topics
GA OU6B2
UT WOS:001209822400001
PM 38524612
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Téllez, T
   Martin-García, D
   Redondo, M
   García-Aranda, M
AF Tellez, Teresa
   Martin-Garcia, Desiree
   Redondo, Maximino
   Garcia-Aranda, Marilina
TI Clusterin Expression in Colorectal Carcinomas
SO INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
LA English
DT Review
DE clusterin; colorectal cancer; biomarker; tumorigenesis; targeted
   treatment; personalized medicine
ID PROSTATE EPITHELIAL-CELLS; DISEASE-FREE SURVIVAL; HEAT-SHOCK PROTEINS;
   CLUSTERIN/APOLIPOPROTEIN-J; TUMOR RADIOSENSITIVITY; NUCLEAR CLUSTERIN;
   OXIDATIVE STRESS; BINDING-ACTIVITY; DRUG-RESISTANCE; CANCER-THERAPY
AB Colorectal cancer is the third most diagnosed cancer, behind only breast and lung cancer. In terms of overall mortality, it ranks second due to, among other factors, problems with screening programs, which means that one of the factors that directly impacts survival and treatment success is early detection of the disease. Clusterin (CLU) is a molecular chaperone that has been linked to tumorigenesis, cancer progression and resistance to anticancer treatments, which has made it a promising drug target. However, it is still necessary to continue this line of research and to adjust the situations in which its use is more favorable. The aim of this paper is to review the current genetic knowledge on the role of CLU in tumorigenesis and cancer progression in general, and discuss its possible use as a therapeutic target in colorectal cancer.
C1 [Tellez, Teresa; Martin-Garcia, Desiree; Redondo, Maximino] Univ Malaga, Fac Med, Surg Specialties Biochem & Immunol Dept, Malaga 29010, Spain.
   [Tellez, Teresa; Martin-Garcia, Desiree; Redondo, Maximino; Garcia-Aranda, Marilina] Inst Invest Biomed Malaga IBIMA, Red Invest Serv Salud Enfermedades Cron REDISSEC, Red Invest Cron, Atenc Primaria & Promoc Salud RICAPPS, Malaga 29590, Spain.
   [Tellez, Teresa; Martin-Garcia, Desiree; Redondo, Maximino; Garcia-Aranda, Marilina] Inst Invest Biomed Malaga & Plataforma Nanomed, IBIMA Plataforma BIONAND, Malaga 29590, Spain.
   [Martin-Garcia, Desiree; Redondo, Maximino; Garcia-Aranda, Marilina] Hosp Costa Sol, Res & Innovat Unit, Marbella 29602, Spain.
C3 Universidad de Malaga; Universidad de Malaga; Instituto de Investigacion
   Biomedica de Malaga y Plataforma en Nanomedicina (IBIMA); Instituto de
   Investigacion Biomedica de Malaga y Plataforma en Nanomedicina (IBIMA)
RP Redondo, M (corresponding author), Univ Malaga, Fac Med, Surg Specialties Biochem & Immunol Dept, Malaga 29010, Spain.; Redondo, M (corresponding author), Inst Invest Biomed Malaga IBIMA, Red Invest Serv Salud Enfermedades Cron REDISSEC, Red Invest Cron, Atenc Primaria & Promoc Salud RICAPPS, Malaga 29590, Spain.; Redondo, M (corresponding author), Inst Invest Biomed Malaga & Plataforma Nanomed, IBIMA Plataforma BIONAND, Malaga 29590, Spain.; Redondo, M (corresponding author), Hosp Costa Sol, Res & Innovat Unit, Marbella 29602, Spain.
EM teresatellez@uma.es; desirermg@uma.es;
   maximino.redondo.sspa@juntadeandalucia.es;
   marilina.garcia.sspa@juntadeandalucia.es
RI ARANDA, MARILINA/AAH-4730-2019
OI Martin-Garcia, Desiree/0009-0009-5007-0529; GARCIA ARANDA,
   MARILINA/0000-0003-3759-4044
FU European Social Fund-Operational Program of Andalusia [RH-0055-2020];
   University of Malaga-Consejeria de Transformacion Economica, Industria,
   Conocimiento y Universidades-Junta de Andalucia [UMA20-FEDERJA-161];
   Instituto de Salud Carlos III [PI18/01181, PI21/00252]; European
   Regional Development fund
FX The researcher Marilina Garcia-Aranda is the benefactor of a
   postdoctoral contract financed by the European Social Fund-Operational
   Program of Andalusia 2014-2020 for the "Incorporation of Research
   Personnel with a PhD degree in the field of Health Sciences and
   Technologies in R&D and Innovation Centers of the Public Health System
   of Andalusia" (RH-0055-2020). This work was partially supported by
   grants from the University of Malaga-Consejeria de Transformacion
   Economica, Industria, Conocimiento y Universidades-Junta de Andalucia
   (UMA20-FEDERJA-161) and from Instituto de Salud Carlos III (PI18/01181,
   PI21/00252) and were co funded by the European Regional Development
   fund. The funders had no role in study design, data collection and
   analysis, decision to publish, or preparation of the manuscript.
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NR 126
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Z9 2
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PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
SN 1661-6596
EI 1422-0067
J9 INT J MOL SCI
JI Int. J. Mol. Sci.
PD OCT
PY 2023
VL 24
IS 19
AR 14641
DI 10.3390/ijms241914641
PG 17
WC Biochemistry & Molecular Biology; Chemistry, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Chemistry
GA X3CK1
UT WOS:001097264100001
PM 37834086
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Mohajershojai, T
   Spangler, D
   Chopra, S
   Frejd, FY
   Yazaki, PJ
   Nestor, M
AF Mohajershojai, Tabassom
   Spangler, Douglas
   Chopra, Saloni
   Frejd, Fredrik Y.
   Yazaki, Paul J.
   Nestor, Marika
TI Enhanced Therapeutic Effects of <SUP>177</SUP>Lu-DOTA-M5A in Combination
   with Heat Shock Protein 90 Inhibitor Onalespib in Colorectal Cancer
   Xenografts
SO CANCERS
LA English
DT Article
DE radioimmunotherapy; combination therapy; carcinoembryonic antigen;
   Lu-177-DOTA-M5A; HSP90 inhibitor onalespib
ID CARCINOEMBRYONIC ANTIGEN LEVELS; PHASE-I TRIAL; CHIMERIC T84.66; SOLID
   TUMORS; RADIOIMMUNOTHERAPY; CEA; ANTIBODY; HSP90; ADENOCARCINOMA;
   CARCINOMA
AB Simple Summary: Cancer treatment is hampered by the limitations of individual therapy modalities and the intricate nature of the disease. The administration of maximal monotherapy doses often leads to undesirable side effects and/or therapy resistance. As a result, there is a growing recognition of the importance of investigating combination therapy to effectively address these obstacles. In the present in vivo study, the therapeutic effects of combination therapy with the heat shock protein 90 inhibitor onalespib, a potential radiosensitizer, and Lu-177-DOTA-M5A for colorectal cancer (CRC) treatment were explored for the first time. The results demonstrated that the combination treatment was so effective that retained or even superior therapeutic effects could be achieved with only half the dose of administered Lu-177-DOTA-M5A, showing enhanced tumor growth suppression and increased apoptosis. Consequently, the combination therapy involving Lu-177-DOTA-M5A and onalespib constitutes a promising approach for treating metastatic CRCs. By enhancing therapeutic effects, minimizing therapy resistance, and reducing side effects, this approach has the potential to expand the patient population that can benefit from targeted treatment.
   Carcinoembryonic antigen (CEA) has emerged as an attractive target for theranostic applications in colorectal cancers (CRCs). In the present study, the humanized anti-CEA antibody hT84.66-M5A (M5A) was labeled with Lu-177 for potential CRC therapy. Moreover, the novel combination of Lu-177-DOTA-M5A with the heat shock protein 90 inhibitor onalespib, suggested to mediate radiosensitizing properties, was assessed in vivo for the first time. M5A antibody uptake and therapeutic effects, alone or in combination with onalespib, were assessed in human CRC xenografts and visualized using SPECT/CT imaging. Although both Lu-177-DOTA-M5A and onalespib monotherapies effectively reduced tumor growth rates, the combination therapy demonstrated the most substantial impact, achieving a fourfold reduction in tumor growth compared to the control group. Median survival increased by 33% compared to Lu-177-DOTA-M5A alone, and tripled compared to control and onalespib groups. Importantly, combination therapy yielded comparable or superior effects to the double dose of Lu-177-DOTA-M5A monotherapy. Lu-177-DOTA-M5A increased apoptotic cell levels, indicating its potential to induce tumor cell death. These findings show promise for Lu-177-DOTA-M5A as a CRC therapeutic agent, and its combination with onalespib could significantly enhance treatment efficacy. Further in vivo studies are warranted to validate these findings fully and explore the treatment's potential for clinical use.
C1 [Mohajershojai, Tabassom; Chopra, Saloni; Frejd, Fredrik Y.; Nestor, Marika] Uppsala Univ, Dept Immunol Genet & Pathol, S-75185 Uppsala, Sweden.
   [Spangler, Douglas] Uppsala Univ, Dept Publ Hlth & Caring Sci, S-75122 Uppsala, Sweden.
   [Yazaki, Paul J.] City Hope Natl Med Ctr, Dept Immunol & Theranost, Beckman Res Inst, Duarte, CA 91010 USA.
C3 Uppsala University; Uppsala University; City of Hope; Beckman Research
   Institute of City of Hope
RP Nestor, M (corresponding author), Uppsala Univ, Dept Immunol Genet & Pathol, S-75185 Uppsala, Sweden.
EM tabassom.mohajer@igp.uu.se; douglas.spangler@pubcare.uu.se;
   saloni.chopra@igp.uu.se; fredrik.frejd@igp.uu.se; pyazaki@coh.org;
   marika.nestor@igp.uu.se
RI Nestor, Marika/HEZ-1169-2022
OI Mohajershojai, Tabassom/0000-0002-7364-5470; Spangler, Douglas
   Nils/0000-0001-6775-5051
FU The authors would like to thank Hanna Berglund for the assistance with
   graphical designs, Bogdan Mitran and Ram Kumar Selvaraju for the
   assistance with SPECT/CT imaging, and Patrick Micke for the assistance
   with assessment of immunohistochemical sections.
FX The authors would like to thank Hanna Berglund for the assistance with
   graphical designs, Bogdan Mitran and Ram Kumar Selvaraju for the
   assistance with SPECT/CT imaging, and Patrick Micke for the assistance
   with assessment of immunohistochemical sections.
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TC 0
Z9 0
U1 3
U2 7
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2072-6694
J9 CANCERS
JI Cancers
PD SEP
PY 2023
VL 15
IS 17
AR 4239
DI 10.3390/cancers15174239
PG 18
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA S3FL6
UT WOS:001070060100001
PM 37686514
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Zhang, BM
   Li, Y
   Song, LQ
   Xi, H
   Wang, SK
   Yu, CF
   Cui, BB
AF Zhang, Bomiao
   Li, Yien
   Song, Liqiang
   Xi, Hua
   Wang, Shaoke
   Yu, Chenfeng
   Cui, Binbin
TI Cuproplasia characterization in colon cancer assists to predict
   prognosis and immunotherapeutic response
SO FRONTIERS IN ONCOLOGY
LA English
DT Article
DE copper; colon cancer; immunotherapy; microsatellite instability; immune
   infiltration
ID TRACE-ELEMENTS; SERUM-LEVELS; COPPER; ZINC; SELENIUM; METALS; IRON
AB IntroductionColon cancer is the 3(rd) most prevalent cancer worldwide, with more than 900,000 deaths annually. Chemotherapy, targeted treatment, and immunotherapeutic treatment are the three cornerstones of colon cancer treatment; however, the occurrence of immune therapy resistance is the most pressing problem to solve. Copper is a mineral nutrient that is both beneficial and potentially toxic to cells and is increasingly implicated in cell proliferation and death pathways. Cuproplasia is characterized by copper-dependent cell growth and proliferation. This term encompasses both neoplasia and hyperplasia and describes the primary and secondary effects of copper. The connection between copper and cancer has been noted for decades. However, the relationship between cuproplasia and colon cancer prognosis remains unclear. MethodIn this study, we applied bioinformatics approaches including WGCNA, GSEA and etc. to delineate cuproplasia characterization of colon cancer, set up a robust Cu_riskScore model based on cuproplasia-relevant genes and found its relevant biological processes use qRT-pCR to validate our results on our cohort. ResultThe Cu_riskScore is found to be relevant to Stage and MSI-H subtype, and some biological processes including MYOGENESIS and MYC TARGETS. The Cu_riskScore high and low groups also showed different immune infiltration pattern and genomic traits. Finally, the result of our cohort showed the Cu_riskScore gene RNF113A has a marked effect in predicting immunotherapy response. DiscussionIn conclusion, we identified a cuproplasia-related gene expression signature consisting of six genes and studied the landscape of the clinical and biological characterization of this model in Colon Cancer. Furthermore, the Cu_riskScore was demonstrated to be a robust prognostic indicator and predictive factor for the benefits of immunotherapy.
C1 [Zhang, Bomiao; Li, Yien; Song, Liqiang; Xi, Hua; Wang, Shaoke; Yu, Chenfeng; Cui, Binbin] Harbin Med Univ, Dept Colorectal Surg Oncol, Canc Hosp, Harbin, Peoples R China.
C3 Harbin Medical University
RP Cui, BB (corresponding author), Harbin Med Univ, Dept Colorectal Surg Oncol, Canc Hosp, Harbin, Peoples R China.
EM binbincui@hrbmu.edu.cn
RI song, liqiang/HPI-0927-2023
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U1 1
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PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 2234-943X
J9 FRONT ONCOL
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PD MAR 16
PY 2023
VL 13
AR 1061084
DI 10.3389/fonc.2023.1061084
PG 9
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA C3VU2
UT WOS:000961239200001
PM 37007132
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Hu, JW
   Ning, YZ
   Ma, YC
   Sun, L
   Chen, GW
AF Hu, Jianwen
   Ning, Yingze
   Ma, Yongchen
   Sun, Lie
   Chen, Guowei
TI Characterization of RNA Processing Genes in Colon Cancer for Predicting
   Clinical Outcomes
SO BIOMARKER INSIGHTS
LA English
DT Article
DE Colon cancer; TCGA; GEO; RNA processing gene; risk score; nomogram;
   prognosis
ID SF3B1; MUTATIONS; MELANOMA; PACKAGE; MODELS
AB Objective: Colon cancer is associated with multiple levels of molecular heterogeneity. RNA processing converts primary transcriptional RNA to mature RNA, which drives tumourigenesis and its maintenance. The characterisation of RNA processing genes in colon cancer urgently needs to be elucidated.Methods: In this study, we obtained 1033 relevant samples from The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) databases to explore the heterogeneity of RNA processing phenotypes in colon cancer. Firstly, Unsupervised hierarchical cluster analysis detected 4 subtypes with specific clinical outcomes and biological features via analysis of 485 RNA processing genes. Next, we adopted the least absolute shrinkage and selection operator (LASSO) as well as Cox regression model with penalty to characterise RNA processing-related prognostic features.Results: An RNA processing-related prognostic risk model based on 10 genes including FXR1, MFAP1, RBM17, SAGE1, SNRPA1, SRRM4, ADAD1, DDX52, ERI1, and EXOSC7 was identified finally. A composite prognostic nomogram was constructed by combining this feature with the remaining clinical variables including TNM, age, sex, and stage. Genetic variation, pathway activation, and immune heterogeneity with risk signatures were also analysed via bioinformatics methods. The outcomes indicated that the high-risk subgroup was associated with higher genomic instability, increased proliferative and cycle characteristics, decreased tumour killer CD8+ T cells and poorer clinical prognosis than the low-risk group.Conclusion: This prognostic classifier based on RNA-edited genes facilitates stratification of colon cancer into specific subgroups according to TNM and clinical outcomes, genetic variation, pathway activation, and immune heterogeneity. It can be used for diagnosis, classification and targeted treatment strategies comparable to current standards in precision medicine. It provides a rationale for elucidation of the role of RNA editing genes and their clinical significance in colon cancer as prognostic markers.
C1 [Hu, Jianwen; Sun, Lie; Chen, Guowei] Peking Univ First Hosp, Gastrointestinal Surg Dept, Beijing, Peoples R China.
   [Hu, Jianwen] Capital Med Univ, Anzhen Hosp, Lab Dept, Beijing, Peoples R China.
   [Ning, Yingze] Peking Univ Third Hosp, Dept Thorac Surg, Beijing, Peoples R China.
   [Ma, Yongchen] Peking Univ First Hosp, Endoscopy Ctr, Beijing, Peoples R China.
C3 Capital Medical University
RP Sun, L (corresponding author), Peking Univ First Hosp, Gastrointestinal Surg Dept, Beijing, Peoples R China.
EM sunliemd@126.com
FU Peking University Medicine Seed Funds for Interdisciplinary Research;
   Fundamental Research Funds for the Central Universities [BMU2022MX018];
   National Science Foundation of China [7214259]; Beijing Natural Science
   Foundation of China [7214259]
FX The author(s) disclosed receipt of the following financial support for
   the research, authorship, and/or publication of this article: Peking
   University Medicine Seed Funds for Interdisciplinary Research and the
   Fundamental Research Funds for the Central <EM><STRONG>
   </STRONG></EM>Universities (No. BMU2022MX018), and the National Science
   and Beijing Natural Science Foundation of China (No. 7214259) supported
   the completion of this project.
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NR 69
TC 0
Z9 0
U1 1
U2 1
PU SAGE PUBLICATIONS LTD
PI LONDON
PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND
SN 1177-2719
J9 BIOMARK INSIGHTS
JI Biomark. Insights
PY 2024
VL 19
AR 11772719241258642
DI 10.1177/11772719241258642
PG 15
WC Medicine, Research & Experimental
WE Emerging Sources Citation Index (ESCI)
SC Research & Experimental Medicine
GA D0E1W
UT WOS:001292995900001
PM 39161926
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Peixoto, RD
   Chakhtoura, JJA
   Aguilar-Ponce, JL
   Garcia-Rivello, H
   Jansen, AM
   Medina, RP
   Ramos-Esquivel, A
   Stefani, SD
AF Peixoto, Renata D.
   Chakhtoura, Jad Joseph Abbas
   Aguilar-Ponce, Jose L.
   Garcia-Rivello, Hernan
   Jansen, Angela M.
   Medina, Rafael Parra
   Ramos-Esquivel, Allan
   Stefani, Stephen Doral
TI Corrected: BRAF Testing in Melanoma and Colorectal Cancer in Latin
   America: Challenges and Opportunities
SO CUREUS JOURNAL OF MEDICAL SCIENCE
LA English
DT Review
DE recommendations; precision medicine; latin america; treatment;
   colorectal cancer; melanoma; braf testing
ID BEVACIZUMAB; FOLFOXIRI; BURDEN; LUNG
AB The incidence of colorectal cancer in Argentina and Brazil has reached levels comparable to those in higher -income countries. Similarly, the incidence of melanoma in Latin America has increased during the past decades. BRAF mutation is seen frequently in melanomas and colorectal cancer. Discovering the expression of this specific biomarker in both cancers has unleashed the potential for targeted molecular therapies. In patients with BRAF-mutated melanoma, adopting a combined targeted treatment approach has shown a dramatic increase in overall survival. However, several barriers impede the development of early BRAF testing in Latin America, jeopardizing the potential for personalized therapies and care. To address this, the Americas Health Foundation convened a virtual meeting of Latin American oncologists to address the barriers to BRAF testing in melanoma and colorectal cancer. During a three-day conference, expert oncologists used literature reviews and personal experience to detail the barriers to early BRAF testing in their region. They proposed actionable steps to overcome the barriers identified, which included deficiencies in knowledge, treatment options, equitable distribution, timely results, and local data on BRAF mutations. Oncologists proposed several actions to overcome barriers, including raising public and healthcare awareness about the importance of BRAF testing, expanding treatment options in clinics across the region, developing centers in underserved areas, and increasing affordable treatment options for patients who test positive for BRAF mutations.
C1 [Peixoto, Renata D.] Ctr Paulista Oncol, Med Oncol, Sao Paulo, Brazil.
   [Chakhtoura, Jad Joseph Abbas] Hosp Rafael Angel Calderon Guardia, Anat Pathol, San Jose, Costa Rica.
   [Aguilar-Ponce, Jose L.] Med Sur, Oncol Ctr, Mexico City, Mexico.
   [Garcia-Rivello, Hernan] Hosp Italiano Buenos Aires, Pathol, Buenos Aires, Argentina.
   [Garcia-Rivello, Hernan] Inst Translat Med & Biomed Engn IMTIB, Pathol, Buenos Aires, Argentina.
   [Jansen, Angela M.] Amer Hlth Fdn, Genet, Laguna Beach, CA USA.
   [Medina, Rafael Parra] Inst Nacl Cancerol, Pathol, Bogota, Colombia.
   [Ramos-Esquivel, Allan] Hosp San Juan Dios, Caja Costarricense Seguro Social, San Jose, Costa Rica.
   [Stefani, Stephen Doral] Hlth Technol Assessment, Unimed, Porto Alegre, Brazil.
C3 University of Buenos Aires; Hospital Italiano de Buenos Aires; American
   Health Foundation
RP Peixoto, RD (corresponding author), Ctr Paulista Oncol, Med Oncol, Sao Paulo, Brazil.
EM renatadalpino@gmail.com
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NR 35
TC 0
Z9 0
U1 0
U2 1
PU SPRINGERNATURE
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON, N1 9XW, ENGLAND
EI 2168-8184
J9 CUREUS J MED SCIENCE
JI Cureus J Med Sci
PD NOV 28
PY 2022
VL 14
IS 11
DI 10.7759/cureus.31972
PG 9
WC Medicine, General & Internal
WE Emerging Sources Citation Index (ESCI)
SC General & Internal Medicine
GA 7W0BY
UT WOS:000913179100039
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Zhang, WN
   Liang, WJ
   Zhang, Y
   Liang, MJ
   Zhang, MJ
   Chen, Q
   Mo, ZP
   Wu, MY
   Weng, XZ
   Han, R
   Liang, YN
   Ke, ML
   Lin, WQ
AF Zhang, Wan-Ning
   Liang, Wei-Jie
   Zhang, Ying
   Liang, Ming-Jian
   Zhang, Ming-Juan
   Chen, Qi
   Mo, Zhou-Pei
   Wu, Mei-Yi
   Weng, Xue-Zi
   Han, Rui
   Liang, Yong-Neng
   Ke, Miao-La
   Lin, Wen-Qian
TI Molecular characteristics of patients with colorectal signet-ring cell
   carcinoma with different ABO blood groups
SO HELIYON
LA English
DT Article
DE Colorectal neoplasms; Carcinoma; Signet ring cell; ABO blood -group
   system; Mutation; HLA antigens
ID CANCER; RISK; ADENOCARCINOMA; RECTUM
AB Background: Colorectal signet-ring cell carcinoma (SRCC) is a rare subtype of malignant adenocarcinoma, accounting for approximately 1 % of colorectal cancer (CRC) cases. Its biomarkers and molecular characteristics remain controversial, and there are no specific therapeutic targets or strategies for its clinical treatment. Methods: A retrospective study was conducted between January 2010 and December 2021. 1058 colorectal cancer cases from the Sun Yat-sen University Cancer Center and 489 cases from the Tumor Genome Atlas Project were included in the analysis, of which 64 were SRCC. Data extraction included patient demographics, blood types and risk factors, including clinical variables and genomics (either a 19-gene panel NGS or 1021-gene panel NGS). Univariate analyses were performed to identify factors significantly associated with overall survival. Results: The blood groups of 27 (42.2 %), 18 (28.1 %), 12 (18.8 %), and seven (10.9 %) patients were classified as O, A, B, and AB, respectively. We found that O was a unique blood group characterized by a low frequency of KRAS mutations, a high frequency of heterozygosity at each HLA class I locus, and a high tumor mutational burden (TMB). Patients in blood group A with high-frequency KRAS mutations and those in blood group B with anemia and metabolic abnormalities required targeted treatment. Furthermore, genetic alterations in SRCC differed from those in adenocarcinoma and mucinous adenocarcinoma. Conclusions: Our study revealed genomic changes in SRCC patients across different blood groups, which could advance the understanding and precise treatment of colorectal SRCC.
C1 [Zhang, Wan-Ning; Zhang, Ying; Liang, Ming-Jian; Zhang, Ming-Juan; Chen, Qi; Mo, Zhou-Pei; Wu, Mei-Yi; Weng, Xue-Zi; Han, Rui; Liang, Yong-Neng; Ke, Miao-La; Lin, Wen-Qian] Sun Yat Sen Univ, State Key Lab Oncol South China, Canc Ctr, Guangzhou 510060, Peoples R China.
   [Liang, Wei-Jie] South China Univ Technol, Guangzhou Peoples Hosp 1, Dept Lab Med, Guangzhou 510180, Peoples R China.
C3 State Key Lab Oncology South China; Sun Yat Sen University; South China
   University of Technology
RP Lin, WQ (corresponding author), Sun Yat Sen Univ, Collaborat Innovat Ctr Canc Med, Dept Blood Transfus, State Key Lab Oncol Southern China,Canc Ctr, Guangzhou 510060, Peoples R China.
EM linwq@sysucc.org.cn
RI Chen, Qi/W-1759-2019; wu, meiyi/ITV-0319-2023; Leung,
   Vijer/HOC-6709-2023
FU Health Commission of Guangdong Province Scientific Research Project
   [A2023098]
FX This research was supported by Health Commission of Guangdong Province
   Scientific Research Project (Grant No. A2023098) .
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NR 33
TC 0
Z9 0
U1 3
U2 3
PU CELL PRESS
PI CAMBRIDGE
PA 50 HAMPSHIRE ST, FLOOR 5, CAMBRIDGE, MA 02139 USA
EI 2405-8440
J9 HELIYON
JI Heliyon
PD JUL 15
PY 2024
VL 10
IS 13
AR e34220
DI 10.1016/j.heliyon.2024.e34220
PG 13
WC Multidisciplinary Sciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Science & Technology - Other Topics
GA YI2K3
UT WOS:001267792800001
PM 39091930
OA Green Published, Green Submitted
DA 2025-01-04
ER

PT J
AU Chang, N
   Zhao, YF
   Ge, N
   Qian, LT
AF Chang, Na
   Zhao, Yufei
   Ge, Ning
   Qian, Liting
TI A pH/ROS cascade-responsive and self-accelerating drug release
   nanosystem for the targeted treatment of multi-drug-resistant colon
   cancer
SO DRUG DELIVERY
LA English
DT Article
DE ROS amplification; self-accelerate drug release; multidrug resistance
ID BETA-LAPACHONE; DELIVERY; DOXORUBICIN; NANOPARTICLES; MICELLES; SWITCH;
   CELLS
AB The efficacy of chemotherapeutic agents for colon cancer treatment is limited by multidrug resistance (MDR) and insufficient intracellular release of the administered nanomedicine. To overcome these limitations, we constructed a pH/ROS cascade-responsive and self-accelerating drug release nanoparticle system (PLP-NPs) for the treatment of multidrug-resistant colon cancer. The PLP-NPs comprised a reactive oxygen species (ROS)-sensitive polymeric paclitaxel (PTX) prodrug (DEX-TK-PTX), a pH-sensitive poly(l-histidine) (PHis), and beta-lapachone (Lapa), a ROS-generating agent. We found that PLP-NPs could accumulate in tumor tissue through enhancement of the permeability and retention (EPR) effect, and were subsequently internalized by cancer cells via the endocytic pathway. Within the acidic endo-lysosomal environment, PHis protonation facilitated the escape of the PLP-NPs from the lysosome and release of Lapa. The released Lapa generated a large amount of ROS, consumed ATP, and downregulated P-glycoprotein (P-gp) production through the activity of NQO1, an enzyme that is specifically overexpressed in tumor cells. In addition, the generated ROS promoted the release of PTX from DEX-TK-PTX to kill cancer cells, while ATP depletion inhibited P-gp-mediated MDR.In vitroandin vivoexperiments subsequently confirmed that PLP-NPs induced tumor-specific cytotoxicity and overcame the MDR of colon cancer. Our findings indicate that the use of the PLP-NPs system represents a promising strategy to counter MDR in the treatment of colon cancer.
C1 [Chang, Na; Zhao, Yufei; Ge, Ning; Qian, Liting] Univ Sci & Technol China, Dept Radiat Oncol, Affiliated Hosp USTC 1, Div Life Sci & Med,Anhui Prov Canc Hosp, Hefei 230000, Anhui, Peoples R China.
C3 Chinese Academy of Sciences; University of Science & Technology of
   China, CAS
RP Qian, LT (corresponding author), Univ Sci & Technol China, Dept Radiat Oncol, Affiliated Hosp USTC 1, Div Life Sci & Med,Anhui Prov Canc Hosp, Hefei 230000, Anhui, Peoples R China.
EM money2004@sina.com
RI Zhao, Yufei/AFL-4714-2022; Ge, Ning/C-3524-2013
OI Reis, AlessanRSS/0000-0001-8486-7469; Ge, Ning/0000-0002-4922-7025
FU National Natural Science Foundation of China [11805198]; National Key
   R&D Program of China [2016YFB1000905]
FX This work was supported by National Natural Science Foundation of China
   [Grant Nos. 11805198] and National Key R&D Program of China [Grant Nos.
   2016YFB1000905].
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   Zhu JH, 2017, J MATER CHEM B, V5, P1339, DOI 10.1039/c6tb03066a
NR 36
TC 25
Z9 26
U1 4
U2 76
PU TAYLOR & FRANCIS LTD
PI ABINGDON
PA 2-4 PARK SQUARE, MILTON PARK, ABINGDON OR14 4RN, OXON, ENGLAND
SN 1071-7544
EI 1521-0464
J9 DRUG DELIV
JI Drug Deliv.
PD JAN 1
PY 2020
VL 27
IS 1
BP 1073
EP 1086
DI 10.1080/10717544.2020.1797238
PG 14
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA MO5VQ
UT WOS:000551593700001
PM 32706272
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Tsilimigras, DI
   Ntanasis-Stathopoulos, I
   Pawlik, TM
AF Tsilimigras, Diamantis I.
   Ntanasis-Stathopoulos, Ioannis
   Pawlik, Timothy M.
TI Molecular Mechanisms of Colorectal Liver Metastases
SO CELLS
LA English
DT Review
DE CRLM; cells; tumor microenvironment
ID HEPATIC STELLATE CELLS; IMMATURE MYELOID CELLS; COLON-CANCER CELLS;
   SUPPRESSOR-CELLS; KUPFFER CELLS; REGULATORY CELLS; NICHE FORMATION;
   PROMOTES; MICROENVIRONMENT; MELANOMA
AB The liver is the most frequently target for metastasis among patients with colorectal cancer mainly because of the portal vein circulation that directly connects the colon and rectum with the liver. The liver tumor microenvironment consists of different cell types each with unique characteristics and functions that modulate the antigen recognition and immune system activation. Primary tumors from other sites "prime" the liver prior to the seeding of cancer cells, creating a pre-metastatic niche. Following invasion into the liver, four different phases are key to the development of liver metastases: a microvascular phase in which cancer cells infiltrate and become trapped in sinusoidal vessels; an extravascular, pre-angiogenic phase; an angiogenic phase that supplies oxygen and nutrients to cancer cells; and a growth phase in which metastatic cells multiply and enlarge to form detectable tumors. Exosomes carry proteins, lipids, as well as genetic information that can create a pre-metastatic niche in distant sites, including the liver. The complexity of angiogenic mechanisms and the exploitation of the vasculature in situ by cancer cells have limited the efficacy of currently available anti-angiogenic therapies. Delineating the molecular mechanisms implicated in colorectal liver metastases is crucial to understand and predict tumor progression; the development of distant metastases; and resistance to chemotherapy, immunotherapy, and targeted treatment.
C1 [Tsilimigras, Diamantis I.; Pawlik, Timothy M.] Ohio State Univ, Wexner Med Ctr, Dept Surg, Div Surg Oncol, 395 W 12th Ave, Columbus, OH 43210 USA.
   [Tsilimigras, Diamantis I.; Pawlik, Timothy M.] James Comprehens Canc Ctr, 395 W 12th Ave, Columbus, OH 43210 USA.
   [Ntanasis-Stathopoulos, Ioannis] Natl & Kapodistrian Univ Athens, Alexandra Gen Hosp, Sch Med, Dept Clin Therapeut, Athens 11527, Greece.
C3 University System of Ohio; Ohio State University; University System of
   Ohio; Ohio State University; James Cancer Hospital & Solove Research
   Institute; Alexandra Hospital; Athens Medical School; National &
   Kapodistrian University of Athens
RP Tsilimigras, DI; Pawlik, TM (corresponding author), Ohio State Univ, Wexner Med Ctr, Dept Surg, Div Surg Oncol, 395 W 12th Ave, Columbus, OH 43210 USA.; Tsilimigras, DI; Pawlik, TM (corresponding author), James Comprehens Canc Ctr, 395 W 12th Ave, Columbus, OH 43210 USA.
EM diamantis.tsilimigras@osumc.edu; johnntanasis@gmail.com;
   tim.pawlik@osumc.edu
RI Pawlik, Timothy/AAO-9335-2020; Ntanasis-Stathopoulos,
   Ioannis/AAD-3692-2019
OI Ntanasis-Stathopoulos, Ioannis/0000-0002-6328-9783; Tsilimigras,
   Diamantis I./0000-0002-3676-9263; Pawlik, Timothy/0000-0002-7994-9870
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NR 113
TC 10
Z9 10
U1 1
U2 10
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2073-4409
J9 CELLS-BASEL
JI Cells
PD JUN
PY 2023
VL 12
IS 12
AR 1657
DI 10.3390/cells12121657
PG 13
WC Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology
GA K6FN7
UT WOS:001017378900001
PM 37371127
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Osman, S
   Çetin, NK
   Erdogdu, IH
   Meteoglu, I
AF Osman, Sibel
   Cetin, Nesibe Kahraman
   Erdogdu, Ibrahim Halil
   Meteoglu, Ibrahim
TI Mutation Profile via Next-Generation Sequencing in Patients with
   Colorectal Adenocarcinoma and Its Clinicopathological Correlation
SO TURKISH JOURNAL OF GASTROENTEROLOGY
LA English
DT Article
DE Colorectal cancer; molecular; mutation; NGS
ID TUMOR SIZE; CANCER; PTEN; SURVIVAL; COLON; BRAF; METASTASIS; KRAS
AB Background/Aims: Recent studies that reveal the molecular profiles of colorectal carcinomas have demonstrated tumor heterogeneity. Characterization of colorectal carcinoma-specific genomic alterations is essential for developing more successful and targeted treatment protocols. Moreover, it is vital in elucidating the pathogenesis and mechanisms of resistance against treatment and predicting prognosis.
   Materials and Methods: The study included 73 cases diagnosed with colorectal carcinomas and subjected to molecular analysis by the next-generation sequencing. The association between the clinicopathologic parameters and pathogenic mutations detected in 32 genes was evaluated.
   Results: Pathogenic mutations were determined in a total of 24 genes. The Cell Division Cycle 27 (CDC27), Kirsten rat sarcoma viral proto-oncogene (KRAS), serine/threonine protein kinase B-raf (BRAF), phosphatase and tensin homolog, breast cancer 2 (BRCA2), and phosphotidylinositol-4,5-biphosphate 3-kinase (PIK3CA) mutations were determined at higher rates, with the adenomatous polyposis coli mutation determined at a lower rate than in the literature. There were significant positive correlations between CDC27 and phosphatase and tensin homolog (PTEN), PTEN and BRCA2, and PTEN and adenomatous polyposis coli (APC) concomitant mutations, whereas negative correlations were present between BRAF and KRAS. Statistically significant relationships were present between KRAS exon 2 and mucinous morphology, PIK3CA and absence of perineural invasion, BRAF and tumor differentiation/localization, MutS homolog 3 (MSH3) and tumor diameter, and BRCA2 and absence of lymph node metastasis.
   Conclusion: It is necessary to have a comprehensive database of genomic alterations of colorectal carcinomas to interpret mutations more accurately clinically. There are no studies on the frequency of mutations in colorectal carcinomas in the Turkish population; thus, follow-up and treatment protocols are organized following the European and American databases and guidelines. A comprehensive study of the colorectal carcinoma patients' mutation profile in the Turkish patient cohort by the next-generation sequencing method will help to provide significant therapeutic, prognostic, and predictive data and design more successful treatment and follow-up strategies.
C1 [Osman, Sibel; Cetin, Nesibe Kahraman; Erdogdu, Ibrahim Halil; Meteoglu, Ibrahim] Aydin Adnan Menderes Univ, Dept Pathol, Fac Med, Aydin, Turkiye.
C3 Adnan Menderes University
RP Çetin, NK (corresponding author), Aydin Adnan Menderes Univ, Dept Pathol, Fac Med, Aydin, Turkiye.
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NR 46
TC 1
Z9 1
U1 0
U2 0
PU AVES
PI SISLI
PA BUYUKDERE CAD 105-9, MECIDIYEKOY, SISLI, ISTANBUL 34394, Turkiye
EI 2148-5607
J9 TURK J GASTROENTEROL
JI Turk. J. Gastroenterol.
PD NOV
PY 2023
VL 34
IS 11
BP 1124
EP 1133
DI 10.5152/tjg.2023.22682
PG 10
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA CU0L4
UT WOS:001127633000003
PM 37737217
OA Green Published
DA 2025-01-04
ER

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TI Enhanced antitumor efficacy in colon cancer using EGF functionalized
   PLGA nanoparticles loaded with 5-Fluorouracil and perfluorocarbon
SO BMC CANCER
LA English
DT Article
DE PLGA nanoparticles; 5-fluorouracil; Perfluorocarbon; EGF; Hypoxia; Colon
   cancer
ID DRUG-DELIVERY; MULTIDRUG-RESISTANCE; CO-DELIVERY; THERAPIES; CURCUMIN;
   SYSTEMS
AB Background Tumor recurrence and metastasis occur at a high rate in patients with colon cancer. Identification of effective strategies for the treatment of colon cancer is critical. Recently, poly (lactic-co-glycolic acid) (PLGA) has been shown to have potential as a broad therapeutic drug delivery system. We designed a dual-loaded nanoparticle drug delivery system to overcome the limitations of chemotherapeutic drugs used to treat colon cancer. Methods We developed epidermal growth factor (EGF) functionalized PLGA nanoparticles (NPs) co-loaded with 5-fluorouracil (5Fu) and perfluorocarbon (PFC) (EGF-PLGA@5Fu/PFC) for targeted treatment of colon cancer. CCK-8 assay, Hoechst33342 staining and flow cytometry were performed to investigate the functions of EGF-PLGA@5Fu/PFC NPs in SW620 cells. Beside, animal experiment, histological analysis and immunofluorescence staining were adopted to further confirm the role of EGF-PLGA@5Fu/PFC NPs in vivo. Results The findings showed that EGF-PLGA@5Fu /PFC NPs had an average size 200 nm and a 5Fu-loading efficiency of 7.29%. Furthermore, in vitro release was pH-sensitive. Targeted EGF-PLGA@5Fu/PFC NPs exhibited higher cellular uptake than non-targeted NPs into colon cancer cells. In addition, EGF-PLGA@5Fu/PFC NPs suppressed cell viability and induced apoptosis in SW620 cells to a greater extent than non-targeted NPs. In tumor xenografted mice, EGF-PLGA@5Fu/PFC NPs suppressed tumor growth more effectively than 5Fu, PLGA@5Fu or PLGA@5Fu/PFC NPs. Histopathological analysis further demonstrated that EGF-targeted NPs inhibited tumor growth to a greater extent than non-targeted or non-NP treatments. The improved therapeutic outcomes observed in this study were due to relief of tumor hypoxia by transport of oxygen by PFC to the tumors. Conclusion We constructed a biocompatible nanodrug delivery system based on functionalized nanoparticles that provided a novel strategy for selective delivery of chemotherapy drugs to tumors.
C1 [Wu, Pingping; Zhou, Qing; Zhu, Huayun; Zhuang, Yan; Bao, Jun] Nanjing Med Univ, Jiangsu Canc Hosp, Dept Med Oncol, Nanjing 210009, Peoples R China.
   [Wu, Pingping; Zhou, Qing; Zhu, Huayun; Zhuang, Yan; Bao, Jun] Nanjing Med Univ, Jiangsu Inst Canc Res, Nanjing 210009, Peoples R China.
   [Wu, Pingping; Zhou, Qing; Zhu, Huayun; Zhuang, Yan; Bao, Jun] Nanjing Med Univ, Affiliated Canc Hosp, Nanjing 210009, Peoples R China.
C3 Nanjing Medical University; Nanjing Medical University; Nanjing Medical
   University
RP Bao, J (corresponding author), Nanjing Med Univ, Jiangsu Canc Hosp, Dept Med Oncol, Nanjing 210009, Peoples R China.; Bao, J (corresponding author), Nanjing Med Univ, Jiangsu Inst Canc Res, Nanjing 210009, Peoples R China.; Bao, J (corresponding author), Nanjing Med Univ, Affiliated Canc Hosp, Nanjing 210009, Peoples R China.
EM baojun@jszlyy.com.cn
FU National Natural Science Youth Foundation of China [81601604]; Natural
   Science Youth Foundation of Jiangsu [BK20161070]; Fifteenth Batch
   High-level Talents Project of "Six Talent Peaks" in Jiangsu Province;
   talents program of Jiangsu Cancer Hospital [YC201809]
FX This project was supported by the National Natural Science Youth
   Foundation of China (No. 81601604), the Natural Science Youth Foundation
   of Jiangsu (No. BK20161070), the Fifteenth Batch High-level Talents
   Project of "Six Talent Peaks" in Jiangsu Province (No.WSW-049) and the
   talents program of Jiangsu Cancer Hospital (No. YC201809). The funding
   bodies played no role in the design of the study and collection,
   analysis, and interpretation of data and in writing the manuscript.
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NR 29
TC 61
Z9 65
U1 7
U2 46
PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
EI 1471-2407
J9 BMC CANCER
JI BMC Cancer
PD APR 28
PY 2020
VL 20
IS 1
AR 354
DI 10.1186/s12885-020-06803-7
PG 10
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA LL9HC
UT WOS:000531863000003
PM 32345258
OA Green Submitted, Green Published, gold
DA 2025-01-04
ER

PT J
AU Franko, J
   Shi, Q
   Meyers, JP
   Maughan, TS
   Adams, RA
   Seymour, MT
   Saltz, L
   Punt, CJA
   Koopman, M
   Tournigand, C
   Tebbutt, NC
   Diaz-Rubio, E
   Souglakos, J
   Falcone, A
   Chibaudel, B
   Heinemann, V
   Moen, J
   De Gramont, A
   Sargent, DJ
   Grothey, A
AF Franko, Jan
   Shi, Qian
   Meyers, Jeffrey P.
   Maughan, Timothy S.
   Adams, Richard A.
   Seymour, Matthew T.
   Saltz, Leonard
   Punt, Cornelis J. A.
   Koopman, Miriam
   Tournigand, Christophe
   Tebbutt, Niall C.
   Diaz-Rubio, Eduardo
   Souglakos, John
   Falcone, Alfredo
   Chibaudel, Benoist
   Heinemann, Volker
   Moen, Joseph
   De Gramont, Aimery
   Sargent, Daniel J.
   Grothey, Axel
CA Anal Res Canc Digestive Syst ARCAD
TI Prognosis of patients with peritoneal metastatic colorectal cancer given
   systemic therapy: an analysis of individual patient data from
   prospective randomised trials from the Analysis and Research in Cancers
   of the Digestive System (ARCAD) database
SO LANCET ONCOLOGY
LA English
DT Article
ID PHASE-III; COMBINATION CHEMOTHERAPY; 1ST-LINE TREATMENT; CARCINOMATOSIS;
   OXALIPLATIN; SURVIVAL; FLUOROURACIL; IRINOTECAN; RESECTION; BEVACIZUMAB
AB Background Patients with peritoneal metastatic colorectal cancer have reduced overall survival compared with patients with metastatic colorectal cancer without peritoneal involvement. Here we further investigated the effect of the number and location of metastases in patients receiving first-line systemic chemotherapy.
   Methods We analysed individual patient data for previously untreated patients enrolled in 14 phase 3 randomised trials done between 1997 and 2008. Trials were included if protocols explicitly pre-specified and solicited for patients with peritoneal involvement in the trial data collection process or had done a formal peritoneum-focused review of individual pre-treatment scans. We used stratified multivariable Cox models to assess the prognostic associations of peritoneal metastatic colorectal cancer with overall survival and progression-free survival, adjusting for other key clinical-pathological factors (age, sex, Eastern Cooperative Oncology Group (ECOG) performance score, primary tumour location [colon vs rectum], previous treatment, and baseline BMI). The primary endpoint was difference in overall survival between populations with and without peritoneal metastases.
   Findings Individual patient data were available for 10 553 patients. 9178 (87%) of 10 553 patients had non-peritoneal metastatic colorectal cancer (4385 with one site of metastasis, 4793 with two or more sites of metastasis), 194 (2%) patients had isolated peritoneal metastatic colorectal cancer, and 1181 (11%) had peritoneal metastatic colorectal cancer and other organ involvement. These groups were similar in age, ethnic origin, and use of targeted treatment. Patients with peritoneal metastatic colorectal cancer were more likely than those with non-peritoneal metastatic colorectal cancer to be women (565 [41%] of 1371 vs 3312 [36%] of 9169 patients; p= 0 . 0003), have colon primary tumours (1116 [84%] of 1334 patients vs 5603 [66%]; p< 0 . 0001), and have performance status of 2 (136 [10%] vs 521 [6%]; p< 0 . 0001). We recorded a higher proportion of patients with mutated BRAF in patients with peritoneal-only (eight [18%] of 44 patients with available data) and peritoneal metastatic colorectal cancer with other sites of metastasis (34 [12%] of 289), compared with patients with non-peritoneal metastatic colorectal cancer (194 [9%] of 2230; p= 0 . 028 comparing the three groups). Overall survival (adjusted HR 0 . 75, 95% CI 0 . 63-0 . 91; p= 0 . 003) was better in patients with isolated non-peritoneal sites than in those with isolated peritoneal metastatic colorectal cancer. Overall survival of patients with two of more non-peritoneal sites of metastasis (adjusted HR 1 . 04, 95% CI 0 . 86-1 . 25, p= 0.69) and those with peritoneal metastatic colorectal cancer plus one other site of metastasis (adjusted HR 1 . 10, 95% CI 0 . 89-1 . 37, p= 0 . 37) was similar to those with isolated peritoneal metastases. Compared with patients with isolated peritoneal metastases, those with peritoneal metastases and two or more additional sites of metastasis had the shortest survival (adjusted HR 1 . 40; CI 1 . 14-1 . 71; p= 0 . 0011).
   Interpretation Patients with peritoneal metastatic colorectal cancer have significantly shorter overall survival than those with other isolated sites of metastases. In patients with several sites of metastasis, poor survival is a function of both increased number of metastatic sites and peritoneal involvement. The pattern of metastasis and in particular, peritoneal involvement, results in prognostic heterogeneity of metastatic colorectal cancer.
C1 [Franko, Jan] Mercy Med Ctr, Div Surg Oncol, Des Moines, IA 50314 USA.
   [Shi, Qian; Meyers, Jeffrey P.; Sargent, Daniel J.] Mayo Clin, Div Biomed Stat & Informat, Rochester, MN USA.
   [Maughan, Timothy S.] MRC, Oxford Inst Radiat Oncol, CRUK, Oxford, England.
   [Adams, Richard A.] Cardiff Univ, Cardiff, S Glam, Wales.
   [Seymour, Matthew T.] Cookridge Hosp, Gastrointestinal Canc Res Unit, Leeds, W Yorkshire, England.
   [Saltz, Leonard] Mem Sloan Kettering Canc Ctr, 1275 York Ave, New York, NY 10021 USA.
   [Punt, Cornelis J. A.] Univ Amsterdam, Acad Med Ctr, Dept Med Oncol, Amsterdam, Netherlands.
   [Koopman, Miriam] Univ Med Ctr Utrecht, Utrecht, Netherlands.
   [Tournigand, Christophe] Hop Henri Mondor, Creteil, France.
   [Tebbutt, Niall C.] Univ Sydney, Sydney Med Sch, Sydney, NSW, Australia.
   [Diaz-Rubio, Eduardo] Hosp Clin San Carlos, Dept Oncol, Madrid, Spain.
   [Souglakos, John] Univ Crete, Sch Med, Iraklion, Greece.
   [Falcone, Alfredo] Univ Pisa, Dept Oncol, Pisa, Italy.
   [Chibaudel, Benoist; De Gramont, Aimery] Franco British Inst, Dept Med Oncol, Levallois Perret, France.
   [Heinemann, Volker] Univ Munich, Dept Med Oncol, Munich, Germany.
   [Heinemann, Volker] Ctr Comprehens Canc, Munich, Germany.
   [Moen, Joseph] Univ Iowa, Dept Biostat, Iowa City, IA USA.
   [Grothey, Axel] Mayo Clin, Dept Oncol, Rochester, MN USA.
C3 Mayo Clinic; University of Oxford; Cardiff University; Cookridge
   Hospital; Memorial Sloan Kettering Cancer Center; University of
   Amsterdam; Academic Medical Center Amsterdam; Utrecht University;
   Utrecht University Medical Center; Universite
   Paris-Est-Creteil-Val-de-Marne (UPEC); Assistance Publique Hopitaux
   Paris (APHP); Hopital Universitaire Henri-Mondor - APHP; University of
   Sydney; Hospital Clinico San Carlos; University of Crete; University of
   Pisa; University of Munich; University of Iowa; Mayo Clinic
RP Franko, J (corresponding author), Mercy Med Ctr, Div Surg Oncol, Des Moines, IA 50314 USA.
EM jan.franko@gmail.com
RI Shi, Qian/AAW-8907-2020; Maughan, Tim/AAV-7636-2021; Falcone,
   Alfredo/G-5217-2013; Tournigand, Christophe/Q-2831-2018
OI Chibaudel, Benoist/0000-0003-1279-2044; Adams,
   Richard/0000-0003-3915-7243; Diaz-Rubio, Eduardo/0000-0003-2792-5348;
   Falcone, Alfredo/0000-0001-5840-2529; Seymour,
   Matthew/0000-0002-2441-9629; Shi, Qian/0000-0002-4640-8832
FU Cancer Research UK [15954] Funding Source: Medline
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NR 44
TC 468
Z9 480
U1 3
U2 50
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1470-2045
EI 1474-5488
J9 LANCET ONCOL
JI Lancet Oncol.
PD DEC
PY 2016
VL 17
IS 12
BP 1709
EP 1719
DI 10.1016/S1470-2045(16)30500-9
PG 11
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA EE3YG
UT WOS:000389537700039
PM 27743922
OA Green Accepted
HC Y
HP N
DA 2025-01-04
ER

PT J
AU Xiao, Y
   Lin, HC
   Li, JL
   Wu, JX
AF Xiao, Yu
   Lin, Hancui
   Li, Jinluan
   Wu, Junxin
TI Disulfidptosis-related prognostic signature correlates with
   immunotherapy response in colorectal cancer
SO SCIENTIFIC REPORTS
LA English
DT Article
ID CELLS; RESISTANCE; EXPRESSION; KEGG
AB Disulfidptosis (DSP), a form of cell death caused by disulphide stress, plays an important role in tumour progression. However, the mechanisms by which DSP regulates the tumour microenvironment remain unclear. Thus, we analysed the transcriptome profiles and clinical data, which were obtained from the TCGA database, of 540 patients with colorectal cancer. Compared with the patients with low DSP expression, those with high DSP expression exhibited significantly better survival outcomes; lower stromal and ESTIMATE scores; significantly higher numbers of CD4+ T cells, M2 macrophages, dendritic cells, and neutrophils; higher expression of immune checkpoint-related genes; and lower Tregs and HLA-DQB2 levels. A prognostic signature established based on DSP-related genes demonstrated an increase in risk score with a higher clinical stage. Risk scores negatively correlated with dendritic cells, eosinophils, and CD4+ T cells and significantly positively correlated with Treg cells. Patients with higher risk scores experienced significantly worse survival outcomes and immunotherapy non-response. Our nomogram model, combining clinicopathological features and risk scores, exhibited robust prognostic and predictive power. In conclusion, DSP-related genes actively participated in regulating the tumour microenvironment. Thus, they can serve as biomarkers to provide targeted treatment for colorectal cancer.
C1 [Xiao, Yu; Lin, Hancui; Li, Jinluan; Wu, Junxin] Fujian Med Univ, Fujian Canc Hosp, Clin Oncol Sch, Dept Radiat Oncol, Fuzhou 350014, Peoples R China.
C3 Fujian Medical University
RP Li, JL; Wu, JX (corresponding author), Fujian Med Univ, Fujian Canc Hosp, Clin Oncol Sch, Dept Radiat Oncol, Fuzhou 350014, Peoples R China.
EM lijinluan@pku.org.cn; junxinwufj@aliyun.com
RI Li, Jinluan/J-8096-2013
FU Fujian Research and Training Grants for Young and Middle-aged Leaders in
   Healthcare
FX We acknowledge the TCGA and GEO databases for providing platforms for
   uploading meaningful datasets.
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NR 51
TC 2
Z9 3
U1 2
U2 6
PU NATURE PORTFOLIO
PI BERLIN
PA HEIDELBERGER PLATZ 3, BERLIN, 14197, GERMANY
SN 2045-2322
J9 SCI REP-UK
JI Sci Rep
PD JAN 2
PY 2024
VL 14
IS 1
AR 81
DI 10.1038/s41598-023-49954-w
PG 13
WC Multidisciplinary Sciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Science & Technology - Other Topics
GA EZ5U3
UT WOS:001142781100768
PM 38168553
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Zhou, XR
   Cao, CP
   Li, N
   Yuan, SF
AF Zhou, Xiaorong
   Cao, Chuanpei
   Li, Nan
   Yuan, Shaofei
TI SYL3C aptamer-anchored microemulsion co-loading β-elemene and PTX
   enhances the treatment of colorectal cancer
SO DRUG DELIVERY
LA English
DT Article
DE PTX; beta-elemene; colorectal cancer; AS1411 aptamer; EpCAM
ID TUMOR-CELLS; IN-VIVO; THERAPY; PACLITAXEL; PHASE; COMBINATION;
   EXPRESSION; CISPLATIN; MOLECULE; EFFICACY
AB The aim of this study is to construct a SYL3C aptamer-anchored microemulsion based on beta-elemene and PTX (SYL3C/EP-MEs) for enhancement on colorectal cancer therapy. Such microemulsion is consist of encapsulated drugs (beta-elemene and PTX), tumor targeting ligand (3'-end thiolated SYL3C aptamer), thiol conjugated site (maleimide-modified PEGylated 1,2-dioleoyl-sn-glycero-3-phosphoethanolamine, mal-DOPE-PEG), pH-sensitive component (DOPE) and other necessary excipients. SYL3C/EP-MEs showed a spherical particle with an average particle size around 30 nm and a high encapsulation efficiency (>80%) for both drugs. beta-elemene and PTX could be released controllably from SYL3C/EP-MEs as pH values changed. SYL3C/EP-MEs displayed a selective affinity to HT-29 cells, leading to an obvious increase in cellular uptake, cell apoptosis and cytotoxicity. In the HT-29 tumor xenograft-bearing nude mice model studies, SYL3C/EP-MEs showed an overwhelming tumor growth inhibition, the longest survival time and the lowest systemic toxicity among all the treatments. The potential mechanism of enhanced anti-cancer ability was probably associated with the induction of M1 macrophage polarization, the downregulation of mutant p53 protein and the reduction of bcl-2 protein expression. Collectively, the microemulsion codelivery of beta-elemene and PTX using functionalization with SYL3C aptamer provides a novel approach for combinational colorectal cancer-targeted treatment.
C1 [Zhou, Xiaorong; Li, Nan; Yuan, Shaofei] Jiangsu Canc Hosp, Dept Med, Nanjing, Jiangsu, Peoples R China.
   [Cao, Chuanpei] Jiujiang Univ, Affiliated Hosp, Gastrointestinal Surg, Jiujiang, Peoples R China.
   [Yuan, Shaofei] Wenzhou Med Univ, Affiliated Hosp 3, Dept Med Oncol, Wenzhou, Peoples R China.
C3 Nanjing Medical University; Jiujiang University; Wenzhou Medical
   University
RP Yuan, SF (corresponding author), Wansong Rd 108, Ruian, Zhejiang, Peoples R China.
EM ysf1004@163.com
RI Li, Naishi/ABI-7607-2020
FU Medical Talent Foundation of Nanjing City [NJRC2018472]
FX We are financially supported by the Medical Talent Foundation of Nanjing
   City [NJRC2018472].
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NR 45
TC 14
Z9 16
U1 6
U2 48
PU TAYLOR & FRANCIS LTD
PI ABINGDON
PA 2-4 PARK SQUARE, MILTON PARK, ABINGDON OR14 4RN, OXON, ENGLAND
SN 1071-7544
EI 1521-0464
J9 DRUG DELIV
JI Drug Deliv.
PD JAN 1
PY 2019
VL 26
IS 1
BP 886
EP 897
DI 10.1080/10717544.2019.1660733
PG 12
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA IY2ST
UT WOS:000486242700001
PM 31524012
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Karatay, E
   Lacin, S
   Eren, A
AF Karatay, Emrah
   Lacin, Sahin
   Eren, Abdulkadir
TI Evaluation of the Relationship Between Portal Vein Diameter and
   Colorectal Liver Metastases on Computed Tomography
SO IN VIVO
LA English
DT Article
DE Colorectal cancer; liver metastasis; computed tomography; portal vein;
   metastasis diameter
ID CANCER; CT; CHEMOTHERAPY; MANAGEMENT; SURGERY; PET/CT
AB Background/Aim: The most common and often first metastatic site of colorectal cancer (CRC) is the liver, and radiological modalities have a critical role in the diagnosis of colorectal liver metastasis (CRLM). In this study, the possible relationship between portal vein diameter, number of metastases, and metastasis diameter was evaluated in CRLM patients who underwent computed tomography (CT) examination with intravenous contrast (IV). Patients and Methods: Cases diagnosed with CRLM who underwent abdominal CT examination with IV contrast between December 2020 and January 2024 were retrospectively scanned. People over the age of 18 were included, and cases were divided into three subgroups according to the number of metastases: a (single), b (two), and c (three and/or more). Results: There were 101 male and 74 female cases; the youngest case was 39 (male) and the oldest case was 87 (male) years old. According to the number of CRLMs, group a had 47 cases, group b had 23, and group c had 105 cases. The minimum diameter of metastasis was 0.74 cm, the maximum was 11.86 cm, and the mean diameter was 4.45 +/- 2.67 cm. There was a significant correlation between the presence of metastasis in the left lobe and the diameter of the metastases (p<0.05). Conclusion: The relationship between portal vein diameter and CRLM using contrast-enhanced CT scans was explored. While no significant correlation was found between portal vein diameters and metastasis size, a notable association was observed between metastasis size and their presence in the left liver lobe. These findings suggest that CRLMs in the left lobe may respond better to preoperative chemotherapy and surgical interventions. This novel insight could help develop targeted treatment strategies for CRLM, though further research with larger cohorts is needed.
C1 [Karatay, Emrah] Sureyyapasa Chest Dis & Thorac Surg Res & Training, Dept Radiol, Basibuyuk Mahallesi Sureyyapasa Yerleskesi,34844 C, Istanbul, Turkiye.
   [Lacin, Sahin] Koc Univ Hosp, Dept Med Oncol, Istanbul, Turkiye.
   [Eren, Abdulkadir] Istanbul Medipol Univ, Mega Hosp, Dept Radiol, Istanbul, Turkiye.
C3 Istanbul Sureyyapasa Chest Diseases & Thoracic Surgery Training &
   Research Hospital; Koc University; Istanbul Medipol University
RP Karatay, E (corresponding author), Sureyyapasa Chest Dis & Thorac Surg Res & Training, Dept Radiol, Basibuyuk Mahallesi Sureyyapasa Yerleskesi,34844 C, Istanbul, Turkiye.
EM emrahkaratay1984@gmail.com
RI Karatay, Emrah/AAE-7657-2022
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NR 23
TC 0
Z9 0
U1 5
U2 5
PU INT INST ANTICANCER RESEARCH
PI ATHENS
PA EDITORIAL OFFICE 1ST KM KAPANDRITIOU-KALAMOU RD KAPANDRITI, PO BOX 22,
   ATHENS 19014, GREECE
SN 0258-851X
EI 1791-7549
J9 IN VIVO
JI In Vivo
PD SEP-OCT
PY 2024
VL 38
IS 5
BP 2471
EP 2477
DI 10.21873/invivo.13717
PG 7
WC Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine
GA E0U6W
UT WOS:001300248100047
PM 39187350
OA gold
DA 2025-01-04
ER

PT J
AU Han, ZQ
   Song, B
   Yang, JY
   Wang, B
   Ma, ZQ
   Yu, L
   Li, YH
   Xu, HJ
   Qiao, MQ
AF Han, Zhiqiang
   Song, Bo
   Yang, Jiyuan
   Wang, Bo
   Ma, Zhongqiang
   Yu, Long
   Li, Yuanhao
   Xu, Haijin
   Qiao, Mingqiang
TI Curcumin-Encapsulated Fusion Protein-Based Nanocarrier Demonstrated
   Highly Efficient Epidermal Growth Factor Receptor-Targeted Treatment of
   Colorectal Cancer
SO JOURNAL OF AGRICULTURAL AND FOOD CHEMISTRY
LA English
DT Article
DE curcumin; GE11; hydrophobin; targeted drug delively
ID DRUG-DELIVERY; HYDROPHOBIN; MICELLES; SURFACE; EGFR; ADSORPTION;
   STABILITY; HYDROGELS; NANOCAGES; PEPTIDE
AB Curcumin, a polyphenol derived from turmeric, has multiple biological functions, such as anti-inflammatory, antioxidant, antibacterial and, above all, antitumor activity. Colorectal cancer is a common malignancy of the gastrointestinal tract with an extremely high mortality rate. However, the low bioavailability and poor targeting properties of curcumin generally limit its clinical application. In the present study, we designed a fusion protein GE11-HGFI as a nanodrug delivery system. The protein was connected by flexible linkers, inheriting the self-assembly properties of hydrophobin HGFI and the targeting ability of GE11. The data show that the encapsulation of curcumin by fusion protein GE11-HGFI can form uniform and stable nanoparticles with a size of only 80 nm. In addition, the nanocarrier had high encapsulation efficiency for curcumin and made it to release sustainably. Notably, the drug-loaded nanosystem selectively targeted colorectal cancer cells with high epidermal growth factor receptor expression, resulting in high aggregated concentrations of curcumin at tumor sites, thus showing a significant anticancer effect. These results suggest that the nanocarrier fusion protein has the potential to be a novel strategy for enhancing molecular bioactivity and drug targeting in cancer therapy.
C1 [Han, Zhiqiang; Song, Bo; Yang, Jiyuan; Wang, Bo; Ma, Zhongqiang; Yu, Long; Xu, Haijin; Qiao, Mingqiang] Nankai Univ, Coll Life Sci, Minist Educ, Key Lab Mol Microbiol & Technol, Tianjin 300071, Peoples R China.
   [Li, Yuanhao] Remegen Co Ltd, Yantai 264000, Shandong, Peoples R China.
   [Qiao, Mingqiang] Shanxi Univ, Sch Life Sci, Taiyuan 030000, Shanxi, Peoples R China.
C3 Nankai University; Shanxi University
RP Xu, HJ; Qiao, MQ (corresponding author), Nankai Univ, Coll Life Sci, Minist Educ, Key Lab Mol Microbiol & Technol, Tianjin 300071, Peoples R China.; Qiao, MQ (corresponding author), Shanxi Univ, Sch Life Sci, Taiyuan 030000, Shanxi, Peoples R China.
EM nkxuhaijin@163.com; qiaomq@nankai.edu.cn
RI Liu, Yuxuan/JVO-7759-2024; Song, Bo/HJP-1326-2023; HAN,
   ZHIQIANG/KWU-4849-2024
FU National Key Research and Development Program [2018YFA0900100]; Natural
   Science Fund for Young Scholars of Tianjin [21JCQNJC00110]
FX This work was financially supported by the National Key Research and
   Development Program (2018YFA0900100) and Natural Science Fund for Young
   Scholars of Tianjin (21JCQNJC00110).
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NR 54
TC 10
Z9 10
U1 4
U2 33
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 0021-8561
EI 1520-5118
J9 J AGR FOOD CHEM
JI J. Agric. Food Chem.
PD DEC 14
PY 2022
VL 70
IS 49
BP 15464
EP 15473
DI 10.1021/acs.jafc.2c04668
EA DEC 2022
PG 10
WC Agriculture, Multidisciplinary; Chemistry, Applied; Food Science &
   Technology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Agriculture; Chemistry; Food Science & Technology
GA 7B0WW
UT WOS:000892630400001
PM 36454954
DA 2025-01-04
ER

PT J
AU Wang, CH
   Yang, SX
   Gao, L
   Wang, LL
   Cao, L
AF Wang, Canhong
   Yang, Shuxian
   Gao, Li
   Wang, Lili
   Cao, Li
TI Carboxymethyl pachyman (CMP) reduces intestinal mucositis and regulates
   the intestinal microflora in 5-fluorouracil-treated CT26 tumour-bearing
   mice
SO FOOD & FUNCTION
LA English
DT Article
ID INFLAMMATORY-BOWEL-DISEASE; COLORECTAL-CANCER; OXIDATIVE STRESS;
   CYCLOPHOSPHAMIDE; MICROBIOTA; RATS; DYSBIOSIS; INTEGRITY; EXTRACT;
   PATHWAY
AB The compound 5-fluorouracil (5-FU) is the first choice chemotherapeutic agent for the treatment of colorectal cancer (CRC), but intestinal mucositis is a primary limiting factor in anticancer therapy. There is currently no broadly effective targeted treatment to cure this side effect. Carboxymethylated pachyman (CMP) is a polysaccharide that is modified from the structure of pachyman isolated from Poria cocos (Chinese name: Fu Ling). Meanwhile, recent studies have shown that CMP exhibits immune regulatory, anti-inflammatory and antioxidant activities. Therefore, the purpose of this study was to evaluate the intestinal protective effect of CMP in 5-FU-treated CT26 tumour-bearing mice and to further explore its underlying mechanism(s) of action. Initially, a CT26 colon carcinoma xenograft mice model was established. The colon length, colon tissue injury, intestinal flora, short-chain fatty acids (SCFAs) and indicators linked to inflammation, antioxidation and apoptosis were then measured. Our results showed that CMP in combination with 5-FU reversed intestinal shortening (p < 0.01) and alleviated 5-FU-induced colon injury (p < 0.001) via suppression of ROS production; increasing the levels of CAT, GSH-Px and GSH; decreasing expression of NF-.B, p-p38 and Bax; and elevating the levels of Nrf2 and Bcl-2. More importantly, CMP had a significant impact and counteracted the intestinal microflora disorders produced by 5-FU by increasing the proportion of Bacteroidetes, lactobacilli, and butyric acid-producing and acetic acid-producing bacteria and restoring the intestinal flora diversity. Overall, this work suggested that CMP could regulate the ecological balance of the intestinal flora and reduce colon injuries induced by 5-FU in CT26 tumour-bearing mice, and the mechanism involved may be associated with the regulation of the NF-.B, Nrf2-ARE and MAPK/ P38 pathways.
C1 [Wang, Canhong; Yang, Shuxian; Gao, Li; Cao, Li] Chinese Acad Med Sci, Inst Med Plant Dev, Beijing 100193, Peoples R China.
   [Wang, Canhong; Yang, Shuxian; Gao, Li; Cao, Li] Peking Union Med Coll, Beijing 100193, Peoples R China.
   [Wang, Canhong] Chinese Acad Med Sci, Inst Med Plant Dev, Hainan Branch, Haikou 570311, Hainan, Peoples R China.
   [Wang, Canhong] Peking Union Med Coll, Haikou 570311, Hainan, Peoples R China.
   [Wang, Lili] Chinese Acad Agr Sci, Inst Agrofood Sci & Technol, Beijing 100193, Peoples R China.
C3 Chinese Academy of Medical Sciences - Peking Union Medical College;
   Institute of Medicinal Plant Development - CAMS; Chinese Academy of
   Medical Sciences - Peking Union Medical College; Peking Union Medical
   College; Chinese Academy of Medical Sciences - Peking Union Medical
   College; Institute of Medicinal Plant Development - CAMS; Chinese
   Academy of Medical Sciences - Peking Union Medical College; Peking Union
   Medical College; Chinese Academy of Agricultural Sciences
RP Cao, L (corresponding author), Chinese Acad Med Sci, Inst Med Plant Dev, Beijing 100193, Peoples R China.; Cao, L (corresponding author), Peking Union Med Coll, Beijing 100193, Peoples R China.
EM lcao@implad.ac.cn
RI Wang, Lili/AAG-9458-2020
OI Yang, Shuxian/0000-0001-9837-5721
FU Key Laboratory of Bioactive Substances and Resources Utilization of
   Chinese Herbal Medicine, Ministry of Education; Beijing Key Laboratory
   of Innovative Drug Discovery of Traditional Chinese Medicine (Natural
   Medicine) and Translational Medicine, Institute of Medical Plant
   Development, Peking Union Medical College; Chinese Academy of Medical
   Sciences [2012ZX09301-002-001-026, 2012ZX09501001-004]
FX This work was supported by the Key Laboratory of Bioactive Substances
   and Resources Utilization of Chinese Herbal Medicine, Ministry of
   Education, and by the Beijing Key Laboratory of Innovative Drug
   Discovery of Traditional Chinese Medicine (Natural Medicine) and
   Translational Medicine, Institute of Medical Plant Development, Peking
   Union Medical College and the Chinese Academy of Medical Sciences (no.
   2012ZX09301-002-001-026 and no. 2012ZX09501001-004).
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NR 36
TC 66
Z9 74
U1 1
U2 91
PU ROYAL SOC CHEMISTRY
PI CAMBRIDGE
PA THOMAS GRAHAM HOUSE, SCIENCE PARK, MILTON RD, CAMBRIDGE CB4 0WF, CAMBS,
   ENGLAND
SN 2042-6496
EI 2042-650X
J9 FOOD FUNCT
JI Food Funct.
PD MAY 1
PY 2018
VL 9
IS 5
BP 2695
EP 2704
DI 10.1039/c7fo01886j
PG 10
WC Biochemistry & Molecular Biology; Food Science & Technology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Food Science & Technology
GA GH1YH
UT WOS:000433198000013
PM 29756138
DA 2025-01-04
ER

PT J
AU Gonzalez, J
   Bahmad, HF
   Ocejo, S
   Abreu, A
   Popp, M
   Gogola, S
   Fernandez, V
   Recine, M
   Poppiti, R
AF Gonzalez, Jeffrey
   Bahmad, Hisham F.
   Ocejo, Stephanie
   Abreu, Alvaro
   Popp, Meagan
   Gogola, Samantha
   Fernandez, Vielka
   Recine, Monica
   Poppiti, Robert
TI The Usefulness of Elastin Staining to Detect Vascular Invasion in Cancer
SO INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
LA English
DT Review
DE lymphovascular invasion; angioinvasion; venous invasion; TNM
   classification; staging; immunohistochemistry; elastin stain; College of
   American Pathologists; World Health Organization
ID VENOUS INVASION; COLORECTAL-CANCER; LYMPHOVASCULAR INVASION;
   PROGNOSTIC-SIGNIFICANCE; ENDOTHELIAL-CELLS; VESSEL INVASION;
   BREAST-CANCER; FACTOR-VIII; CARCINOMA; IMPACT
AB Tumor prognosis hinges on accurate cancer staging, a pivotal process influenced by the identification of lymphovascular invasion (LVI), i.e., blood vessel and lymphatic vessel invasion. Protocols by the College of American Pathologists (CAP) and the World Health Organization (WHO) have been established to assess LVI in various tumor types, including, but not limited to, breast cancer, colorectal cancer (CRC), pancreatic exocrine tumors, and thyroid carcinomas. The CAP refers to blood vessel invasion as "angioinvasion" (vascular invasion) to differentiate it from lymphatic vessel invasion (lymphatic invasion). For clarity, the latter terms will be used throughout this review. The presence of lymphatic and/or vascular invasion has emerged as a pivotal prognostic factor; therefore, its accurate identification is crucial not only for staging but also for providing the patient with an honest understanding of his/her prognosis. Given the prognostic importance of the correct identification of LVI, specific staining techniques are employed to distinguish lymphatic vessel invasion from angioinvasion and to differentiate true LVI from artifact. These encompass hematoxylin and eosin (H&E) staining, elastic staining, Factor VIII staining, Ulex europaeus I agglutinin staining, CD31, CD34, D2-40, ERG, and D2-40 (podoplanin) immunohistochemical (IHC) stains among others. Based on a review of numerous publications regarding the efficacy of various methods for LVI detection, elastin staining demonstrated superior accuracy and prognostic value, allowing for more targeted treatment strategies. The clinical significance of accurately detecting LVI cannot be overstated, as it is strongly linked to higher cancer-related mortality and an increased risk of tumor recurrence. This review aims to examine the existing literature on the use of elastin stains in the detection of vascular invasion among different types of tumors and its prognostic value.
C1 [Gonzalez, Jeffrey; Ocejo, Stephanie; Abreu, Alvaro; Popp, Meagan; Gogola, Samantha] Florida Int Univ, Herbert Wertheim Coll Med, Miami, FL 33199 USA.
   [Bahmad, Hisham F.; Fernandez, Vielka; Recine, Monica; Poppiti, Robert] Mt Sinai Med Ctr, Arkadi M Rywlin MD Dept Pathol & Lab Med, Miami Beach, FL 33140 USA.
   [Recine, Monica; Poppiti, Robert] Florida Int Univ, Herbert Wertheim Coll Med, Dept Pathol, Miami, FL 33199 USA.
C3 State University System of Florida; Florida International University;
   Mount Sinai Medical Center; State University System of Florida; Florida
   International University
RP Bahmad, HF (corresponding author), Mt Sinai Med Ctr, Arkadi M Rywlin MD Dept Pathol & Lab Med, Miami Beach, FL 33140 USA.
EM jgonz1074@med.fiu.edu; hfbahmad@gmail.com; socej001@med.fiu.edu;
   aabre070@med.fiu.edu; mpopp002@med.fiu.edu; sgogo002@med.fiu.edu;
   vielka.fernandez@msmc.com; monica.recine@msmc.com;
   robert.poppiti@msmc.com
RI ; Bahmad, Hisham/A-5369-2019
OI Abreu, Alvaro/0009-0002-1509-3855; Popp, Meagan/0000-0003-0201-6420;
   Gogola, Samantha/0000-0003-2979-9648; Gonzalez,
   Jeffrey/0009-0001-3327-1988; Bahmad, Hisham/0000-0003-3799-2595
FU Figures were created with <uri>BioRender.com</uri> (accessed on 13
   August 2023). All rights and ownership of BioRender content are reserved
   by BioRender (Agreement numbers SD25Q6E68K, CE25Q6HVWB, and CZ25Q6KQOF).
   BioRender content included in the completed [SD25Q6E68K, CE25Q6HVWB,
   CZ25Q6KQOF]
FX Figures were created with <URI>BioRender.com</URI> (accessed on 13
   August 2023). All rights and ownership of BioRender content are reserved
   by BioRender (Agreement numbers SD25Q6E68K, CE25Q6HVWB, and CZ25Q6KQOF).
   BioRender content included in the completed graphic is not licensed for
   any commercial uses beyond publication in a journal. For any commercial
   use of these figures, users may, if allowed, recreate the figures in
   BioRender under an Industry BioRender Plan.
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NR 69
TC 2
Z9 2
U1 1
U2 2
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
SN 1661-6596
EI 1422-0067
J9 INT J MOL SCI
JI Int. J. Mol. Sci.
PD OCT
PY 2023
VL 24
IS 20
AR 15264
DI 10.3390/ijms242015264
PG 17
WC Biochemistry & Molecular Biology; Chemistry, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Chemistry
GA W1RA5
UT WOS:001089463200001
PM 37894944
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Carvalho, MR
   Reis, RL
   Oliveira, JM
AF Carvalho, M. R.
   Reis, R. L.
   Oliveira, J. M.
TI Dendrimer nanoparticles for colorectal cancer applications
SO JOURNAL OF MATERIALS CHEMISTRY B
LA English
DT Review
ID IRON-OXIDE NANOPARTICLES; ANTICANCER DRUG-DELIVERY; MAGNETIC-RESONANCE;
   TARGETED DENDRIMER; PAMAM DENDRIMER; IN-VITRO; CONTROLLED-RELEASE;
   CONTRAST AGENTS; DOXORUBICIN; THERAPEUTICS
AB Cancer nanotechnology is a prolific field of research, where nanotools are employed to diagnose and treat cancer with unprecedented precision. Targeted drug delivery is fundamental for more efficient cancer treatments. For this, nanoparticles have been extensively used during the past few years in order to improve the specificity, selectivity and controlled release of drug delivery. It holds potential in minimizing systemic toxicity through the development of functionalized particles for targeted treatment. Among all the type of nanoparticles, dendrimers display several advantages, which make them ideal candidates for improved and targeted drug delivery in cancer research. Dendrimers can transport large amounts of drug into specific areas. In addition, they can be employed for monitoring the progress of the treatment process, with an unprecedented theranostic capability. Special emphasis is given to colorectal cancer and to the preferred employed strategies for producing drug-loaded/functionalized NPs for cancer therapy in the past few years.
C1 [Carvalho, M. R.; Reis, R. L.; Oliveira, J. M.] Univ Minho, European Inst Excellence Tissue Engn & Regenerat, I3Bs Res Inst Biomat Biodegradables & Biomimet, 3Bs Res Grp, AvePk,Parque Ciencia & Tecnol, P-4805017 Barco, Guimaraes, Portugal.
   [Carvalho, M. R.; Reis, R. L.; Oliveira, J. M.] ICVS 3Bs PT Govt Associate Lab, Braga, Portugal.
   [Carvalho, M. R.; Reis, R. L.; Oliveira, J. M.] Univ Minho, Discoveries Ctr Regenerat & Precis Med, Guimaraes, Portugal.
C3 Universidade do Minho; Universidade do Minho
RP Oliveira, JM (corresponding author), Univ Minho, European Inst Excellence Tissue Engn & Regenerat, I3Bs Res Inst Biomat Biodegradables & Biomimet, 3Bs Res Grp, AvePk,Parque Ciencia & Tecnol, P-4805017 Barco, Guimaraes, Portugal.; Oliveira, JM (corresponding author), ICVS 3Bs PT Govt Associate Lab, Braga, Portugal.; Oliveira, JM (corresponding author), Univ Minho, Discoveries Ctr Regenerat & Precis Med, Guimaraes, Portugal.
EM miguel.oliveira@i3bs.uminho.pt
RI Reis, Rui/A-8938-2008; Oliveira, Joaquim Miguel/H-8636-2012
OI Carvalho, Mariana/0000-0003-2081-3909; Oliveira, Joaquim
   Miguel/0000-0001-7052-8837
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NR 99
TC 74
Z9 76
U1 1
U2 55
PU ROYAL SOC CHEMISTRY
PI CAMBRIDGE
PA THOMAS GRAHAM HOUSE, SCIENCE PARK, MILTON RD, CAMBRIDGE CB4 0WF, CAMBS,
   ENGLAND
SN 2050-750X
EI 2050-7518
J9 J MATER CHEM B
JI J. Mat. Chem. B
PD FEB 14
PY 2020
VL 8
IS 6
BP 1128
EP 1138
DI 10.1039/c9tb02289a
PG 11
WC Materials Science, Biomaterials
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Materials Science
GA KN1WR
UT WOS:000514632000004
PM 31971528
OA Green Accepted, Bronze
DA 2025-01-04
ER

PT J
AU Penney, ME
   Parfrey, PS
   Savas, S
   Yilmaz, YE
AF Penney, Michelle E.
   Parfrey, Patrick S.
   Savas, Sevtap
   Yilmaz, Yildiz E.
TI Associations of single nucleotide polymorphisms with mucinous colorectal
   cancer: genome-wide common variant and gene-based rare variant analyses
SO BIOMARKER RESEARCH
LA English
DT Article
DE Colorectal cancer; Mucinous adenocarcinoma; Genome-wide association
   study; Common single nucleotide polymorphisms; Rare single nucleotide
   polymorphisms
ID FINGER PROTEIN ZBTB20; CLINICOPATHOLOGICAL CHARACTERISTICS;
   MICROSATELLITE INSTABILITY; HISTOLOGY PREDICTS; GASTRIC MUCIN; CORE
   PROTEINS; CARCINOMA; EXPRESSION; SURVIVAL; COLON
AB Background: Colorectal cancer has significant impact on individuals and healthcare systems. Many genes have been identified to influence its pathogenesis. However, the genetic basis of mucinous tumor histology, an aggressive subtype of colorectal cancer, is currently not well-known. This study aimed to identify common and rare genetic variations that are associated with the mucinous tumor phenotype.
   Methods: Genome-wide single nucleotide polymorphism (SNP) data was investigated in a colorectal cancer patient cohort (n = 505). Association analyses were performed for 729,373 common SNPs and 275,645 rare SNPs. Common SNP association analysis was performed using univariable and multivariable logistic regression under different genetic models. Rare-variant association analysis was performed using a multi-marker test.
   Results: No associations reached the traditional genome-wide significance. However, promising genetic associations were identified. The identified common SNPs significantly improved the discriminatory accuracy of the model for mucinous tumor phenotype. Specifically, the area under the receiver operating characteristic curve increased from 0.703 (95% CI: 0.634-0.773) to 0.916 (95% CI: 0.873-0.960) when considering the most significant SNPs. Additionally, the rare variant analysis identified a number of genetic regions that potentially contain causal rare variants associated with the mucinous tumor phenotype.
   Conclusions: This is the first study applying both common and rare variant analyses to identify genetic associations with mucinous tumor phenotype using a genome-wide genotype data. Our results suggested novel associations with mucinous tumors. Once confirmed, these results will not only help us understand the biological basis of mucinous histology, but may also help develop targeted treatment options for mucinous tumors.
C1 [Penney, Michelle E.; Savas, Sevtap; Yilmaz, Yildiz E.] Mem Univ Newfoundland, Fac Med, Discipline Genet, St John, NF, Canada.
   [Parfrey, Patrick S.; Yilmaz, Yildiz E.] Mem Univ Newfoundland, Fac Med, Discipline Med, St John, NF, Canada.
   [Savas, Sevtap] Mem Univ Newfoundland, Fac Med, Discipline Oncol, St John, NF, Canada.
   [Yilmaz, Yildiz E.] Mem Univ Newfoundland, Fac Med, Dept Math & Stat, St John, NF, Canada.
C3 Memorial University Newfoundland; Memorial University Newfoundland;
   Memorial University Newfoundland; Memorial University Newfoundland
RP Yilmaz, YE (corresponding author), Mem Univ Newfoundland, Fac Med, Discipline Genet, St John, NF, Canada.; Yilmaz, YE (corresponding author), Mem Univ Newfoundland, Fac Med, Discipline Med, St John, NF, Canada.
EM yyilmaz@mun.ca
FU Research and Development Corporation (RDC) Newfoundland and Labrador
   (NL) [5404.1723.101]; Faculty of Medicine of Memorial University of
   Newfoundland; Translational and Personalized Medicine Initiative
   (TPMI)/NP SUPPORT fellowship
FX This work was funded by the Research and Development Corporation (RDC)
   Newfoundland and Labrador (NL) [5404.1723.101] and the Faculty of
   Medicine of Memorial University of Newfoundland (awarded to Y.E.
   Yilmaz). M.E. Penney is partly supported by a Translational and
   Personalized Medicine Initiative (TPMI)/NP SUPPORT fellowship. The
   funding sources were not involved in the study design; in the
   collection, analysis or interpretation of data; in the writing of the
   report; or in the decision to submit the paper for publication.
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NR 78
TC 5
Z9 6
U1 0
U2 3
PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
EI 2050-7771
J9 BIOMARK RES
JI Biomark. Res.
PD JUN 13
PY 2018
VL 6
AR 17
DI 10.1186/s40364-018-0133-z
PG 10
WC Oncology; Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Research & Experimental Medicine
GA GJ2OZ
UT WOS:000435112100001
PM 29942513
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Plavec, TV
   Mitrovic, A
   Nanut, MP
   Strukelj, B
   Kos, J
   Berlec, A
AF Plavec, Tina Vida
   Mitrovic, Ana
   Nanut, Milica Perisic
   Strukelj, Borut
   Kos, Janko
   Berlec, Ales
TI Targeting of fluorescent <i>Lactococcus lactis</i> to colorectal cancer
   cells through surface display of tumour-antigen binding proteins
SO MICROBIAL BIOTECHNOLOGY
LA English
DT Article
ID ACID BACTERIA; EPCAM; DELIVERY; HER2
AB Development of targeted treatment for colorectal cancer is crucial to avoid side effects. To harness the possibilities offered by microbiome engineering, we prepared safe multifunctional cancer cell-targeting bacteria Lactococcus lactis. They displayed, on their surface, binding proteins for cancer-associated transmembrane receptors epithelial cell adhesion molecule (EpCAM) and human epidermal growth factor receptor 2 (HER2) and co-expressed an infrared fluorescent protein for imaging. Binding of engineered L. lactis to tumour antigens EpCAM and HER2 was confirmed and characterised in vitro using soluble receptors. The proof-of-principle of targeting was demonstrated on human cell lines HEK293, HT-29 and Caco-2 with fluorescent microscopy and flow cytometry. The highest L. lactis adhesion was seen for the HEK293 cells with the overexpressed tumour antigens, where colocalisation with their tumour antigens was seen for 39% and 67% of EpCAM-targeting and HER2-targeting bacteria, respectively. On the other hand, no binding was observed to HEK293 cells without tumour antigens, confirming the selectivity of the engineered L. lactis. Apart from cell targeting in static conditions, targeting ability of engineered L. lactis was also shown in conditions of constant flow of bacterial suspension over the HEK293 cells. Successful targeting by engineered L. lactis support the future use of these bacteria in biopharmaceutical delivery for the treatment of colorectal cancer.
C1 [Plavec, Tina Vida; Mitrovic, Ana; Nanut, Milica Perisic; Strukelj, Borut; Kos, Janko; Berlec, Ales] Jozef Stefan Inst, Dept Biotechnol, Jamova 39, Ljubljana, Slovenia.
   [Plavec, Tina Vida; Strukelj, Borut; Kos, Janko; Berlec, Ales] Univ Ljubljana, Fac Pharm, Askerceva 7, Ljubljana, Slovenia.
C3 Slovenian Academy of Sciences & Arts (SASA); Jozef Stefan Institute;
   University of Ljubljana
RP Berlec, A (corresponding author), Jozef Stefan Inst, Dept Biotechnol, Jamova 39, Ljubljana, Slovenia.; Berlec, A (corresponding author), Univ Ljubljana, Fac Pharm, Askerceva 7, Ljubljana, Slovenia.
EM ales.berlec@ijs.si
RI Kos, Janko/AAX-6462-2021; Berlec, Aleš/AAG-5922-2019
OI Berlec, Ales/0000-0002-8095-6998; Perisic Nanut,
   Milica/0000-0003-2314-2733; Mitrovic, Ana/0000-0002-6996-4831
FU Slovenian Research Agency [P4-0127, J4-9327]
FX This study was funded by the Slovenian Research Agency (Grant Numbers
   P4-0127 and J4-9327).
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NR 51
TC 10
Z9 11
U1 3
U2 20
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1751-7915
J9 MICROB BIOTECHNOL
JI Microb. Biotechnol.
PD SEP
PY 2021
VL 14
IS 5
BP 2227
EP 2240
DI 10.1111/1751-7915.13907
EA AUG 2021
PG 14
WC Biotechnology & Applied Microbiology; Microbiology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biotechnology & Applied Microbiology; Microbiology
GA UR8LO
UT WOS:000680943500001
PM 34347360
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Huang, K
   Zhang, X
   Hao, YH
   Feng, RX
   Wang, HJ
   Shu, ZW
   Li, A
   Du, MH
AF Huang, Kun
   Zhang, Xin
   Hao, Yanhui
   Feng, Ruixing
   Wang, Haojie
   Shu, Zhiwan
   Li, An
   Du, Minghu
TI RETRACTED: Hypoxia Tumor Microenvironment Activates GLI2 through
   HIF-1<i>α</i> and TGF-<i>β</i>2 to Promote Chemotherapy Resistance of
   Colorectal Cancer (Retracted Article)
SO COMPUTATIONAL AND MATHEMATICAL METHODS IN MEDICINE
LA English
DT Article; Retracted Publication
ID CELLS; CISPLATIN
AB Background. A majority of relapse cases have been reported in colorectal cancer patients due to cancer stem cell progenitors. The factors responsible for chemoresistance have yet to be discovered and investigated as CSCs have reported escaping from chemotherapy's killing action. Objective. In this study, we have investigated the effects of HIF-1 alpha and TGF-beta 2 in hypoxia conditions on the expression of GLI2, which is a potential factor for causing chemoresistance. Material and Methods. Colorectal samples of treated patients were collected from the Hospital Biological Sample Library. Culture of patient-derived TSs and fibroblasts was performed. The collected patient samples and cells were used for immunohistochemistry, quantitative PCR, and western blotting studies which were performed. Results. It was reported that HIF-1 alpha (hypoxia-inducible factor) and TGF-beta 2 secreted from cancer-associated fibroblasts (CAFs) synergistically work to express GLI2 in cancer stem cells. Hence, it increased the stemness as well as resistance to chemotherapy. Conclusion. The HIF-1 alpha/TGF-beta 2-mediated GLI2 signaling was responsible for causing chemoresistance in the hypoxia environment. High expressions of HIF1 alpha/TGF-beta 2/GLI2 cause the relapsing of colorectal cancer, thus making this a potential biomarker for identifying the relapse and resistance in patients. The study uncovers the mechanism involved in sternness and chemotherapy resistance which will help in targeted treatment.
C1 [Huang, Kun] Cent Hosp Jiangjin Dist, Dept Gen Surg, Chongqing, Peoples R China.
   [Zhang, Xin; Shu, Zhiwan] Qinghai Univ, Res Ctr Basic Med Sci, Coll Med, Xining, Peoples R China.
   [Hao, Yanhui] Qinghai Univ, Dept Radiat Oncol, Affiliated Hosp, Xining, Peoples R China.
   [Feng, Ruixing; Wang, Haojie] Qinghai Univ, Affiliated Hosp, Xining, Peoples R China.
   [Li, An] Xinxiang Med Coll, Zhengzhou Cent Hosp, Dept Neurol, Xinxiang, Peoples R China.
   [Du, Minghu] Wuwei City Peoples Hosp, Wuwei, Peoples R China.
C3 Qinghai University; Qinghai University; Qinghai University; Xinxiang
   Medical University
RP Du, MH (corresponding author), Wuwei City Peoples Hosp, Wuwei, Peoples R China.
EM 1013532486@qq.com; wangwangyt@yandex.ru; hyhlee@163.com;
   1311474058@qq.com; whj19805440916@163.com; shuzhiwan1120@163.com;
   la199581@163.com; dmtig1@163.com
RI Wang, Hesheng/P-3192-2015
FU Qinghai Provincial Health Commission [2020-wjzdx-50]
FX The authors gratefully acknowledge all individuals who participated in
   this study. This study was supported by the general guiding task of
   Qinghai Provincial Health Commission, "Comparison of SBRT and IMRT in
   Lung Oligometastatic of Colorectal Cancer" (number: 2020-wjzdx-50).
CR Choi JY, 2011, J BREAST CANCER, V14, P88, DOI 10.4048/jbc.2011.14.2.88
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NR 12
TC 12
Z9 12
U1 0
U2 3
PU HINDAWI LTD
PI LONDON
PA ADAM HOUSE, 3RD FLR, 1 FITZROY SQ, LONDON, W1T 5HF, ENGLAND
SN 1748-670X
EI 1748-6718
J9 COMPUT MATH METHOD M
JI Comput. Math. Method Med.
PD FEB 10
PY 2022
VL 2022
AR 2032895
DI 10.1155/2022/2032895
PG 7
WC Mathematical & Computational Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Mathematical & Computational Biology
GA 0A2SV
UT WOS:000773810700002
PM 35186110
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Kanat, O
   Ertas, H
   Caner, B
AF Kanat, Ozkan
   Ertas, Hulya
   Caner, Burcu
TI Dual HER2 inhibition strategies in the management of
   treatment-refractory metastatic colorectal cancer: History and status
SO WORLD JOURNAL OF CLINICAL CASES
LA English
DT Review
DE Epidermal growth factor receptor; Cetuximab; Panitumumab; Human
   epidermal growth factor receptor 2; Anti-epidermal growth factor
   receptor resistance; Trastuzumab; Dual inhibition
ID PLUS CETUXIMAB; RAS MUTATIONS; PHASE-II; OVEREXPRESSION; THERAPY; ERBB2;
   RESISTANCE; PREDICTOR; RECEPTORS; BENEFIT
AB Human epidermal growth factor receptor 2 (HER2) signaling pathway activation has been identified as a contributor to de novo or acquired resistance to epidermal growth factor receptor (EGFR) inhibitors in a small subset of patients with metastatic colorectal cancer (mCRC). Dual anti-HER2-targeted treatment exhibits strong antitumor activity in preclinical models of HER2-positive mCRC, supporting its testing in clinical trials. The HERACLES trial at four Italian academic cancer centers has confirmed the effectiveness of dual blockage of HER2 with trastuzumab plus lapatinib in patients with heavily pretreated HER2-positive mCRC, refractory to the anti-EGFR antibodies cetuximab or panitumumab. Here, we reviewed the preclinical studies exploring the role of HER2 signaling in the development of anti-EGFR therapy resistance and discussed the status of clinical trials assessing the activity of HER2 inhibitors in this setting.
C1 [Kanat, Ozkan; Ertas, Hulya; Caner, Burcu] Uludag Univ, Med Oncol, Fac Med, TR-16059 Bursa, Turkey.
C3 Uludag University
RP Kanat, O (corresponding author), Uludag Univ, Dept Med Oncol, Fac Med, TR-16059 Gorukle, Bursa, Turkey.
EM ozkanat@uludag.edu.tr
RI Caner, Burcu/AAE-8549-2022
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NR 47
TC 8
Z9 10
U1 0
U2 4
PU BAISHIDENG PUBLISHING GROUP INC
PI PLEASANTON
PA 7041 Koll Center Parkway, Suite 160, PLEASANTON, CA, UNITED STATES
SN 2307-8960
J9 WORLD J CLIN CASES
JI World J. Clin. Cases
PD OCT 6
PY 2018
VL 6
IS 11
BP 418
EP 425
DI 10.12998/wjcc.v6.i11.418
PG 8
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA GV0JE
UT WOS:000445745100003
PM 30294606
OA gold, Green Published, Green Submitted
DA 2025-01-04
ER

PT J
AU Yue, ZQ
   Zhu, Y
   Chen, T
   Feng, TT
   Zhou, Y
   Zhang, JJ
   Zhang, N
   Yang, J
   Luo, G
   Wang, ZH
AF Yue, Zhongqun
   Zhu, Yue
   Chen, Teng
   Feng, Tingting
   Zhou, Ying
   Zhang, Jiaojiao
   Zhang, Ning
   Yang, Jing
   Luo, Gang
   Wang, Zuhua
TI <i>Bletilla striata</i> polysaccharide-coated andrographolide
   nanomicelles for targeted drug delivery to enhance anti-colon cancer
   efficacy
SO FRONTIERS IN IMMUNOLOGY
LA English
DT Article
DE colon cancer; Bletilla striata polysaccharide; andrographolide; polymer;
   nano-micelle
ID IN-VIVO; NANOPARTICLES; MICELLES; TUMORS; THERAPY
AB Background: Vitamin E, which is also known as tocopherol, is a compound with a polyphenol structure. Its esterified derivative, Vitamin E succinate (VES), exhibits unique anticancer and healthcare functions as well as immunomodulatory effects. Natural polysaccharides are proved to be a promising material for nano-drug delivery systems, which show excellent biodegradability and biocompatibility. In this study, we employed a novel bletilla striata polysaccharide-vitamin E succinate polymer (BSP-VES) micelles to enhance the tumor targeting and anti-colon cancer effect of andrographolide (AG). Methods: BSP-VES polymer was synthesized through esterification and its structure was confirmed using 1H NMR. AG@BSP-VES was prepared via the dialysis method and the drug loading, entrapment efficiency, stability, and safety were assessed. Furthermore, the tumor targeting ability of AG@BSP-VES was evaluated through targeted cell uptake and in vivo imaging. The antitumor activity of AG@BSP-VES was measured in vitro using MTT assay, Live&Dead cell staining, and cell scratch test. Results: In this study, we successfully loaded AG into BSP-VES micelles (AG@BSP-VES), which exhibited good stability, biosafety and sustained release effect. In addition, AG@BSP-VES also showed excellent internalization capability into CT26 cells compared with NCM460 cells in vitro. Meanwhile, the specific delivery of AG@BSP-VES micelles into subcutaneous and in-situ colon tumors was observed compared with normal colon tissues in vivo during the whole experiment process (1-24 h). What's more, AG@BSP-VES micelles exhibited significant antitumor activities than BSP-VES micelles and free AG. Conclusion: The study provides a meaningful new idea and method for application in drug delivery system and targeted treatment of colon cancer based on natural polysaccharides.
C1 [Yue, Zhongqun; Zhu, Yue; Chen, Teng; Feng, Tingting; Zhou, Ying; Yang, Jing; Wang, Zuhua] Guizhou Univ Tradit Chinese Med, Coll Pharmaceut Sci, Guiyang 550025, Peoples R China.
   [Yue, Zhongqun; Zhu, Yue; Chen, Teng; Wang, Zuhua] Guizhou Univ Tradit Chinese Med, Nanodrug Technol Res Ctr, Guiyang 550025, Peoples R China.
   [Zhang, Jiaojiao] Zhejiang A&F Univ, Coll Food & Hlth, Hangzhou, Peoples R China.
   [Zhang, Ning] Guizhou Univ Tradit Chinese Med, Sch Acupuncture Moxibust & Tuina, Guiyang 550025, Peoples R China.
   [Luo, Gang] Guizhou Med Univ, Sch Basic Med Sci, Key Lab Med Microbiol & Parasitol, Minist Educ, Guiyang, Peoples R China.
   [Luo, Gang] Guizhou Med Univ, Sch Basic Med Sci, Key Lab Environm Pollut Monitoring & Dis Control, Minist Educ, Guiyang, Peoples R China.
C3 Guizhou University of Traditional Chinese Medicine; Guizhou University
   of Traditional Chinese Medicine; Zhejiang A&F University; Guizhou
   University of Traditional Chinese Medicine; Guizhou Medical University;
   Guizhou Medical University
RP Wang, ZH (corresponding author), Guizhou Univ Tradit Chinese Med, Coll Pharmaceut Sci, Guiyang 550025, Peoples R China.; Wang, ZH (corresponding author), Guizhou Univ Tradit Chinese Med, Nanodrug Technol Res Ctr, Guiyang 550025, Peoples R China.
EM wangrui551601@163.com
RI Wang, Zuhua/AAH-1549-2019; Zhang, Jiaojiao/AAN-1038-2020
FU National Natural Science Foundation of China [82360852, 81760643];
   Science and Technology Program of Guizhou Province (Qiankehe Basics) [ZK
   [2023] Key 046]; Guizhou Province Graduate Student Research Fund Project
   [[2021]166]; High-level Innovative Talents of Guizhou Province [[2023]
   047]; Natural Science Research Project of Guizhou Department of
   Education [[2023] 069]; Guizhou Province's 14th Five-Year Plan Key
   disciplines of Traditional Chinese Medicine and Ethnic Medicine
   [(JS)-2021-03]
FX The author(s) declare that financial support was received for the
   research, authorship, and/or publication of this article. The research
   was supported by grants from the National Natural Science Foundation of
   China (82360852, 81760643); Science and Technology Program of Guizhou
   Province (Qiankehe Basics ZK [2023] Key 046); Guizhou Province Graduate
   Student Research Fund Project (QiankeheYJSKYJJ[2021]166); High-level
   Innovative Talents of Guizhou Province (QianKeHe platform talents-GCC
   [2023] 047); Natural Science Research Project of Guizhou Department of
   Education (Qianjiaoji [2023] 069). The research was and technical
   supported by Guizhou Province's 14th Five-Year Plan Key disciplines of
   Traditional Chinese Medicine and Ethnic Medicine (QZYYZDXK(JS)-2021-03).
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NR 45
TC 1
Z9 1
U1 14
U2 14
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 1664-3224
J9 FRONT IMMUNOL
JI Front. Immunol.
PD JUN 7
PY 2024
VL 15
AR 1380229
DI 10.3389/fimmu.2024.1380229
PG 13
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA UY7V3
UT WOS:001251698700001
PM 38911867
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Shnaikat, SG
   Shakya, AK
   Bardaweel, SK
AF Shnaikat, Sewar G.
   Shakya, Ashok K.
   Bardaweel, Sanaa K.
TI Formulation, development and evaluation of hyaluronic acid-conjugated
   liposomal nanoparticles loaded with regorafenib and curcumin and their
   in vitro evaluation on colorectal cancer cell lines
SO SAUDI PHARMACEUTICAL JOURNAL
LA English
DT Article
DE Liposome; Hyaluronic acid; Regorafenib; Curcumin; CD44; Targeted drug
   delivery; Colorectal cancer
ID SENSITIVITY ASSAYS; COATED LIPOSOMES; PACLITAXEL; DELIVERY; DOXORUBICIN;
   EXTRUSION; BILAYERS; DESIGN; CD44
AB Colorectal cancer is one of the major causes of global cancer, with chemotherapy and radiation therapy being effective but limited due to low specificity. Regorafenib, a multikinase inhibitor, provides hope to patients with metastatic colorectal cancer and was approved by the FDA in 2012. However, due to resistance issues and adverse events, its efficacy is compromised, necessitating further refinement. Meanwhile, curcumin, a compound of turmeric, exhibits anticancer effects through antioxidant and anti-inflammatory actions, induction of the apoptosis, arrest of cell cycle, inhibition of angiogenesis, and modulation of signaling pathways. Unfortunately, its clinical utility is limited by its poor bioavailability, pointing towards innovative drug delivery strategies for enhanced efficacy in colorectal cancer treatment. Hyaluronic acid (HA)-decorated liposomes (LIPO) have been developed to target colorectal cells through an overexpressed CD44 receptor, increasing antitumor and antimetastasis efficacy. This study investigates the possibility of loading curcumin (CUR) or regorafenib (REGO) into a liposomal formulation for passive and HA- actively targeted treatment, evaluating its critical quality attributes (CQA) (size, zeta potential, polydispersity index) and cytotoxic activity in the HT29 colorectal cancer cell line. The average particle size of the plain liposomes and those decorated with HA was 144.00 f 0.78 nm and 140.77 f 1.64 nm, respectively. In contrast, curcumin-loaded plain liposomes and HA-decorated liposomes had 140 f 2.46 nm and 164.53 f 15.13 nm, respectively. The prepared liposomes had a spherical shape with a narrow size distribution and an acceptable zeta potential of less than-30 mV. The encapsulation efficiency was 99.2 % f 0.3 and 99.9 f 0.2 % for HA- decorated and bare regorafenib loaded. The % EE was 98.9 f 0.2 % and 97.5 f 0.2 % for bare liposomal nanoparticles loaded with curcumin and coated with curcumin. The IC50 50 of free REGO, CUR, REGO-LIPO, CURLIPO, REGO-LIPO-HA and CUR-LIPO-HA were 20.17 f 0.78, 64.4 f 0.33, 224.8 f 0.06, 49.66 f 0.22, 73.66 f 0.6, and 27.86 f 0.49 mu M, respectively. The MTT assay in HT29 cells showed significant cytotoxic activity of the HA-decorated liposomal formulation compared to the base uncoated formulation, indicating that hyaluronic acid-targeted liposomes loaded with regorafenib or curcumin could be a promising targeted formulation against colorectal cancer cells.
C1 [Shnaikat, Sewar G.; Shakya, Ashok K.] Al Ahliyya Amman Univ, Fac Pharm, Amman, Jordan.
   [Bardaweel, Sanaa K.] Univ Jordan, Sch Pharm, Amman, Jordan.
C3 Al-Ahliyya Amman University; University of Jordan
RP Shakya, AK (corresponding author), Al Ahliyya Amman Univ, Fac Pharm, Pharmacol & Diagnost Res Ctr, Amman, Jordan.
EM ak_shakya@ammanu.edu.jo
RI Shakya, Ashok/AEM-3853-2022; Shakya, Ashok K./A-8411-2015
OI G. shnaikat, sewar/0009-0004-2794-5968; Shakya, Ashok
   K./0000-0002-2387-6940
FU Deanship of Higher Education and Research, Al-Ahliyya Amman University,
   Amman, Jordan
FX This project was supported by Deanship of Higher Education and Research,
   Al-Ahliyya Amman University, Amman, Jordan.
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NR 71
TC 0
Z9 0
U1 2
U2 2
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
SN 1319-0164
EI 2213-7475
J9 SAUDI PHARM J
JI Saudi Pharm. J.
PD JUL
PY 2024
VL 32
IS 7
DI 10.1016/j.jsps.2024.102099
EA MAY 2024
PG 13
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA D8G7D
UT WOS:001298516800001
PM 38817822
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Khodarahmi, M
   Abbasi, H
   Kouchak, M
   Mahdavinia, M
   Handali, S
   Rahbar, N
AF Khodarahmi, Mohsen
   Abbasi, Hanieh
   Kouchak, Maryam
   Mahdavinia, Masoud
   Handali, Somayeh
   Rahbar, Nadereh
TI Nanoencapsulation of aptamer-functionalized 5-Fluorouracil liposomes
   using alginate/chitosan complex as a novel targeting strategy for
   colon-specific drug delivery
SO JOURNAL OF DRUG DELIVERY SCIENCE AND TECHNOLOGY
LA English
DT Article
DE Liposome; Nanocapsule; 5-Fluorouracil; Nucleolin aptamer; Colon targeted
   drug delivery; Sodium alginate/chitosan complex
ID ALGINATE-CARBOXYMETHYL CELLULOSE; ORGANOPHOSPHOROUS PESTICIDES; SOYBEAN
   PHOSPHATIDYLCHOLINE; CANCER CELLS; CHITOSAN; NANOPARTICLES; DESIGN;
   SYSTEMS; BEADS; WATER
AB Two important challenges in clinical application of 5-Fluorouracil (5-FU) in the treatment of colon cancer are preventing the release or degradation of the drug in the stomach/small intestine, and its delivering the colon as the site of action. The preparation of targeted liposomes using a suitable ligand and their encapsulation may be a promising method for the targeted treatment of colon cancer. The targeted liposomes were prepared by the optimized thin film method, and anti-nucleolin aptamer (AS1411) was used as the ligand. The nanocapsules were then prepared by coating of the synthesized liposomes with alginate and chitosan solution. The chemical structure, particle size and morphology of the liposomes and the nanocapsules were examined by Fourier transform infrared spectroscopy (FT-IR), dynamic light scattering (DLS), zeta potentiometer and field emission scanning electron microscopy (FESEM). MTT cytotoxicity studies were performed in vitro on the colon cancer cell line (HT-29). The liposomes and nanocapsules prepared were spherical with approximate sizes of 120 and 170 nm, respectively. The cytotoxicity studies on HT-29 cells showed that aptamer-conjugated liposomes induced significantly more cell death than aptamer-free liposomes and free drug. The results of the drug release experiments under simulated conditions including stomach, small intestine, and colon showed the excellent efficiency of the nanocapsules in releasing their cargo only under colonic condition.
C1 [Khodarahmi, Mohsen; Abbasi, Hanieh; Kouchak, Maryam; Rahbar, Nadereh] Ahvaz Jundishapur Univ Med Sci, Nanotechnol Res Ctr, Ahvaz, Iran.
   [Khodarahmi, Mohsen; Abbasi, Hanieh; Rahbar, Nadereh] Ahvaz Jundishapur Univ Med Sci, Sch Pharm, Dept Med Chem, Ahvaz, Iran.
   [Kouchak, Maryam] Ahvaz Jundishapur Univ Med Sci, Sch Pharm, Dept Pharmaceut, Ahvaz, Iran.
   [Mahdavinia, Masoud] Ahvaz Jundishapur Univ Med Sci, Toxicol Res Ctr, Ahvaz, Iran.
   [Mahdavinia, Masoud] Ahvaz Jundishapur Univ Med Sci, Sch Pharm, Dept Toxicol, Ahvaz, Iran.
   [Handali, Somayeh] Univ Tehran Med Sci, Med Biomat Res Ctr MBRC, Tehran, Iran.
C3 Ahvaz Jundishapur University of Medical Sciences (AJUMS); Ahvaz
   Jundishapur University of Medical Sciences (AJUMS); Ahvaz Jundishapur
   University of Medical Sciences (AJUMS); Ahvaz Jundishapur University of
   Medical Sciences (AJUMS); Ahvaz Jundishapur University of Medical
   Sciences (AJUMS); Tehran University of Medical Sciences
RP Abbasi, H (corresponding author), Ahvaz Jundishapur Univ Med Sci, Sch Pharm, Dept Med Chem, Ahvaz, Iran.; Rahbar, N (corresponding author), Ahvaz Jundishapur Univ Med Sci, Dept Med Chem, Ahvaz, Iran.
EM hanieabasi6@gmail.com; n_rahbar2001@yahoo.com
RI Mahdavinia, Masoud/AAB-7689-2020; Kouchak, Maryam/I-6546-2017; Rahbar,
   Nadereh/AAC-6684-2021; Mahdavinia, Masoud/ABB-9375-2020
OI Mahdavinia, Masoud/0000-0001-9448-1500
FU Nanotechnology Research Center; Research Council of Ahvaz Jundishapur
   University of Medical Sciences; Hanieh Abbasi's thesis [N-9802]; Mohsen
   Khodarahmi's thesis [N-9808]
FX The authors wish to thank for financial support of this research work
   provided by Nanotechnology Research Center and Research Council of Ahvaz
   Jundishapur University of Medical Sciences. This paper is extracted from
   Hanieh Abbasi's thesis (grant No. N-9802) and Mohsen Khodarahmi's thesis
   (grant No. N-9808). We are also especially grateful for the help of
   Professor Eskandar Moghimipour to provide some of the necessities of
   these projects.
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NR 86
TC 25
Z9 25
U1 1
U2 46
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
SN 1773-2247
EI 2588-8943
J9 J DRUG DELIV SCI TEC
JI J. Drug Deliv. Sci. Technol.
PD MAY
PY 2022
VL 71
AR 103299
DI 10.1016/j.jddst.2022.103299
EA APR 2022
PG 9
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA 1C1QL
UT WOS:000792902300003
DA 2025-01-04
ER

PT J
AU Dufraing, K
   Keppens, C
   Tack, V
   Siebers, AG
   Kafatos, G
   Dube, S
   Demonty, G
   Lowe, K
   Kroeze, LI
   Ligtenberg, M
   Normanno, N
   Tembuyser, L
   Sara, V
   van Krieken, JH
   Dequeker, EMC
AF Dufraing, Kelly
   Keppens, Cleo
   Tack, Veronique
   Siebers, Albert Gerrit
   Kafatos, George
   Dube, Sabada
   Demonty, Gaston
   Lowe, Kimberly
   Kroeze, Leonie Ilse
   Ligtenberg, Marjolijn
   Normanno, Nicola
   Tembuyser, Lien
   Sara, Vander Borght
   van Krieken, Joannes Henricus
   Dequeker, Elisabeth Marie C.
TI Evolution of <i>RAS</i> testing over time: factors influencing mutation
   rates in metastatic colorectal cancer patients
SO COLORECTAL CANCER
LA English
DT Article
DE biomarker analysis; colorectal cancer; external quality assessment;
   molecular pathology
ID 2ND-LINE TREATMENT; UPDATED ANALYSIS; KRAS MUTATIONS; PHASE-III;
   CETUXIMAB; PLUS; FLUOROURACIL; PANITUMUMAB; LEUCOVORIN; SURVIVAL
AB Aim: Correct identification of RAS gene variants is key for targeted treatment decisions in patients with metastatic colorectal cancer. Published RAS mutation rates differ and could be influenced by several factors including testing methods. This study aimed to describe the performance of laboratories to correctly identify RAS variants over time and to understand how RAS testing has evolved in Europe. Materials & methods: Misclassification and test failure rates were calculated and related to the used test methodology for 239 unique laboratories participating in external quality assessment for metastatic colorectal cancer between 2013 and 2018. In addition, 33 laboratories completed a survey aiming to obtain more details on their routine testing strategies, number of samples analyzed and RAS mutation rates between 2013 and 2017. Results: The mutation status was correctly analyzed in 96.1% (N = 5471) RAS and BRAF tests. A total of 4.6% (N = 2860) RAS tests included false-negative results. In 1.6% (N = 5562) RAS and BRAF tests, an analysis failure occurred. Misclassifications and technical failures both decreased between 2013 and 2018. The number of next-generation sequencing users increased from 6.9% (N = 130) in 2013 to 44.6% (N = 112) in 2018. Over time, more codons were included in the methodologies, yet 23.2% (N = 112) did not offer full RAS testing (exon 2, 3, 4) in 2018. Based on the survey the overall RAS mutation rate was estimated as 45.2% (N = 27,325). Conclusion: This is the largest observational study reporting RAS mutation rates to-date. There was no trend of RAS mutation rates over time despite having a clear shift to more sensitive tests and increased quality of testing.
C1 [Dufraing, Kelly; Keppens, Cleo; Tack, Veronique; Tembuyser, Lien; Dequeker, Elisabeth Marie C.] Univ Leuven, Dept Publ Hlth & Primary Care, Biomed Qual Assurance Res Unit, Leuven, Belgium.
   [Siebers, Albert Gerrit; Kroeze, Leonie Ilse; Ligtenberg, Marjolijn; van Krieken, Joannes Henricus] Radboud Univ Nijmegen, Dept Pathol, Med Ctr, Nijmegen, Netherlands.
   [Kafatos, George; Dube, Sabada] Amgen Ltd, Uxbridge, Middx, England.
   [Demonty, Gaston] Amgen Belgium SA NV, Brussels, Belgium.
   [Lowe, Kimberly] Amgen Inc, Thousand Oaks, CA 91320 USA.
   [Ligtenberg, Marjolijn] Radboud Univ Nijmegen, Dept Human Genet, Med Ctr, Nijmegen, Netherlands.
   [Normanno, Nicola] Ist Nazl Tumori Fdn Pascale, Cell Biol & Biotherapy Unit, Naples, Italy.
   [Sara, Vander Borght] Univ Hosp Leuven, Dept Pathol, Pathol Ontleedkunde, Leuven, Belgium.
C3 KU Leuven; Radboud University Nijmegen; Amgen; Amgen Limited; Amgen;
   Radboud University Nijmegen; IRCCS Fondazione Pascale; KU Leuven;
   University Hospital Leuven
RP Dequeker, EMC (corresponding author), Univ Leuven, Dept Publ Hlth & Primary Care, Biomed Qual Assurance Res Unit, Leuven, Belgium.
EM els.dequeker@kuleuven.be
RI Kroeze, Leonie/D-9673-2016; Ligtenberg, Marjolijn/N-9666-2013; Normanno,
   Nicola/AAT-1107-2021; Siebers, Albert/D-6300-2015; Siebers,
   Albert/H-6974-2015
OI Siebers, Albert/0000-0002-6085-0678; Dufraing,
   Kelly/0000-0002-0418-587X; Keppens, Cleo/0000-0002-4498-8386
FU Amgen Inc., Thousand Oaks, CA, USA; Amgen
FX This study was funded by a research grant from Amgen Inc., Thousand
   Oaks, CA 91320, USA (grant number not applicable). G Kafatos, G Demonty
   and K Lowe are employees and hold shares of Amgen, Sabada Dube is a
   former employee of Amgen. JH Van Krieken received research grant funding
   from Amgen. The authors have no other relevant affiliations or financial
   involvement with any organization or entity with a financial interest in
   or financial conflict with the subject matter or materials discussed in
   the manuscript apart from those disclosed.
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NR 37
TC 4
Z9 4
U1 0
U2 2
PU FUTURE MEDICINE LTD
PI LONDON
PA UNITEC HOUSE, 3RD FLOOR, 2 ALBERT PLACE, FINCHLEY CENTRAL, LONDON, N3
   1QB, ENGLAND
SN 1758-194X
EI 1758-1958
J9 COLORECTAL CANCER
JI Colorectal Cancer
PD MAR
PY 2020
VL 9
IS 1
AR CRC14
DI 10.2217/crc-2019-0013
PG 17
WC Oncology
WE Emerging Sources Citation Index (ESCI)
SC Oncology
GA LL9NS
UT WOS:000531882100001
OA gold, Green Submitted
DA 2025-01-04
ER

PT J
AU Schwartzberg, L
   Daniel, D
   Vaena, D
   Slater, D
   Staszewski, H
   Fang, BN
   Seneviratne, L
   Yu, ELE
   Price, R
   Szado, T
   Meyer, CS
   Shah, AN
   Ma, ES
AF Schwartzberg, Lee
   Daniel, Davey
   Vaena, Daniel
   Slater, Dennis
   Staszewski, Harry
   Fang, Bruno
   Seneviratne, Lasika
   Yu, Elaine
   Price, Richard
   Szado, Tania
   Meyer, Craig S.
   Shah, Anuj
   Ma, Esprit
TI Improving biomarker testing in advanced non-small-cell lung cancer and
   metastatic colorectal cancer: experience from a large community oncology
   network in the USA
SO FUTURE ONCOLOGY
LA English
DT Article
DE biomarkers; breast cancer; community practices; NSCLC; oncology;
   real-world data
AB Plain language summary - Improving biomarker testing in advanced non-small-cell lung cancer and metastatic colorectal cancer: experience from a large community oncology network in the USA What is this article about?Cancer therapies often work better in certain subgroups of patients. Tumors may have characteristics that can predict which therapies may be more likely to work. These cancer biomarkers may be identified by special testing, such as next-generation sequencing (NGS). If a biomarker is detected, the patient can potentially be treated with medicine that targets that biomarker. This study looked at biomarker testing of lung and colon cancers in two community cancer practices (OneOncology [OneOnc] and nationwide database [NAT]). What were the results?The biomarker testing rates were high (>= 81%) and similar between OneOnc and NAT. NGS testing rates were higher at OneOnc than at NAT (58 vs 49% for NSCLC, 55 vs 42% for metastatic colorectal cancer [mCRC]), suggesting the success of OneOnc's networkwide educational, pathway and operational programs. NGS testing was lower in community practices due to operational challenges and insufficient tissue collection. Patients who had NGS versus other biomarker testing were more likely to receive treatment specifically for that biomarker. However, some patients started treatment before their biomarker results were reported, usually because of their disease and a long wait time for biomarker test results. What do the results of the study mean?Community cancer centers can treat patients with targeted medicine based on biomarker testing results. There are opportunities to increase the number of patients getting NGS testing, shorten turnaround times and reduce the number of patients who start treatment before getting their biomarker test results.
   Tweetable abstractCommunity cancer centers deliver biomarker testing to inform 1L targeted treatment for the actionable oncogene mutations detected in aNSCLC and mCRC. Higher NGS testing rates at OneOnc versus Flatiron Health reflect the success of OneOnc's educational and operational initiatives.
   Aim: Biomarker testing detects actionable driver mutations to inform first-line treatment in advanced non-small-cell lung cancer (aNSCLC) and metastatic colorectal cancer (mCRC). This study evaluated biomarker testing in a nationwide database (NAT) versus the OneOncology (OneOnc) community network. Patients & methods: Patients with aNSCLC or mCRC with >= 1 biomarker test in a de-identified electronic health record-derived database were evaluated. OneOnc oncologists were surveyed. Results: Biomarker testing rates were high and comparable between OneOnc and NAT; next-generation sequencing (NGS) rates were higher at OneOnc. Patients with NGS versus other biomarker testing were more likely to receive targeted treatment. Operational challenges and insufficient tissue were barriers to NGS testing. Conclusion: Community cancer centers delivered personalized healthcare through biomarker testing.
C1 [Schwartzberg, Lee] Renown Hlth Inst Canc, Reno, NV 89502 USA.
   [Schwartzberg, Lee; Daniel, Davey; Vaena, Daniel; Slater, Dennis; Staszewski, Harry; Fang, Bruno; Seneviratne, Lasika] OneOncology Inc, Nashville, TN 37219 USA.
   [Daniel, Davey] Tennessee Oncol, Nashville, TN 37203 USA.
   [Vaena, Daniel] West Canc Ctr & Res Inst, Germantown, TN 38138 USA.
   [Slater, Dennis] Eastern Connecticut Hematol & Oncol, Norwich, CT 06360 USA.
   [Staszewski, Harry] New York Canc & Blood Specialists, Port Jefferson Stn, NY 11776 USA.
   [Fang, Bruno] Astera Canc Care, East Brunswick, NJ 08816 USA.
   [Seneviratne, Lasika] Los Angeles Canc Network, Los Angeles, CA 90017 USA.
   [Yu, Elaine; Price, Richard; Szado, Tania; Ma, Esprit] Genentech Inc, South San Francisco, CA 94080 USA.
   [Meyer, Craig S.] Janssen Pharmaceut Johnson & Johnson, South San Francisco, CA 94080 USA.
   [Shah, Anuj] Gilead Sci Inc, Foster City, CA 94404 USA.
C3 Tennessee Oncology; Roche Holding; Genentech; Johnson & Johnson; Janssen
   Pharmaceuticals; Gilead Sciences
RP Schwartzberg, L (corresponding author), Renown Hlth Inst Canc, Reno, NV 89502 USA.; Schwartzberg, L (corresponding author), OneOncology Inc, Nashville, TN 37219 USA.
EM Lee.Schwartzberg@renown.org
OI , Harry Staszewski/0009-0005-2559-1315; Schwartzberg,
   Lee/0000-0002-7433-3428
CR Aisner DL, 2021, J NATL COMPR CANC NE, V19, P610, DOI 10.6004/jnccn.2021.5020
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   [Anonymous], 2023, NCCN CLIN PRACTICE G
   [Anonymous], 2013, R LANG ENV STAT COMP
   Birnbaum B., 2020, ARXIV
   Bruno DS, 2022, JCO PRECIS ONCOL, V6, DOI 10.1200/PO.21.00427
   Centers for Medicare & Medicaid Services, 2020, NAT COV AN NCA NEXT
   Centers for Medicare & Medicaid Services, NAT COV DET NCD NEXT
   Chakravarty D, 2022, J CLIN ONCOL, V40, P1231, DOI 10.1200/JCO.21.02767
   Cobain EF, 2021, JAMA ONCOL, V7, P525, DOI 10.1001/jamaoncol.2020.7987
   Freedman AN, 2018, JCO PRECIS ONCOL, V2, DOI 10.1200/PO.18.00169
   John A, 2020, ONCOLOGIST, V25, pE1743, DOI 10.1634/theoncologist.2019-0864
   Lim W, 2018, QUANT IMAG MED SURG, V8, P709, DOI 10.21037/qims.2018.08.02
   Lindeman NI, 2018, J MOL DIAGN, V20, P129, DOI [10.1016/j.jmoldx.2017.11.004, 10.5858/arpa.2017-0388-CP, 10.1016/j.jtho.2017.12.001]
   Ma X., 2020, medRxiv, DOI DOI 10.1101/2020.03.16.20037143
   Malone ER, 2020, GENOME MED, V12, DOI 10.1186/s13073-019-0703-1
   Miller TE, 2018, J CLIN PATHOL, V71, P1108, DOI 10.1136/jclinpath-2018-205396
   Robert NJ, 2022, LUNG CANCER, V166, P197, DOI 10.1016/j.lungcan.2022.03.004
   Sheinson D, 2020, LUNG CANCER, V143, P86, DOI 10.1016/j.lungcan.2020.03.005
   Sheinson DM, 2021, JAMA NETW OPEN, V4, DOI 10.1001/jamanetworkopen.2021.38219
   Smith RE., 2022, J CLIN ONCOL, V60
   Unger JM, 2019, JNCI-J NATL CANCER I, V111, P245, DOI 10.1093/jnci/djy221
NR 22
TC 0
Z9 0
U1 1
U2 1
PU TAYLOR & FRANCIS LTD
PI ABINGDON
PA 2-4 PARK SQUARE, MILTON PARK, ABINGDON OR14 4RN, OXON, ENGLAND
SN 1479-6694
EI 1744-8301
J9 FUTURE ONCOL
JI Future Oncol.
PD JUN
PY 2023
VL 19
IS 20
BP 1397
EP 1414
DI 10.2217/fon-2022-1216
EA JUN 2023
PG 18
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA O3BL9
UT WOS:001006229600001
PM 37318757
OA hybrid
DA 2025-01-04
ER

PT J
AU De Luca, C
   Vigliar, E
   d'Anna, M
   Pisapia, P
   Bellevicine, C
   Malapelle, U
   Troncone, G
AF De Luca, Caterina
   Vigliar, Elena
   d'Anna, Melania
   Pisapia, Pasquale
   Bellevicine, Claudio
   Malapelle, Umberto
   Troncone, Giancarlo
TI <i>KRAS</i> detection on archival cytological smears by the novel fully
   automated polymerase chain reaction-based Idylla mutation test
SO CYTOJOURNAL
LA English
DT Article
DE Aspiration cytology; Idylla; KRAS; molecular pathology
ID COLORECTAL-CANCER; LUNG-CANCER; EGFR; SPECIMENS
AB Background: Molecular techniques are relevant to modern cytopathology, but their implementation is difficult without molecular expertise and infrastructure. The assessment of KRAS mutational status on cytological preparations may be useful either to refine uncertain diagnoses on pancreatic aspirates or to yield predictive information to plan targeted treatment of metastatic colorectal cancer (mCRC). The novel test Idylla T enables fully automated KRAS genotyping in approximately 2 h, even in less experienced hands. Materials and Methods: This study aims to validate this methodology to detect KRAS mutations on archival cytological preparations of pancreatic cancer (n = 9) and mCRC (n = 9) by comparing the Idylla T performance to that of standard real-time polymerase chain reaction. Results: The same 11 mutations (n = 4: p. G12D; n = 2: p. G12V; n = 2: p. A59E/ G/ T; n = 1: p. G12R; n = 1: p. G13D; n = 1: p. Q61H) were detected by both techniques. Conclusion: Even in less experienced laboratories, a cytopathologist may easily integrate morphological diagnostic report with accurate KRAS mutation detection, which is relevant for diagnostic and treatment decisions.
C1 [De Luca, Caterina; Vigliar, Elena; d'Anna, Melania; Pisapia, Pasquale; Bellevicine, Claudio; Malapelle, Umberto; Troncone, Giancarlo] Univ Naples Federico II, Dept Publ Hlth, Naples, Italy.
C3 University of Naples Federico II
RP Troncone, G (corresponding author), Univ Naples Federico II, Dept Publ Hlth, Naples, Italy.
EM caterideluca@libero.it; elena@vigliar.it; melaniadanna63@gmail.com;
   pasqualepisapia89@gmail.com; claudio.bellevicine@unina.it;
   umberto.malapelle@unina.it; giancarlo.troncone@unina.it
RI Vigliar, Elena/L-2174-2019; Pisapia, Pasquale/L-7473-2019; Bellevicine,
   Claudio/K-8189-2016; De Luca, Caterina/AAZ-1837-2021
OI De Luca, Caterina/0000-0002-6932-763X; Bellevicine,
   Claudio/0000-0002-7479-6457; Malapelle, Umberto/0000-0003-3211-9957;
   Vigliar, Elena/0000-0003-2856-9023; Pisapia,
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NR 17
TC 9
Z9 9
U1 0
U2 2
PU MEDKNOW PUBLICATIONS & MEDIA PVT LTD
PI MUMBAI
PA B-9, KANARA BUSINESS CENTRE, OFF LINK RD, GHAKTOPAR-E, MUMBAI, 400075,
   INDIA
SN 0974-5963
EI 1742-6413
J9 CYTOJOURNAL
JI CytoJournal
PD FEB 24
PY 2017
VL 13
DI 10.4103/1742-6413.200936of
PG 5
WC Pathology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pathology
GA ES6NJ
UT WOS:000399664900003
PM 28331530
DA 2025-01-04
ER

PT J
AU Taman, H
   Fenton, CG
   Anderssen, E
   Florholmen, J
   Paulssen, RH
AF Taman, Hagar
   Fenton, Christopher G.
   Anderssen, Endre
   Florholmen, Jon
   Paulssen, Ruth H.
TI DNA hypo-methylation facilitates anti-inflammatory responses in severe
   ulcerative colitis
SO PLOS ONE
LA English
DT Article
ID T-CELLS; CPG ISLANDS; INTERLEUKIN-10; INFLAMMASOME; RECEPTOR; IL-10;
   HYPOMETHYLATION; ASSOCIATION; SECRETION; GUT
AB Severe ulcerative colitis (UC) is a potentially life-threatening disease with a potential colorectal cancer (CRC) risk. The aim of this study was to explore the relationship between transcriptomic and genome-wide DNA methylation profiles in a well-stratified, treatment-naive severe UC patient population in order to define specific epigenetic changes that could be responsible for the grade of disease severity. Mucosal biopsies from treatment-naive severe UC patients (n = 8), treatment-naive mild UC (n = 8), and healthy controls (n = 8) underwent both whole transcriptome RNA-Seq and genome-wide DNA bisulfite- sequencing, and principal component analysis (PCA), cell deconvolutions and diverse statistical methods were applied to obtain a dataset of significantly differentially expressed genes (DEGs) with correlation to DNA methylation for severe UC. DNA hypo-methylation correlated with approximately 80% of all DEGs in severe UC when compared to mild UC. Enriched pathways of annotated hypo-methylated genes revealed neutrophil degranulation, and immuno-regulatory interactions of the lymphoid system. Specifically, hypo-methylated anti-inflammatory genes found for severe UC were IL10, SIGLEC5, CD86, CLMP and members of inflammasomes NLRP3 and NLRC4. Hypo-methylation of anti-inflammatory genes during severe UC implies an interplay between the epithelium and lamina propria in order to mitigate inflammation in the gut. The specifically DNA hypo-methylated genes found for severe UC can potentially be useful biomarkers for determining disease severity and in the development of new targeted treatment strategies for severe UC patients.
C1 [Taman, Hagar; Paulssen, Ruth H.] UiT Arctic Univ Norway, Clin Bioinformat Res Grp, Dept Clin Med, Tromso, Norway.
   [Taman, Hagar; Fenton, Christopher G.; Anderssen, Endre; Paulssen, Ruth H.] UiT Arctic Univ Norway, Genom Support Ctr Tromso GSCT, Dept Clin Med, Tromso, Norway.
   [Florholmen, Jon] UiT Arctic Univ Norway, Gastroenterol & Nutr Res Grp, Dept Clin Med, Tromso, Norway.
C3 UiT The Arctic University of Tromso; UiT The Arctic University of
   Tromso; UiT The Arctic University of Tromso
RP Paulssen, RH (corresponding author), UiT Arctic Univ Norway, Clin Bioinformat Res Grp, Dept Clin Med, Tromso, Norway.; Paulssen, RH (corresponding author), UiT Arctic Univ Norway, Genom Support Ctr Tromso GSCT, Dept Clin Med, Tromso, Norway.
EM ruth.h.paulssen@uit.no
FU Northern Norway Regional Health Authority HelseNord [SFP-1209-14]
FX THis work was supported by the Northern Norway Regional Health Authority
   HelseNord (SFP-1209-14).s
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NR 60
TC 9
Z9 9
U1 0
U2 6
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD APR 1
PY 2021
VL 16
IS 4
AR e0248905
DI 10.1371/journal.pone.0248905
PG 17
WC Multidisciplinary Sciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Science & Technology - Other Topics
GA RH8NB
UT WOS:000636467000106
PM 33793617
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Price, T
   Ang, A
   Boedigheimer, M
   Kim, TW
   Li, J
   Cascinu, S
   Ruff, P
   Suresh, AS
   Thomas, A
   Tjulandin, S
   Peeters, M
AF Price, Timothy
   Ang, Agnes
   Boedigheimer, Michael
   Kim, Tae Won
   Li, Jin
   Cascinu, Stefano
   Ruff, Paul
   Suresh, Attili Satya
   Thomas, Anne
   Tjulandin, Sergei
   Peeters, Marc
TI Frequency of S492R mutations in the epidermal growth factor receptor:
   analysis of plasma DNA from patients with metastatic colorectal cancer
   treated with panitumumab or cetuximab monotherapy
SO CANCER BIOLOGY & THERAPY
LA English
DT Article
DE Colorectal cancer; gene mutations; resistance; cetuximab; panitumumab;
   anti-epidermal growth factor receptor
ID RAS MUTATIONS; RESISTANCE; CARCINOMA
AB Background Antibodies against epidermal growth factor receptor (EGFR), panitumumab, a fully human monoclonal antibody, and cetuximab, a human/mouse chimeric monoclonal antibody, have shown clinical efficacy in metastatic colorectal cancer (mCRC). In the phase 3 noninferiority ASPECCT (ClinicalTrials.gov, NCT01001377) study, panitumumab was demonstrated to be noninferior to cetuximab and provided a similar overall survival benefit for patients with chemotherapy-refractory wild-typeKRASexon 2 mCRC. However, some patients eventually develop resistance to anti-EGFR therapy. EGFR p.S492R mutation was previously identified as conferring resistance to cetuximab, but not to panitumumab. Methods This biomarker study analyzed plasma samples from ASPECCT collected at both baseline and posttreatment. Results No EGFR p.S492R mutations were identified at baseline; however, after treatment the EGFR p.S492R mutation was detected in 1% of patients treated with panitumumab versus 16% of those treated with cetuximab, supporting that, in a large population, this mutation is more likely to be induced by cetuximab than by panitumumab. There were, however, no significant differences in progression-free survival or overall survival between patients who were wild-type compared with those with the S492R mutation within the cetuximab arm or the overall population. Conclusions These results may support targeting treatment to small patient subgroups based on the presence of emerging EGFR mutations and provide a molecular rationale for rechallenging with a different anti-EGFR agent in patients who develop resistance. Prospective studies are needed to evaluate the efficacy of panitumumab in the EGFR p.S492R mutant population.
C1 [Price, Timothy] Queen Elizabeth Hosp, Clin Oncol Res Dept, Woodville, SA, Australia.
   [Price, Timothy] Univ Adelaide, Haematol & Med Oncol Serv Dept, Woodville, SA, Australia.
   [Ang, Agnes; Boedigheimer, Michael] Amgen Inc, Clin Biomarkers, Thousand Oaks, CA USA.
   [Kim, Tae Won] Univ Ulsan, Asan Med Ctr, Dept Oncol, Coll Med, Seoul, South Korea.
   [Li, Jin] Tongji Univ, Dept Oncol, East Hosp, Shanghai, Peoples R China.
   [Cascinu, Stefano] Univ Politecn Marche, Dept Med Oncol, Ancona, Italy.
   [Ruff, Paul] Univ Witwatersrand, Fac Hlth Sci, Johannesburg, South Africa.
   [Suresh, Attili Satya] Apollo Hosp, Dept Med Oncol, Hyderabad, India.
   [Thomas, Anne] Univ Leicester, Dept Oncol, Leicester, Leics, England.
   [Tjulandin, Sergei] NN Blokhin Canc Res Ctr Rams, Dept Clin Pharmacol & Chemotherapy, Moscow, Russia.
   [Peeters, Marc] Antwerp Univ Hosp, Dept Oncol, Edegem, Belgium.
C3 University of Adelaide; Amgen; University of Ulsan; Asan Medical Center;
   Tongji University; Marche Polytechnic University; University of
   Witwatersrand; University of Leicester; Russian Academy of Medical
   Sciences; N.N. Blokhin Russian Cancer Research Center; University of
   Antwerp
RP Price, T (corresponding author), Queen Elizabeth Hosp, Adelaide, SA 5011, Australia.
EM Timothy.Price@sa.gov.au
RI Peeters, Marc/C-5525-2013; Price, Timothy/AFN-1360-2022; Wang,
   Jie/H-3638-2015; Kim, Tae Won/GRX-7323-2022; Price, Timothy/G-1404-2012
OI Thomas, Anne/0000-0003-1998-3134; Price, Timothy/0000-0002-3922-2693
FU Amgen Inc.
FX This work was supported by the Amgen Inc.
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NR 27
TC 17
Z9 17
U1 0
U2 4
PU TAYLOR & FRANCIS INC
PI PHILADELPHIA
PA 530 WALNUT STREET, STE 850, PHILADELPHIA, PA 19106 USA
SN 1538-4047
EI 1555-8576
J9 CANCER BIOL THER
JI Cancer Biol. Ther.
PD OCT 2
PY 2020
VL 21
IS 10
BP 891
EP 898
DI 10.1080/15384047.2020.1798695
EA OCT 2020
PG 8
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA OD5HV
UT WOS:000575984700001
PM 33026965
OA Green Published, hybrid
DA 2025-01-04
ER

PT J
AU Zhang, YH
   Li, Y
   Wang, QY
   Su, B
   Xu, H
   Sun, Y
   Sun, P
   Li, RM
   Peng, XC
   Cai, J
AF Zhang, Yanhua
   Li, Yue
   Wang, Quanyue
   Su, Bo
   Xu, Hui
   Sun, Yang
   Sun, Pei
   Li, Rumeng
   Peng, Xiaochun
   Cai, Jun
TI Role of RASA1 in cancer: A review and update
SO ONCOLOGY REPORTS
LA English
DT Review
DE tumour; Ras p21 protein activator 1; microRNA; Ras; therapy
ID SQUAMOUS-CELL CARCINOMA; GTPASE-ACTIVATING PROTEIN-1; LUNG-CANCER;
   CAPILLARY MALFORMATION; MESSENGER-RNA; BREAST-CANCER; NEURONAL
   APOPTOSIS; COLORECTAL-CANCER; REGULATES RASA1; TARGETING RASA1
AB Ras p21 protein activator 1 (RASA1) is a regulator of Ras GDP and GTP and is involved in numerous physiological processes such as angiogenesis, cell proliferation, and apoptosis. As a result, RASA1 also contributes to pathological processes in vascular diseases and tumour formation. This review focuses on the role of RASA1 in multiple tumours types in the lung, intestines, liver, and breast. Furthermore, we discuss the potential mechanisms of RASA1 and its downstream effects through Ras/RAF/MEK/ERK or Ras/PI3K/AKT signalling. Moreover, miRNAs are capable of regulating RASA1 and could be a novel targeted treatment strategy for tumours.
C1 [Zhang, Yanhua; Li, Yue; Xu, Hui; Sun, Yang; Cai, Jun] Yangtze Univ, Dept Oncol, Affiliated Hosp 1, 1 Nanhuan Rd, Jingzhou 434023, Hubei, Peoples R China.
   [Wang, Quanyue] Qinghai Inst Hlth Sci, Xining 810000, Qinghai, Peoples R China.
   [Su, Bo; Sun, Pei; Li, Rumeng; Peng, Xiaochun] Yangtze Univ, Ctr Mol Med, Lab Oncol, Jingzhou 434023, Hubei, Peoples R China.
   [Su, Bo] Yangtze Univ, Hlth Sci Ctr, Sch Basic Med, Dept Pathol, Jingzhou 434023, Hubei, Peoples R China.
   [Peng, Xiaochun] Yangtze Univ, Hlth Sci Ctr, Sch Basic Med, Dept Pathophysiol, 1 Nanhuan Rd, Jingzhou 434023, Hubei, Peoples R China.
C3 Yangtze University; Yangtze University; Yangtze University; Yangtze
   University
RP Cai, J (corresponding author), Yangtze Univ, Dept Oncol, Affiliated Hosp 1, 1 Nanhuan Rd, Jingzhou 434023, Hubei, Peoples R China.; Peng, XC (corresponding author), Yangtze Univ, Hlth Sci Ctr, Sch Basic Med, Dept Pathophysiol, 1 Nanhuan Rd, Jingzhou 434023, Hubei, Peoples R China.
EM pxcwd789@sina.com; 529369023@qq.com
RI peng, xiaochun/HJI-4832-2023
FU Nature Science Foundation of Hubei Province [2017CFB786]; Hubei Province
   Health and Family Planning Scientific Research Project [WJ2016Y10];
   Jingzhou Science and Technology Bureau Project [2017-93]; National
   innovation and entrepreneurship training program for College Students
   [202010489017]
FX The present study was supported by the Nature Science Foundation of
   Hubei Province (grant no. 2017CFB786), the Hubei Province Health and
   Family Planning Scientific Research Project (grant no. WJ2016Y10), the
   Jingzhou Science and Technology Bureau Project (grant no. 2017-93), and
   the National innovation and entrepreneurship training program for
   College Students (grant no. 202010489017). All funding was provided to
   XP.
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NR 127
TC 37
Z9 39
U1 2
U2 21
PU SPANDIDOS PUBL LTD
PI ATHENS
PA POB 18179, ATHENS, 116 10, GREECE
SN 1021-335X
EI 1791-2431
J9 ONCOL REP
JI Oncol. Rep.
PD DEC
PY 2020
VL 44
IS 6
BP 2386
EP 2396
DI 10.3892/or.2020.7807
PG 11
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA OZ9RZ
UT WOS:000595257400007
PM 33125148
OA hybrid, Green Published
DA 2025-01-04
ER

PT J
AU Fleming, K
   McGuinness, J
   Kipgen, D
   Glen, H
   Spiliopoulou, P
AF Fleming, Kathryn
   McGuinness, James
   Kipgen, David
   Glen, Hilary
   Spiliopoulou, Pavlina
TI A Case of Lenvatinib-Induced Focal Segmental Glomerulosclerosis (FSGS)
   in Metastatic Medullary Thyroid Cancer
SO CASE REPORTS IN ONCOLOGICAL MEDICINE
LA English
DT Article
ID ENDOTHELIAL GROWTH-FACTOR; TYROSINE KINASE INHIBITOR; COLORECTAL-CANCER;
   INTERSTITIAL NEPHRITIS; VEGF INHIBITION; PHASE-I; E7080; PLACEBO;
   CHEMOTHERAPY; REGORAFENIB
AB We describe a case of lenvatinib (E7080) associated focal segmental glomerulosclerosis (FSGS) encountered during the treatment of metastatic medullary thyroid cancer. Proteinuria is a relatively common side effect of VEGF-targeted treatments and can occasionally result in treatment discontinuation. Here, we describe a patient who developed secondary FSGS necessitating discontinuation of treatment at first but who was subsequently rechallenged with anti-VEGF-targeted treatment without recurrence of proteinuria. Lenvatinib was a novel experimental agent at the time the treatment took place; however, its recent licensing for the treatment of thyroid malignancies in the UK makes reporting of these adverse effects all the more important now.
C1 [Fleming, Kathryn; McGuinness, James; Glen, Hilary; Spiliopoulou, Pavlina] Beatson West Scotland Canc Ctr BWoSCC, Glasgow, Lanark, Scotland.
   [Kipgen, David] Queen Elizabeth Univ Hosp, Glasgow, Lanark, Scotland.
   [Spiliopoulou, Pavlina] Imperial Coll London, Hammersmith Hosp, London, England.
C3 Beatson Oncology Centre; Queen Elizabeth University Hospital (QEUH);
   Imperial College London
RP Spiliopoulou, P (corresponding author), Beatson West Scotland Canc Ctr BWoSCC, Glasgow, Lanark, Scotland.; Spiliopoulou, P (corresponding author), Imperial Coll London, Hammersmith Hosp, London, England.
EM p.spiliopoulou@imperial.ac.uk
RI Kipgen, David/T-6014-2019
OI Fleming, Kathryn/0000-0003-1737-6840; Spiliopoulou,
   Pavlina/0000-0002-6486-6319; Kipgen, David/0000-0002-0339-9921
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NR 41
TC 5
Z9 6
U1 0
U2 1
PU HINDAWI LTD
PI LONDON
PA ADAM HOUSE, 3RD FLR, 1 FITZROY SQ, LONDON, W1T 5HF, ENGLAND
SN 2090-6706
EI 2090-6714
J9 CASE REP ONCOL MED
JI Case Rep. Oncol. Med.
PY 2018
VL 2018
AR 6927639
DI 10.1155/2018/6927639
PG 6
WC Oncology
WE Emerging Sources Citation Index (ESCI)
SC Oncology
GA GX2GX
UT WOS:000447538100001
PM 30402314
OA Green Published, Green Submitted, Green Accepted, gold
DA 2025-01-04
ER

PT J
AU Battaglin, F
   Lenz, HJ
AF Battaglin, Francesca
   Lenz, Heinz-Josef
TI Clinical Applications of Circulating Tumor DNA Profiling in GI Cancers
SO JCO ONCOLOGY PRACTICE
LA English
DT Review
ID CELL-FREE DNA; ACQUIRED-RESISTANCE; COLORECTAL-CANCER; RAS MUTATIONS;
   LIQUID BIOPSY; PLASMA; THERAPY; BIOMARKER; MARKER; CHEMOTHERAPY
AB Over the next few years, the analysis of circulating tumor DNA (ctDNA) through liquid biopsy is expected to enter clinical practice and revolutionize the approach to biomarker testing and treatment selection in GI cancers. In fact, growing evidence support the use of ctDNA testing as a noninvasive, effective, and highly specific tool for molecular profiling in GI cancers. Analysis of blood ctDNA has been investigated in multiple settings including early tumor detection, minimal residual disease evaluation, tumor diagnosis and evaluation of prognostic/predictive biomarkers for targeted treatment selection, longitudinal monitoring of treatment response, and identification of resistance mechanisms. Here, we review the clinical applications, advantages, and limitations of ctDNA profiling for precision oncology in GI cancers.
C1 [Battaglin, Francesca; Lenz, Heinz-Josef] Univ Southern Calif, Keck Sch Med, Norris Comprehens Canc Ctr, Los Angeles, CA 90089 USA.
C3 University of Southern California
RP Lenz, HJ (corresponding author), Univ Southern Calif, Keck Sch Med, Norris Comprehens Canc Ctr, Los Angeles, CA 90089 USA.
EM lenz@med.usc.edu
RI Battaglin, Francesca/C-2746-2017
FU National Cancer Institute of the National Institutes of Health
   [P30CA014089]; Gloria Borges WunderGlo Foundation; Dhont Family
   Foundation; Victoria and Philip Wilson Research Fund; San Pedro
   Peninsula Cancer Guild; Ming Hsieh Research; Daniel Butler Research Fund
FX Supported in part by the National Cancer Institute of the National
   Institutes of Health under Award Number P30CA014089 (to H.-J.L.), the
   Gloria Borges WunderGlo Foundation, the Dhont Family Foundation, the
   Victoria and Philip Wilson Research Fund, the San Pedro Peninsula Cancer
   Guild, the Ming Hsieh Research and the Daniel Butler Research Fund. The
   content is solely the responsibility of the authors and does not
   necessarily represent the official views of the National Institutes of
   Health.
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NR 117
TC 1
Z9 1
U1 1
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 2688-1527
EI 2688-1535
J9 JCO ONCOL PRACT
JI JCO Oncol. Pract.
PD NOV
PY 2024
VL 20
IS 11
DI 10.1200/OP.24.00167
PG 11
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA O4M2Y
UT WOS:001370883000009
PM 39531845
DA 2025-01-04
ER

PT J
AU Hamblin, A
   Wordsworth, S
   Fermont, JM
   Page, S
   Kaur, K
   Camps, C
   Kaisaki, P
   Gupta, A
   Talbot, D
   Middleton, M
   Henderson, S
   Cutts, A
   Vavoulis, DV
   Housby, N
   Tomlinson, I
   Taylor, JC
   Schuh, A
AF Hamblin, Angela
   Wordsworth, Sarah
   Fermont, Jilles M.
   Page, Suzanne
   Kaur, Kulvinder
   Camps, Carme
   Kaisaki, Pamela
   Gupta, Avinash
   Talbot, Denis
   Middleton, Mark
   Henderson, Shirley
   Cutts, Anthony
   Vavoulis, Dimitrios V.
   Housby, Nick
   Tomlinson, Ian
   Taylor, Jenny C.
   Schuh, Anna
TI Clinical applicability and cost of a 46-gene panel for genomic analysis
   of solid tumours: Retrospective validation and prospective audit in the
   UK National Health Service
SO PLOS MEDICINE
LA English
DT Article
ID CELL LUNG-CANCER; 1ST-LINE TREATMENT; OPEN-LABEL; COLORECTAL-CANCER;
   PHASE-III; MUTATION; EGFR; RESISTANCE; CETUXIMAB; MELANOMA
AB Background
   Single gene tests to predict whether cancers respond to specific targeted therapies are performed increasingly often. Advances in sequencing technology, collectively referred to as next generation sequencing (NGS), mean the entire cancer genome or parts of it can now be sequenced at speed with increased depth and sensitivity. However, translation of NGS into routine cancer care has been slow. Healthcare stakeholders are unclear about the clinical utility of NGS and are concerned it could be an expensive addition to cancer diagnostics, rather than an affordable alternative to single gene testing.
   Methods and findings
   We validated a 46-gene hotspot cancer panel assay allowing multiple gene testing from small diagnostic biopsies. From 1 January 2013 to 31 December 2013, solid tumour samples (including non-small-cell lung carcinoma [NSCLC], colorectal carcinoma, and melanoma) were sequenced in the context of the UK National Health Service from 351 consecutively submitted prospective cases for which treating clinicians thought the patient had potential to benefit from more extensive genetic analysis. Following histological assessment, tumour-rich regions of formalin-fixed paraffin-embedded (FFPE) sections underwent macrodissection, DNA extraction, NGS, and analysis using a pipeline centred on Torrent Suite software. With a median turnaround time of seven working days, an integrated clinical report was produced indicating the variants detected, including those with potential diagnostic, prognostic, therapeutic, or clinical trial entry implications. Accompanying phenotypic data were collected, and a detailed cost analysis of the panel compared with single gene testing was undertaken to assess affordability for routine patient care.
   Panel sequencing was successful for 97% (342/351) of tumour samples in the prospective cohort and showed 100% concordance with known mutations (detected using cobas assays). At least one mutation was identified in 87% (296/342) of tumours. A locally actionable mutation (i.e., available targeted treatment or clinical trial) was identified in 122/351 patients (35%). Forty patients received targeted treatment, in 22/40 (55%) cases solely due to use of the panel. Examination of published data on the potential efficacy of targeted therapies showed theoretically actionable mutations (i. e., mutations for which targeted treatment was potentially appropriate) in 66% (71/107) and 39% (41/105) of melanoma and NSCLC patients, respectively. At a cost of sic 339 (US$ 449) per patient, the panel was less expensive locally than performing more than two or three single gene tests.
   Study limitations include the use of FFPE samples, which do not always provide highquality DNA, and the use of "real world" data: submission of cases for sequencing did not always follow clinical guidelines, meaning that when mutations were detected, patients were not always eligible for targeted treatments on clinical grounds.
   Conclusions
   This study demonstrates that more extensive tumour sequencing can identify mutations that could improve clinical decision-making in routine cancer care, potentially improving patient outcomes, at an affordable level for healthcare providers.
C1 [Hamblin, Angela; Page, Suzanne; Henderson, Shirley; Cutts, Anthony; Vavoulis, Dimitrios V.; Housby, Nick; Schuh, Anna] Oxford Univ Hosp NHS Fdn Trust, Mol Diagnost Ctr, Oxford, England.
   [Hamblin, Angela; Wordsworth, Sarah; Page, Suzanne; Kaur, Kulvinder; Camps, Carme; Kaisaki, Pamela; Talbot, Denis; Middleton, Mark; Henderson, Shirley; Cutts, Anthony; Vavoulis, Dimitrios V.; Housby, Nick; Tomlinson, Ian; Taylor, Jenny C.; Schuh, Anna] Natl Inst Hlth Res, Biomed Res Ctr, Oxford, England.
   [Wordsworth, Sarah] Univ Oxford, Nuffield Dept Populat Hlth, Hlth Econ Res Ctr, Oxford, England.
   [Fermont, Jilles M.] Univ Cambridge, Dept Med, Expt Med & Immunotherapeut, Cambridge, England.
   [Kaur, Kulvinder; Camps, Carme; Kaisaki, Pamela; Vavoulis, Dimitrios V.; Tomlinson, Ian; Taylor, Jenny C.] Univ Oxford, Wellcome Trust Ctr Human Genet, Oxford, England.
   [Gupta, Avinash; Talbot, Denis; Middleton, Mark; Schuh, Anna] Univ Oxford, Dept Oncol, Oxford, England.
C3 Oxford University Hospitals NHS Foundation Trust; University of Oxford;
   University of Oxford; University of Cambridge; University of Oxford;
   Wellcome Centre for Human Genetics; University of Oxford
RP Wordsworth, S (corresponding author), Natl Inst Hlth Res, Biomed Res Ctr, Oxford, England.; Wordsworth, S (corresponding author), Univ Oxford, Nuffield Dept Populat Hlth, Hlth Econ Res Ctr, Oxford, England.
EM sarah.wordsworth@dph.ox.ac.uk
RI Camps, Cédric/O-1120-2017; Schuh, Anna/D-8954-2014; Camps,
   Carlos/L-3073-2017
OI Fermont, Jilles/0000-0001-5042-5785; Wordsworth,
   Sarah/0000-0002-2361-3040; Anna, schuh/0000-0002-3938-8490; Camps,
   Carlos/0000-0002-0648-5403; Taylor, Jenny/0000-0003-3602-5704; Kaur,
   Kulvinder/0009-0009-1872-9346
FU UK Technology Strategy Board; Wellcome Trust Centre for Human Genetics
   Wellcome Trust Core Award [090532/Z/09/Z]
FX The study was funded by the UK Technology Strategy Board (now called
   Innovate UK). We also acknowledge the Wellcome Trust Centre for Human
   Genetics Wellcome Trust Core Award Grant Number 090532/Z/09/Z. The
   funders of the study had no role in the study design, data collection,
   data analysis, data interpretation, or writing of the paper.
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NR 57
TC 48
Z9 50
U1 1
U2 9
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1549-1277
EI 1549-1676
J9 PLOS MED
JI PLos Med.
PD FEB
PY 2017
VL 14
IS 2
AR e1002230
DI 10.1371/journal.pmed.1002230
PG 26
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA EN0ZR
UT WOS:000395740500004
PM 28196074
OA gold, Green Published, Green Submitted
DA 2025-01-04
ER

PT J
AU Thao, LQ
   Byeon, HJ
   Lee, C
   Lee, S
   Lee, ES
   Choi, YW
   Choi, HG
   Park, ES
   Lee, KC
   Youn, YS
AF Thao, Le Quang
   Byeon, Hyeong Jun
   Lee, Changkyu
   Lee, Seunghyun
   Lee, Eun Seong
   Choi, Yeon Woong
   Choi, Han-Gon
   Park, Eun-Seok
   Lee, Kang Choon
   Youn, Yu Seok
TI Doxorubicin-Bound Albumin Nanoparticles Containing a TRAIL Protein for
   Targeted Treatment of Colon Cancer
SO PHARMACEUTICAL RESEARCH
LA English
DT Article
DE albumin; doxorubicin; nanoparticles; targeting; TRAIL
ID APOPTOSIS-INDUCING LIGAND; DRUG-DELIVERY; CHEMOTHERAPEUTIC-AGENTS;
   ANTITUMOR-ACTIVITY; COMBINATION; PACLITAXEL; IMPACT
AB We developed a new nanoparticle formulation comprised of human serum albumin (HSA) for co-delivery of doxorubicin (Dox) and tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) with the goal of apoptotic synergy in the treatment of colon cancer.
   TRAIL (0.2, 0.4, 1.0%)- and Dox-loaded HSA nanoparticles (TRAIL/Dox HSA NPs) were prepared by using the nab(TM) technology. Morphological and physicochemical characterizations were investigated by dynamic light scattering and transmission electron microscopy. Synergistic cytotoxicity, apoptotic activity, and potential penetration into mass tumor were determined in HCT116 cell-based systems. Furthermore, antitumor efficacy and tumor targeting were also investigated.
   TRAIL/Dox HSA NPs were uniformly spherical with sizes of 60 similar to 120 nm. The encapsulation efficacy of Dox and TRAIL was 68.9-77.2% and 80.4-86.0%, respectively. TRAIL 1.0%/Dox HSA NPs displayed the best inhibition of HCT116 colon cancer cells; inhibition was 6 times higher than achieved with Dox HSA NPs. The TRAIL 1.0%/Dox HSA NPs formulation was studied further. Flow cytometry analysis and TUNEL assay revealed that TRAIL 1.0%/Dox HSA NPs had markedly greater apoptotic activity than Dox HSA NPs. In HCT116 tumor-bearing BALB/c nu/nu mice, TRAIL 1.0%/Dox HSA NPs had significantly higher antitumor efficacy than Dox HSA NPs (tumor volume; 933.4 mm(3) vs. 3183.7 mm(3), respectively). TRAIL 1.0%/Dox HSA NPs penetrated deeply into tumor masses in a HCT116 spheroid model and localized in tumor sites after tail vein injection.
   Data indicate that TRAIL 1.0%/Dox HSA NPs offer advantages of co-delivery of Dox and TRAIL in tumors, with potential synergistic apoptosis-based anticancer therapy.
C1 [Thao, Le Quang; Byeon, Hyeong Jun; Lee, Changkyu; Lee, Seunghyun; Park, Eun-Seok; Lee, Kang Choon; Youn, Yu Seok] Sungkyunkwan Univ, Sch Pharm, Suwon 16419, South Korea.
   [Lee, Eun Seong] Catholic Univ Korea, Div Biotechnol, Bucheon Si 14662, Gyeonggi Do, South Korea.
   [Choi, Yeon Woong] Korea United Pharm INC, Seoul 06114, South Korea.
   [Choi, Han-Gon] Hanyang Univ, Coll Pharm, Ansan 15588, South Korea.
C3 Sungkyunkwan University (SKKU); Catholic University of Korea; Hanyang
   University
RP Youn, YS (corresponding author), Sungkyunkwan Univ, Sch Pharm, 300 Cheoncheon Dong, Suwon 16419, South Korea.
EM ysyoun@skku.edu
RI LEE, EUN/R-2320-2017; Lee, Kang/A-9556-2010
FU Basic Science Research Program through the National Research Foundation
   of Korea - Ministry of Science, ICT, and future Planning [2014002133]
FX This research was supported by the Basic Science Research Program
   through the National Research Foundation of Korea funded by the Ministry
   of Science, ICT, and future Planning (#2014002133).
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NR 32
TC 56
Z9 59
U1 4
U2 79
PU SPRINGER/PLENUM PUBLISHERS
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0724-8741
EI 1573-904X
J9 PHARM RES-DORDR
JI Pharm. Res.
PD MAR
PY 2016
VL 33
IS 3
BP 615
EP 626
DI 10.1007/s11095-015-1814-z
PG 12
WC Chemistry, Multidisciplinary; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Chemistry; Pharmacology & Pharmacy
GA DD5EV
UT WOS:000369946400007
PM 26526555
DA 2025-01-04
ER

PT J
AU Yin, AY
   van Hasselt, JGC
   Guchelaar, HJ
   Friberg, LE
   Moes, DJAR
AF Yin, Anyue
   van Hasselt, Johan G. C.
   Guchelaar, Henk-Jan
   Friberg, Lena E.
   Moes, Dirk Jan A. R.
TI Anti-cancer treatment schedule optimization based on tumor dynamics
   modelling incorporating evolving resistance
SO SCIENTIFIC REPORTS
LA English
DT Article
ID CLINICAL DRUG DEVELOPMENT; COLORECTAL-CANCER; CLONAL EVOLUTION; EGFR
   BLOCKADE; PHASE-II; INTERMITTENT; ONCOLOGY; DNA; FUTURE; HETEROGENEITY
AB Quantitative characterization of evolving tumor resistance under targeted treatment could help identify novel treatment schedules, which may improve the outcome of anti-cancer treatment. In this study, a mathematical model which considers various clonal populations and evolving treatment resistance was developed. With parameter values fitted to the data or informed by literature data, the model could capture previously reported tumor burden dynamics and mutant KRAS levels in circulating tumor DNA (ctDNA) of patients with metastatic colorectal cancer treated with panitumumab. Treatment schedules, including a continuous schedule, intermittent schedules incorporating treatment holidays, and adaptive schedules guided by ctDNA measurements were evaluated using simulations. Compared with the continuous regimen, the simulated intermittent regimen which consisted of 8-week treatment and 4-week suspension prolonged median progression-free survival (PFS) of the simulated population from 36 to 44 weeks. The median time period in which the tumor size stayed below the baseline level (T-TS<TS0) was prolonged from 52 to 60 weeks. Extending the treatment holiday resulted in inferior outcomes. The simulated adaptive regimens showed to further prolong median PFS to 56-64 weeks and T-TS<TS0 to 114-132 weeks under different treatment designs. A prospective clinical study is required to validate the results and to confirm the added value of the suggested schedules.
C1 [Yin, Anyue; Guchelaar, Henk-Jan; Moes, Dirk Jan A. R.] Leiden Univ, Med Ctr, Dept Clin Pharm & Toxicol, Albinusdreef 2, NL-2333 ZA Leiden, Netherlands.
   [Yin, Anyue; Guchelaar, Henk-Jan; Moes, Dirk Jan A. R.] Leiden Univ, Med Ctr, Leiden Network Personalized Therapeut, Leiden, Netherlands.
   [van Hasselt, Johan G. C.] Leiden Univ, Leiden Acad Ctr Drug Res LACDR, Div Syst Biomed & Pharmacol, Leiden, Netherlands.
   [Friberg, Lena E.] Uppsala Univ, Dept Pharm, Uppsala, Sweden.
C3 Leiden University; Leiden University Medical Center (LUMC); Leiden
   University - Excl LUMC; Leiden University; Leiden University Medical
   Center (LUMC); Leiden University - Excl LUMC; Leiden University - Excl
   LUMC; Leiden University; Uppsala University
RP Moes, DJAR (corresponding author), Leiden Univ, Med Ctr, Dept Clin Pharm & Toxicol, Albinusdreef 2, NL-2333 ZA Leiden, Netherlands.; Moes, DJAR (corresponding author), Leiden Univ, Med Ctr, Leiden Network Personalized Therapeut, Leiden, Netherlands.
EM D.J.A.R.Moes@lumc.nl
RI van Hasselt, Coen/H-5593-2019; Friberg, Lena/AAW-5888-2021; Yin,
   Anyue/AAP-4566-2021; guchelaar, henk-jan/AAP-1381-2021
OI van Hasselt, J.G.C./0000-0002-1664-7314; Yin, Anyue/0000-0001-9924-6040
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NR 44
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PU NATURE PORTFOLIO
PI BERLIN
PA HEIDELBERGER PLATZ 3, BERLIN, 14197, GERMANY
SN 2045-2322
J9 SCI REP-UK
JI Sci Rep
PD MAR 10
PY 2022
VL 12
IS 1
AR 4206
DI 10.1038/s41598-022-08012-7
PG 14
WC Multidisciplinary Sciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Science & Technology - Other Topics
GA ZX8ZM
UT WOS:000772182900001
PM 35273301
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Han, ZQ
   Wen, LN
AF Han, Zong-Qiang
   Wen, Li-Na
TI Application of G-quadruplex targets in gastrointestinal cancers:
   Advancements, challenges and prospects
SO WORLD JOURNAL OF GASTROINTESTINAL ONCOLOGY
LA English
DT Review
DE G-quadruplex; Pancreatic cancer; Liver cancer; Gastric cancer;
   Colorectal cancer; Gastrointestinal stromal tumor
ID TELOMERIC G-QUADRUPLEX; NUCLEASE HYPERSENSITIVE ELEMENT; STRUCTURE-BASED
   DESIGN; RNA G-QUADRUPLEXES; MYC G-QUADRUPLEX; PANCREATIC-CANCER; DNA
   STRUCTURES; MESSENGER-RNA; OLIGONUCLEOTIDE AS1411; PROMOTER REGION
AB Genomic instability and inflammation are considered to be two enabling characteristics that support cancer development and progression. G-quadruplex structure is a key element that contributes to genomic instability and inflammation. G-quadruplexes were once regarded as simply an obstacle that can block the transcription of oncogenes. A ligand targeting G-quadruplexes was found to have anticancer activity, making G-quadruplexes potential anticancer targets. However, further investigation has revealed that G-quadruplexes are widely distributed throughout the human genome and have many functions, such as regulating DNA replication, DNA repair, transcription, translation, epigenetics, and inflammatory response. G-quadruplexes play double regulatory roles in transcription and translation. In this review, we focus on G-quadruplexes as novel targets for the treatment of gastrointestinal cancers. We summarize the application basis of G-quadruplexes in gastrointestinal cancers, including their distribution sites, structural characteristics, and physiological functions. We describe the current status of applications for the treatment of esophageal cancer, pancreatic cancer, hepatocellular carcinoma, gastric cancer, colorectal cancer, and gastrointestinal stromal tumors, as well as the associated challenges. Finally, we review the prospective clinical applications of G-quadruplex targets, providing references for targeted treatment strategies in gastrointestinal cancers.
C1 [Han, Zong-Qiang] Beijing Xiaotangshan Hosp, Dept Lab Med, Beijing 102211, Peoples R China.
   [Wen, Li-Na] Capital Med Univ, Beijing Shijitan Hosp, Dept Clin Nutr, Beijing 100038, Peoples R China.
   [Wen, Li-Na] Capital Med Univ, Beijing Shijitan Hosp, Dept Clin Nutr, 10 Tieyi Rd Yang-fangdian St, Beijing 100038, Peoples R China.
C3 Capital Medical University; Capital Medical University
RP Wen, LN (corresponding author), Capital Med Univ, Beijing Shijitan Hosp, Dept Clin Nutr, 10 Tieyi Rd Yang-fangdian St, Beijing 100038, Peoples R China.
EM wenlina3074@bjsjth.cn
FU National Natural Science Foundation of China [81803773]
FX Supported by the National Natural Science Foundation of China, No.
   81803773.
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NR 223
TC 4
Z9 4
U1 6
U2 22
PU BAISHIDENG PUBLISHING GROUP INC
PI PLEASANTON
PA 7041 Koll Center Parkway, Suite 160, PLEASANTON, CA, UNITED STATES
SN 1948-5204
J9 WORLD J GASTRO ONCOL
JI World J. Gastrointest. Oncol.
PD JUL 15
PY 2023
VL 15
IS 7
BP 1149
EP +
DI 10.4251/wjgo.v15.i7.1149
PG 26
WC Oncology; Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Gastroenterology & Hepatology
GA O5VF5
UT WOS:001044477100004
PM 37546556
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Moorcraft, SY
   Jones, T
   Walker, BA
   Ladas, G
   Kalaitzaki, E
   Yuan, LN
   Begum, R
   Eltahir, Z
   Wotherspoon, A
   Montero-Fernandez, A
   Mendes, LST
   de Castro, DG
   Wilson, SH
   Proszek, P
   To, YM
   Hawkes, E
   Roy, A
   Cunningham, D
   Rao, S
   Watkins, D
   Starling, N
   Bowcock, AM
   Chau, I
AF Moorcraft, Sing Y.
   Jones, Thomas
   Walker, Brian A.
   Ladas, George
   Kalaitzaki, Eleftheria
   Yuan, Lina
   Begum, Ruwaida
   Eltahir, Zakaria
   Wotherspoon, Andrew
   Montero-Fernandez, Angeles
   Mendes, Larissa S. Teixeira
   de Castro, David Gonzalez
   Wilson, Sanna Hulkki
   Proszek, Paula
   To, Ye M.
   Hawkes, Eliza
   Roy, Amitesh
   Cunningham, David
   Rao, Sheela
   Watkins, David
   Starling, Naureen
   Bowcock, Anne M.
   Chau, Ian
TI Molecular profiling of colorectal pulmonary metastases and primary
   tumours: implications for targeted treatment
SO ONCOTARGET
LA English
DT Article
DE colorectal cancer; heterogeneity; metastasectomy; pulmonary metastases;
   RAS
ID LUNG METASTASES; SURGICAL RESECTION; RAS MUTATIONS; KRAS MUTATION;
   CANCER; BRAF; LIVER; EGFR
AB This study aimed to molecularly characterise colorectal pulmonary metastases (PM) and investigate whether their molecular profiles were concordant with those of the primary tumour. Clinical data and archival formalin fixed paraffin embedded tissue samples were retrospectively collected from patients who underwent >= 1 pulmonary metastasectomies for colorectal cancer between 1997-2012. Primary tumour and metastatic samples were analysed using a targeted capture sequencing panel of 46 cancer-associated genes. The 5-year progression-free and overall survival rates for the 81 patients in this study were 32% (95% CI 22-42%) and 77% (95% CI 66-85%) respectively. Fifty-four patients had samples available from >= 1 PM, and sequencing data were successfully obtained from 33 PM from 24 patients. The most frequently mutated genes were APC (71%), KRAS (58%) and TP53 (46%). Seventy-three percent of the 15 patients with matched primary and PM samples and 6 of the 7 patients (86%) with data from >= 2 PM had concordant molecular profiles. The concordance for KRAS and NRAS was 100%. At our institutions, patients with resectable colorectal PM had a favourable prognosis. RAS mutations were commonly detected in PM and the molecular profiles of colorectal PM were highly concordant with the primary tumour.
C1 [Moorcraft, Sing Y.; Walker, Brian A.; Kalaitzaki, Eleftheria; Yuan, Lina; Begum, Ruwaida; Eltahir, Zakaria; Wotherspoon, Andrew; Mendes, Larissa S. Teixeira; de Castro, David Gonzalez; Wilson, Sanna Hulkki; Proszek, Paula; To, Ye M.; Hawkes, Eliza; Roy, Amitesh; Cunningham, David; Rao, Sheela; Watkins, David; Starling, Naureen; Chau, Ian] Royal Marsden NHS Fdn Trust, London, England.
   [Moorcraft, Sing Y.; Walker, Brian A.; Kalaitzaki, Eleftheria; Yuan, Lina; Begum, Ruwaida; Eltahir, Zakaria; Wotherspoon, Andrew; Mendes, Larissa S. Teixeira; de Castro, David Gonzalez; Wilson, Sanna Hulkki; Proszek, Paula; To, Ye M.; Hawkes, Eliza; Roy, Amitesh; Cunningham, David; Rao, Sheela; Watkins, David; Starling, Naureen; Chau, Ian] Royal Marsden NHS Fdn Trust, Sutton, Surrey, England.
   [Jones, Thomas; Ladas, George; Montero-Fernandez, Angeles] Royal Brompton & Harefield NHS Fdn Trust, London, England.
   [Bowcock, Anne M.] Imperial Coll, Natl Heart & Lung Inst, London, England.
C3 Royal Marsden NHS Foundation Trust; Royal Marsden NHS Foundation Trust;
   Royal Brompton & Harefield NHS Foundation Trust; Imperial College London
RP Chau, I (corresponding author), Royal Marsden NHS Fdn Trust, London, England.; Chau, I (corresponding author), Royal Marsden NHS Fdn Trust, Sutton, Surrey, England.
EM ian.chau@rmh.nhs.uk
RI Chau, Ian/ABC-2023-2020; Cunningham, David/ABT-0193-2022; Roy,
   Amitesh/AGQ-4929-2022; Walker, Brian/A-4984-2013; Starling,
   Naureen/JQV-9577-2023; Hawkes, Eliza/G-2847-2019
OI Roy, Amitesh/0000-0002-3583-7981; Chau, Ian/0000-0003-0286-8703; Walker,
   Brian/0000-0002-8615-6254; Starling, Naureen/0000-0002-1496-6792;
   Eltahir, Zakaria/0000-0001-6815-4100; Bowcock, Anne/0000-0001-8691-9090;
   Teixeira Mendes, Larissa/0000-0002-2417-1109; Cunningham,
   David/0000-0001-5158-1069; Proszek, Paula/0000-0002-0780-6790; Hawkes,
   Eliza/0000-0002-0376-2559
FU Royal Marsden/Institute of Cancer Research National Institute for Health
   Research Biomedical Research Centre [A95]; STFC [ST/N000331/1] Funding
   Source: UKRI
FX This work was supported by the Royal Marsden/Institute of Cancer
   Research National Institute for Health Research Biomedical Research
   Centre (Grant Number A95).
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NR 25
TC 12
Z9 12
U1 0
U2 5
PU IMPACT JOURNALS LLC
PI ORCHARD PARK
PA 6666 E QUAKER ST, STE 1, ORCHARD PARK, NY 14127 USA
EI 1949-2553
J9 ONCOTARGET
JI Oncotarget
PD SEP 12
PY 2017
VL 8
IS 39
BP 64999
EP 65008
DI 10.18632/oncotarget.17048
PG 10
WC Oncology; Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Cell Biology
GA FG4YC
UT WOS:000410291200026
PM 29029407
OA gold, Green Submitted, Green Published
DA 2025-01-04
ER

PT J
AU Taghizadeh, E
   Taheri, F
   Rostami, D
   Renani, PG
   Ferns, GA
   Pasdar, A
   Mobarhan, MG
AF Taghizadeh, Eskandar
   Taheri, Forough
   Rostami, Daryoush
   Renani, Pedram G.
   Ferns, Gordon A.
   Pasdar, Alireza
   Mobarhan, Majid G.
TI MiR-492 as an Important Biomarker for Early Diagnosis and Targeted
   Treatment in Different Cancers
SO CURRENT CANCER THERAPY REVIEWS
LA English
DT Review
DE MiR-492; breast cancer; microRNAs; colorectal cancer; RNA-silencing;
   biomarker
ID MICRORNA EXPRESSION; MIRNAS; RETINOBLASTOMA; IDENTIFICATION;
   PROLIFERATION; GENES; CELLS
AB Recent studies have led to a more detailed understanding of the roles played by microRNAs in health and disease, and their potential use as biomarkers in physiological and pathophysiological processes involving cancer initiation and progression. MiR-492 is encoded by a pseudogene, has a key role in some human cancer cells and its overexpression in tissues, and it has been proposed that it can be used as a good biomarker for management and early diagnosis of some cancers including breast cancer, colorectal and ovarian cancer, hepatocellular cancer, retinoblastoma and pancreatic cancer. The aim of this review was to summarize the data of MiR-492 for early diagnosis and treatment of some types of related cancers.
C1 [Taghizadeh, Eskandar] Yasuj Univ Med Sci, Cellular & Mol Res Ctr, Yasuj, Iran.
   [Taghizadeh, Eskandar; Pasdar, Alireza] Mashhad Univ Med Sci, Fac Med, Dept Med Genet, Mashhad, Razavi Khorasan, Iran.
   [Taheri, Forough; Renani, Pedram G.] Islamic Azad Univ, Sharekord Branch, Sharekord, Iran.
   [Rostami, Daryoush] Zabol Univ Med Sci, Dept Sch Allied, Zabol, Iran.
   [Ferns, Gordon A.] Brighton & Sussex Med Sch, Dept Med Educ, Brighton, E Sussex, England.
   [Mobarhan, Majid G.] Mashhad Univ Med Sci, Sch Med, Metab Syndrome Res Ctr, Mashhad, Razavi Khorasan, Iran.
C3 Yasouj University; Mashhad University of Medical Sciences; Islamic Azad
   University; University of Sussex; University of Brighton; Mashhad
   University of Medical Sciences
RP Pasdar, A (corresponding author), Mashhad Univ Med Sci, Fac Med, Dept Med Genet, Mashhad, Razavi Khorasan, Iran.; Mobarhan, MG (corresponding author), Mashhad Univ Med Sci, Sch Med, Metab Syndrome Res Ctr, Mashhad, Razavi Khorasan, Iran.
EM pasdarA@mums.ac.ir; ghayourm@mums.ac.ir
RI Ghayour-Mobarhan, Majid/AAY-5963-2020; Taghizadeh,
   Eskandar/AAY-5149-2020; rostami, daryoush/B-5964-2018
OI Taghizadeh, Eskandar/0000-0002-7394-2539; Pasdar,
   Alireza/0000-0002-7864-9729; rostami, daryoush/0000-0002-4698-4944
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NR 50
TC 2
Z9 2
U1 0
U2 1
PU BENTHAM SCIENCE PUBL LTD
PI SHARJAH
PA EXECUTIVE STE Y-2, PO BOX 7917, SAIF ZONE, 1200 BR SHARJAH, U ARAB
   EMIRATES
SN 1573-3947
EI 1875-6301
J9 CURR CANCER THER REV
JI Curr. Cancer Ther. Rev.
PY 2020
VL 16
IS 4
BP 269
EP 275
DI 10.2174/1573394716666200309124048
PG 7
WC Oncology
WE Emerging Sources Citation Index (ESCI)
SC Oncology
GA OW3YQ
UT WOS:000592826900002
DA 2025-01-04
ER

PT J
AU Siu, LL
   Conley, BA
   Boerner, S
   LoRusso, PM
AF Siu, Lillian L.
   Conley, Barbara A.
   Boerner, Scott
   LoRusso, Patricia M.
TI Next-Generation Sequencing to Guide Clinical Trials
SO CLINICAL CANCER RESEARCH
LA English
DT Article
ID COLORECTAL-CANCER; PHASE-II; BIOMARKERS; GENOME; MUTATIONS; MEDICINE;
   ONCOLOGY; THERAPY; DESIGN; BREAST
AB Rapidly accruing knowledge of the mutational landscape of malignant neoplasms, the increasing facility of massively parallel genomic sequencing, and the availability of drugs targeting many "driver" molecular abnormalities have spurred the oncologic community to consider how to use these new tools to improve cancer treatment. In order to assure that assignment of patients to a particular targeted treatment is likely to be beneficial to the patient, it will be necessary to conduct appropriate clinical research. It is clear that clinical (histology and stage) eligibility criteria are not sufficient for most clinical trials using agents that target mutations that are present in only a minority of patients. Recently, several clinical trial designs have been suggested to test the benefit of targeted treatment in molecular and/or clinical subgroups of patients. However, challenges remain in the implementation of such trials, including choice of assay, levels of evidence regarding gene variants, tumor heterogeneity, identifying resistance mechanisms, the necessity of screening large numbers of patients, infrastructure needs, and collaboration of investigators and industry. This article reviews current trial designs and discusses some of the considerations, advantages, and drawbacks of designing clinical trials that depend on particular molecular variants as eligibility criteria. (C) 2015 AACR.
C1 [Siu, Lillian L.] Univ Toronto, Princess Margaret Canc Ctr, Toronto, ON, Canada.
   [Conley, Barbara A.] NCI, Div Canc Treatment & Diag, Bethesda, MD 20892 USA.
   [Boerner, Scott; LoRusso, Patricia M.] Yale Univ, Sch Med, Yale Canc Ctr, New Haven, CT USA.
C3 University of Toronto; University Health Network Toronto; Princess
   Margaret Cancer Centre; National Institutes of Health (NIH) - USA; NIH
   National Cancer Institute (NCI); Yale University
RP Siu, LL (corresponding author), Univ Hlth Network, 610 Univ Ave,Suite 5-718, Toronto, ON M5G 2M9, Canada.
EM lillian.siu@uhn.ca
FU NCI NIH HHS [UM1 CA186644] Funding Source: Medline
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NR 34
TC 52
Z9 56
U1 0
U2 6
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1078-0432
EI 1557-3265
J9 CLIN CANCER RES
JI Clin. Cancer Res.
PD OCT 15
PY 2015
VL 21
IS 20
BP 4536
EP 4544
DI 10.1158/1078-0432.CCR-14-3215
PG 9
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA CV7WH
UT WOS:000364486300008
PM 26473189
OA Green Accepted, Bronze
DA 2025-01-04
ER

PT J
AU Robinson, HR
   Messersmith, WA
   Lentz, RW
AF Robinson, Hannah R.
   Messersmith, Wells A.
   Lentz, Robert W.
TI HER2-Positive Metastatic Colorectal Cancer
SO CURRENT TREATMENT OPTIONS IN ONCOLOGY
LA English
DT Review
DE Colorectal cancer; HER2; ERBB2; Trastuzumab; Tucatinib; Pertuzumab
ID RANDOMIZED-TRIAL; PLUS TRASTUZUMAB; COPY NUMBER; OPEN-LABEL;
   AMPLIFICATION; MULTICENTER; THERAPY
AB Targeted treatment strategies are available for human epidermal growth factor receptor 2 (HER2)-positive (amplified and/or overexpressed) metastatic colorectal cancer (mCRC), and HER2 testing is indicated in patients with mCRC. At present, standard of care first-line treatment for those with HER2-positive mCRC remains chemotherapy in combination with epidermal growth factor receptor (EGFR) inhibitors or bevacizumab, depending on RAS/BRAF mutational status and tumor sidedness. HER2-targeted agents should be considered for those with RAS/BRAF wild-type disease in subsequent-line treatment and in first-line treatment for patients not appropriate for intensive therapy. While the choice of anti-HER2 therapy is empiric given lack of head-to-head comparisons, the combination of trastuzumab plus tucatinib has received FDA accelerated approval for use in this setting and is generally the authors' preference. Trastuzumab plus lapatinib, trastuzumab plus pertuzumab, and trastuzumab deruxtecan (T-DXd) also have evidence of efficacy in this setting. As T-DXd has demonstrated activity following treatment with other HER2-targeted regimens and carries an increased risk of high-grade toxicities, the authors favor reserving it for use after progression on prior anti-HER2 therapy. HER2-targeted therapies that inhibit signal transduction appear to have limited activity in those with RAS mutations, including trastuzumab-containing regimens. However, the antibody drug conjugate T-DXd has some data showing efficacy in this setting, and the authors would consider T-DXd in subsequent-line therapy for HER2-positive, RAS-mutated mCRC. Several areas of uncertainty remain regarding how to best utilize HER2-targeted therapies in mCRC. These include the optimal sequence of anti-HER2 therapies with chemotherapy and anti-EGFR therapies, the optimal combination partners for anti-HER2 therapies, and the incorporation of predictive biomarkers to guide use of anti-HER2 therapies. Results of ongoing studies may thus alter the treatment paradigm above in the coming years.
C1 [Robinson, Hannah R.; Messersmith, Wells A.; Lentz, Robert W.] Univ Colorado, Sch Med, Dept Med, Div Med Oncol, MS 8117, 12801 E 17Th Ave, Aurora, CO 80045 USA.
C3 University of Colorado System; University of Colorado Anschutz Medical
   Campus
RP Lentz, RW (corresponding author), Univ Colorado, Sch Med, Dept Med, Div Med Oncol, MS 8117, 12801 E 17Th Ave, Aurora, CO 80045 USA.
EM robert.lentz@cuanschutz.edu
OI Robinson, Hannah/0000-0002-9150-8015
FU NIH [5K12CA086913-21]
FX This work was supported by NIH 5K12CA086913-21 (to RWL).
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NR 77
TC 2
Z9 2
U1 2
U2 4
PU SPRINGER
PI NEW YORK
PA ONE NEW YORK PLAZA, SUITE 4600, NEW YORK, NY, UNITED STATES
SN 1527-2729
EI 1534-6277
J9 CURR TREAT OPTION ON
JI Curr. Treat. Options Oncol.
PD MAY
PY 2024
VL 25
IS 5
BP 585
EP 604
DI 10.1007/s11864-024-01183-7
EA MAR 2024
PG 20
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA PX4E7
UT WOS:001194629100001
PM 38539034
DA 2025-01-04
ER

PT J
AU Montes, AF
   Orduña, VA
   Martínez, EA
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   Lavín, DC
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   Oliva, JC
   Cirera, L
   Gómez, JG
   Pericay, C
AF Fernandez Montes, Ana
   Alonso Orduna, Vicente
   Asensio Martinez, Elena
   Rodriguez Salas, Nuria
   Torres, Esperanza
   Cacho Lavin, Diego
   Rodriguez Alonso, Rosa Maria
   Falco, Esther
   Carles Oliva, Joan
   Cirera, Lluis
   Garcia Gomez, Jesus
   Pericay, Carles
TI The Frequency of Specific KRAS Mutations, and Their Impact on Treatment
   Choice and Survival, in Patients With Metastatic Colorectal Cancer
SO ONCOLOGIST
LA English
DT Article
DE colonic neoplasms; mutation; codon; genes (ras); prognosis
ID FUTURE PERSPECTIVES; BRAF
AB Background Patients with metastatic colorectal cancer (mCRC) and KRAS mutations have a poor prognosis, seemingly dependent on the location of the mutation. This multicenter, retrospective, cohort study assessed the frequency and prognostic value of specific KRAS mutation codon locations in mCRC patients, and survival outcomes in relation to treatment. Materials and Methods Data from mCRC patients treated in 10 Spanish hospitals between January 2011 and December 2015 were analyzed. The main objective was to investigate (1) the impact of KRAS mutation location on overall survival (OS), and (2) the effect of targeted treatment plus metastasectomy and primary tumor location on OS in patients with KRAS mutations. Results The KRAS mutation location was known for 337/2002 patients. Of these, 177 patients received chemotherapy only, 155 received bevacizumab plus chemotherapy, and 5 received anti-epidermal growth factor receptor therapy plus chemotherapy; 94 patients underwent surgery. The most frequent KRAS mutation locations were G12A (33.8%), G12D (21.4%), and G12V (21.4%). Compared with other locations, patients with a G12S mutation had the shortest median OS (10.3 [95% CI, 2.5-18.0] months). OS was longer in patients who underwent surgery versus those who did not, with a trend toward prolonged survival with bevacizumab (median OS 26.7 [95% CI, 21.8-31.7] months) versus chemotherapy alone (median OS 23.2 [95% CI, 19.4-27.0] months). Conclusion These findings confirm that KRAS mutation location may predict survival outcomes in patients with mCRC, and suggest that pre-/post-operative bevacizumab plus metastasectomy provides survival benefits in patients with KRAS mutations.
   Patients with metastatic colorectal cancer (mCRC) and KRAS mutations have a poor prognosis, seemingly dependent on the location of the mutation. This study assessed the frequency and prognostic value of specific KRAS mutation codon locations in mCRC and survival outcomes in relation to treatment.
C1 [Fernandez Montes, Ana; Garcia Gomez, Jesus] Complexo Hosp Univ Ourense, Serv Oncol Med, Calle Ramon Puga Noguerol, Orense, Spain.
   [Alonso Orduna, Vicente] Hosp Univ Miguel Servet, Inst Invest Sanitaria Aragon, Serv Oncol Med, Zaragoza, Spain.
   [Asensio Martinez, Elena] Hosp Gen Univ Elche, Serv Oncol Med, Carrer Almazara, Alicante, Spain.
   [Rodriguez Salas, Nuria] Hosp Univ La Paz, Serv Oncol Med, Madrid, Spain.
   [Torres, Esperanza] Hospit Univ Reg & Virgen de la Victoria, UGC Interctr Oncol Med, Campus Teatinos, Malaga, Spain.
   [Torres, Esperanza] Inst Invest Biomed Malaga IBIMA, Campus Teatinos, Malaga, Spain.
   [Cacho Lavin, Diego] Hosp Univ Marques de Valdecilla, Serv Oncol Med, Santander, Cantabria, Spain.
   [Rodriguez Alonso, Rosa Maria] Hosp Univ Reina Sofia Cordoba, Serv Oncol Med, Ave Menendez Pidal, Cordoba, Spain.
   [Falco, Esther] Hosp Son Llatzer, Serv Oncol Med, Carretera Manacor, Palma De Mallorca, Illes Balears, Spain.
   [Carles Oliva, Joan] Fundacio Parc Tauli, Inst Invest Innovacio I3PT, Barcelona, Spain.
   [Cirera, Lluis] Hosp Univ Mutua Terrassa, Serv Oncol Med, Barcelona, Spain.
   [Pericay, Carles] Hosp Univ Parc Tauli, Serv Oncol Med, Barcelona, Spain.
C3 Complexo Hospitalario Universitario de Ourense, Verin e O Barco de
   Valdeorras; Miguel Servet University Hospital; Hospital Universitario La
   Paz; Universidad de Malaga; Instituto de Investigacion Biomedica de
   Malaga y Plataforma en Nanomedicina (IBIMA); Hospital Universitario
   Marques de Valdecilla (HUMV); Hospital Universitario Reina Sofia -
   Cordoba; Hospital Universitari Son Llatzer; Autonomous University of
   Barcelona; Parc Tauli Hospital Universitari; Hospital Universitario
   Mutua Terrassa; Autonomous University of Barcelona; Parc Tauli Hospital
   Universitari
RP Montes, AF (corresponding author), Complexo Hosp Univ Ourense, Serv Oncol Med, Calle Ramon Puga Noguerol 54, Orense 32005, Spain.
EM afm1003@hotmail.com
RI ALONSO, ROSA/M-3047-2014
OI Ana, Fernandez Montes/0000-0003-4630-5830
FU Merck, S.L., Spain, an affiliate of Merck KGaA, Darmstadt, Germany
FX This study was funded by Merck, S.L., Spain, an affiliate of Merck KGaA,
   Darmstadt, Germany.
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NR 27
TC 3
Z9 3
U1 0
U2 4
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 1083-7159
EI 1549-490X
J9 ONCOLOGIST
JI Oncologist
PD OCT
PY 2023
VL 28
IS 10
BP e902
EP e909
DI 10.1093/oncolo/oyad117
EA MAY 2023
PG 8
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA FD4C2
UT WOS:000992687100001
PM 37141400
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Liu, NN
   Zhou, X
   Lu, SY
   Luo, G
   Wu, ZG
   Zhang, CC
   Li, JH
   Zhang, YJ
   Zhang, LL
AF Liu, Nannan
   Zhou, Xiao
   Lu, Siyao
   Luo, Guang
   Wu, Zhongguang
   Zhang, Chuchu
   Li, Jiehan
   Zhang, Yingjie
   Zhang, Lingling
TI Injectable Hydrogel Delivery System with Nintedanib and Chloroquine
   Triggers Apoptosis and Inhibits Protective Autophagy
SO ACS APPLIED POLYMER MATERIALS
LA English
DT Article
DE PEG hydrogel; nintedanib; CQ; apoptosis; autophagy; PUMA
ID SUSTAINED-RELEASE; BAX TRANSLOCATION; CELL-DEATH; CANCER; PUMA; PATHWAY;
   EXPRESSION; DOCETAXEL; DISEASE
AB The hydrogel drug delivery system has demonstrated significant potential in addressing the limitations of chemotherapeutic medicines and tumor-targeted treatment. Nintedanib, an FDA-approved potent triple vascular kinase inhibitor, has exhibited effective antitumor activity in a variety of malignancies, although its underlying mechanism remains elusive. In this investigation, an innovative sustained-release hydrogel delivery system for medication was established using the Michael addition reaction of the polyethylene glycol diacrylate and 4-arm poly(ethylene glycol)-thiol (4 Arm PEG-SH). It was discovered that the nintedanib@PEG hydrogel induced cell apoptosis and inhibited tumor progression. Subsequently, analysis revealed that nintedanib caused apoptosis in colon cancer cells by upregulating PUMA (p53 upregulated modulator of apoptosis) expression while also activating protective autophagy. Mechanistically, nintedanib inhibited Akt/mTOR (mechanistic target of rapamycin kinase) pathway activation, thereby inducing PUMA-dependent apoptosis and triggering protective autophagy. Moreover, the combination of nintedanib and CQ (chloroquine, an autophagy inhibitor) contained in the hydrogel delivery system showed a synergistically antitumor effect both in vitro and in vivo. Consequently, an in situ-targeted, long-term, effective, and safe antitumor strategy using an innovative injectable hydrogel delivery system combined with complementary medication. These findings propose a promising therapeutic approach for clinical patients, particularly in the realm of colon cancer therapy, thereby illuminating potential avenues for further research and clinical application.
C1 [Liu, Nannan; Zhou, Xiao; Lu, Siyao; Luo, Guang; Wu, Zhongguang; Zhang, Yingjie; Zhang, Lingling] Cent South Univ, Third Xiangya Hosp, Dept Lab Med, Changsha 410013, Peoples R China.
   [Liu, Nannan; Zhou, Xiao; Lu, Siyao; Luo, Guang; Wu, Zhongguang; Zhang, Yingjie; Zhang, Lingling] Cent South Univ, Third Xiangya Hosp, Dept Hlth Management, Changsha 410013, Peoples R China.
   [Liu, Nannan; Zhang, Chuchu; Zhang, Yingjie] Hunan Univ, Sch Biomed Sci, Changsha 410082, Peoples R China.
   [Zhang, Yingjie] Fudan Univ, Huadong Hosp, Shanghai Med Coll, Dept Gastroenterol, Shanghai 200040, Peoples R China.
   [Li, Jiehan] Zhengzhou Univ, Dept Gastroenterol, Affiliated Hosp 1, Zhengzhou 450052, Peoples R China.
C3 Central South University; Central South University; Hunan University;
   Fudan University; Zhengzhou University
RP Zhang, LL (corresponding author), Cent South Univ, Third Xiangya Hosp, Dept Lab Med, Changsha 410013, Peoples R China.; Zhang, LL (corresponding author), Cent South Univ, Third Xiangya Hosp, Dept Hlth Management, Changsha 410013, Peoples R China.
EM zhll0807@csu.edu.cn
RI LU, SIYAO/AAG-1434-2020
FU National Natural Science Foundation of China [82273172]; National
   Natural Science Foundation of China (NSFC) [2024JJ5526]; Natural Science
   Foundation of Hunan Province
FX We would like to thank the support of the National Natural Science
   Foundation of China (NSFC) (no. 82273172) and the Natural Science
   Foundation of Hunan Province (no. 2024JJ5526).
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NR 49
TC 1
Z9 1
U1 6
U2 6
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 2637-6105
J9 ACS APPL POLYM MATER
JI ACS Appl. Polym. Mater.
PD JUN 15
PY 2024
VL 6
IS 12
BP 7148
EP 7160
DI 10.1021/acsapm.4c00893
EA JUN 2024
PG 13
WC Materials Science, Multidisciplinary; Polymer Science
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Materials Science; Polymer Science
GA WZ2D1
UT WOS:001248640600001
DA 2025-01-04
ER

PT J
AU Zhang, N
   Yang, YN
   Wang, ZY
   Yang, J
   Chu, X
   Liu, J
   Zhao, YX
AF Zhang, Nan
   Yang, Yanan
   Wang, Ziyi
   Yang, Jing
   Chu, Xiao
   Liu, Jin
   Zhao, Yongxing
TI Polypeptide-engineered DNA tetrahedrons for targeting treatment of
   colorectal cancer <i>via</i> apoptosis and autophagy
SO JOURNAL OF CONTROLLED RELEASE
LA English
DT Article
DE Colorectal cancer; DNA tetrahedron; Cell apoptosis; Cell autophagy;
   Anti-cancer peptides
ID CD SPECTRA; NANOPARTICLES; DELIVERY
AB Smart delivery of therapeutic peptides that target cellular signaling pathways holds high specificity and great promise for cancer therapy. Here, DNA tetrahedrons (TDs) are designed to carry two therapeutic peptides-FAS peptide and FK-16 peptide. DNA TDs are designed with varied numbers and spatial placement of FAS peptides and FK-16 peptides, and tested for their anti-cancer efficacy. Trimerization of FAS receptors using TDs that are assembled with three FAS peptides enhances FAS-induced cell apoptosis. FK-16 peptides are conjugated to TDs via a peptide sequence sensitive to MMP-2/9 in tumor microenvironment. Therefore, FK-16 peptides are expected to detach from TDs once arrived the tumor microenvironment. A cell penetrating peptide (TAT) is also conjugated to the FK-16 peptide to facilitate its intracellular delivery, which increases the FK-16 peptide-induced cell apoptosis and autophagy. TD-3(TFM)3(FAS) (TFM: TAT+ FK-16+ MMP-2/9) exhibits the highest HT-29 inhibition in vitro and in vivo among all therapies. In addition to the high anti-cancer efficacy, TD-3(TFM)3(FAS) shows a high specificity to HT-29 cells in vitro and in vivo. Low cell inhibition rates and cellular uptake are observed in normal cells. In sum, the multifunctional TD-3(TFM)3(FAS) provides a new platform for the smart delivery of anti-cancer peptides to achieve enhanced efficacy and high specificity.
C1 [Zhang, Nan; Yang, Yanan; Wang, Ziyi; Yang, Jing; Chu, Xiao; Zhao, Yongxing] Zhengzhou Univ, Sch Pharmaceut Sci, Dept Pharmaceut, Zhengzhou 450001, Henan, Peoples R China.
   [Zhang, Nan; Zhao, Yongxing] Key Lab Targeting Therapy & Diag Crit Dis, Zhengzhou 450001, Henan, Peoples R China.
   [Zhang, Nan; Zhao, Yongxing] Minist Educ China, Key Lab Adv Pharmaceut Technol, Zhengzhou 450001, Henan, Peoples R China.
   [Liu, Jin] Fudan Univ, Inst Biomed Sci, Zhongshan Hosp, Shanghai, Peoples R China.
   [Liu, Jin] Fudan Univ, Shanghai Inst Cardiovasc Dis, Zhongshan Hosp, Shanghai, Peoples R China.
C3 Zhengzhou University; Fudan University; Fudan University
RP Zhang, N; Zhao, YX (corresponding author), Zhengzhou Univ, Sch Pharmaceut Sci, 100 KeXue Ave,Room A315, Zhengzhou 450001, Henan, Peoples R China.
EM nanzhang@zzu.edu.cn; zhaoyx@zzu.edu.cn
RI Zhao, Yongxing/AAD-4079-2019; Cheng, Xiaoxiao/ABA-6326-2020; Zhang,
   Nan/J-6823-2016
OI Zhang, Nan/0000-0002-0941-482X
FU National Natural Science Foundation of China (NSFC) [81573011,
   81861138004]; Key Project of Ministry of Education of HeNan Province for
   Higher Education Institutions [16A350012]
FX Financial support from the National Natural Science Foundation of China
   (NSFC No. 81573011 and 81861138004) and Key Project of Ministry of
   Education of HeNan Province for Higher Education Institutions (No.
   16A350012) are gratefully acknowledged. We also thank the Center of
   Advanced Analysis & Computational Science, Zhengzhou University for the
   assistance of data acquirement.
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NR 31
TC 19
Z9 19
U1 2
U2 55
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
SN 0168-3659
EI 1873-4995
J9 J CONTROL RELEASE
JI J. Control. Release
PD SEP 10
PY 2019
VL 309
BP 48
EP 58
DI 10.1016/j.jconrel.2019.07.012
PG 11
WC Chemistry, Multidisciplinary; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Chemistry; Pharmacology & Pharmacy
GA JG2NS
UT WOS:000491913100005
PM 31301339
DA 2025-01-04
ER

PT J
AU Pesta, M
   Kulda, V
   Narsanska, A
   Fichtl, J
   Topolcan, O
AF Pesta, Martin
   Kulda, Vlastimil
   Narsanska, Andrea
   Fichtl, Jakub
   Topolcan, Ondrej
TI May CTC technologies promote better cancer management?
SO EPMA JOURNAL
LA English
DT Review
DE Circulating tumor cells; Tumor markers; PPPM; Breast cancer; Colorectal
   cancer
ID CIRCULATING TUMOR-CELLS; METASTATIC BREAST-CANCER; COLORECTAL-CANCER;
   PERIPHERAL-BLOOD; BONE-MARROW; KRAS MUTATION; HER2 STATUS;
   PROGNOSTIC-SIGNIFICANCE; CLINICAL-SIGNIFICANCE; PREDICTIVE MARKERS
AB In the case of cancer, death is usually not due to the primary tumor itself but due to dissemination. Analysis of the circulating tumor cells (CTCs), i.e., cells responsible for a formation of metastases, should provide information useful for the management of cancer patients, fulfilling the objectives of predictive, preventive, and personalized medicine (PPPM). Despite promising results, the decisions on stage of disease and how to guide the adjuvant treatment still do not include results of CTC assessment. We want to describe two major reasons why the recent diagnostic value of CTC analysis is not sufficient for clinical use. The first reason arises from the biological nature of the tumor itself and the second reason is associated with an interdisciplinary status of CTC diagnostics in the sense that it is neither a theme purely for pathologists nor for haemato-oncologists nor clinical biochemists. We anticipate that there are at least three areas where CTCs can be useful for clinical practice. The first is monitoring of treatment efficacy of cancer patients. The second is a molecular characterization of captured CTCs for targeted treatment, and the third is a cultivation of captured CTCs for drug sensitivity testing. All of these approaches allow researchers recognize and respond to changes of phenotype of cancer cells during disease progression and introduce PPPM into clinical practice.
C1 [Pesta, Martin] Charles Univ Prague, Fac Med Pilsen, Dept Biol, Karlovarska 48, Plzen 30166, Czech Republic.
   [Pesta, Martin] Charles Univ Prague, Fac Med Pilsen, Biomed Ctr, Plzen 30166, Czech Republic.
   [Kulda, Vlastimil] Charles Univ Prague, Fac Med Pilsen, Dept Biochem, Plzen 30166, Czech Republic.
   [Narsanska, Andrea; Fichtl, Jakub] Charles Univ Prague, Fac Med Pilsen, Dept Surg, Plzen 30166, Czech Republic.
   [Topolcan, Ondrej] Charles Univ Prague, Fac Med Pilsen, Dept Internal Med 2, Plzen 30166, Czech Republic.
C3 Charles University Prague; Charles University Prague; Charles University
   Prague; Charles University Prague; Charles University Prague
RP Pesta, M (corresponding author), Charles Univ Prague, Fac Med Pilsen, Dept Biol, Karlovarska 48, Plzen 30166, Czech Republic.
EM martin.pesta@lfp.cuni.cz
RI Kulda, Vlastimil/I-3165-2017; Topolcan, Ondrej/K-7753-2017
OI Kulda, Vlastimil/0000-0001-7926-994X; Topolcan,
   Ondrej/0000-0001-6622-390X
FU Ministry of Health, Czech Republic-conceptual development of research
   organization (Faculty Hospital in Pilsen-FNPl) [00669806]; grand IGA
   MZCR [NT 14332-3/2013]; EU [CZ1.07./2.3.00/20.0040]
FX This work was supported by the Ministry of Health, Czech
   Republic-conceptual development of research organization (Faculty
   Hospital in Pilsen-FNPl, 00669806) and by the grand IGA MZCR, NT
   14332-3/2013 and EU project CZ1.07./2.3.00/20.0040.
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NR 84
TC 19
Z9 20
U1 0
U2 7
PU SPRINGER INT PUBL AG
PI CHAM
PA GEWERBESTRASSE 11, CHAM, CH-6330, SWITZERLAND
SN 1878-5077
EI 1878-5085
J9 EPMA J
JI EPMA J.
PD JAN 22
PY 2015
VL 6
AR 1
DI 10.1186/s13167-014-0023-x
PG 9
WC Medicine, General & Internal; Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine; Research & Experimental Medicine
GA CU6HB
UT WOS:000363631500001
PM 25628770
OA hybrid, Green Published
DA 2025-01-04
ER

PT J
AU Patelli, G
   Mauri, G
   Tosi, F
   Amatu, A
   Bencardino, K
   Bonazzina, E
   Pizzutilo, EG
   Villa, F
   Calvanese, G
   Agostara, AG
   Stabile, S
   Ghezzi, S
   Crisafulli, G
   Di Nicolantonio, F
   Marsoni, S
   Bardelli, A
   Siena, S
   Sartore-Bianchi, A
AF Patelli, Giorgio
   Mauri, Gianluca
   Tosi, Federica
   Amatu, Alessio
   Bencardino, Katia
   Bonazzina, Erica
   Pizzutilo, Elio Gregory
   Villa, Federica
   Calvanese, Gabriele
   Agostara, Alberto Giuseppe
   Stabile, Stefano
   Ghezzi, Silvia
   Crisafulli, Giovanni
   Di Nicolantonio, Federica
   Marsoni, Silvia
   Bardelli, Alberto
   Siena, Salvatore
   Sartore-Bianchi, Andrea
TI Circulating Tumor DNA to Drive Treatment in Metastatic Colorectal Cancer
SO CLINICAL CANCER RESEARCH
LA English
DT Review
ID EGFR MONOCLONAL-ANTIBODIES; FOLFIRI PLUS CETUXIMAB; CELL-FREE DNA;
   ACQUIRED-RESISTANCE; MICROSATELLITE INSTABILITY; RAS MUTATIONS;
   PHASE-III; THERAPY; PANITUMUMAB; BRAF
AB In the evolving molecular treatment landscape of metastatic colorectal cancer (mCRC), the identification of druggable alterations is pivotal to achieve the best therapeutic opportunity for each patient. Because the number of actionable targets is expanding, there is the need to timely detect their presence or emergence to guide the choice of different available treatment options. Liquid biopsy, through the analysis of circulating tumor DNA (ctDNA), has proven safe and effective as a complementary method to address cancer evolution while overcoming the limitations of tissue biopsy. Even though data are accumulating regarding the potential for ctDNA-guided treatments applied to targeted agents, still major gaps in knowledge exist as for their application to different areas of the continuum of care. In this review, we recapitulate how ctDNA information could be exploited to drive different targeted treatment strategies in mCRC patients, by refining molecular selection before treatment by addressing tumor heterogeneity beyond tumor tissue biopsy; longitudinally monitoring early-tumor response and resistance mechanisms to targeted agents, potentially leading to tailored, molecular-driven, therapeutic options; guiding the molecular triage towards rechallenge strategies with anti-EGFR agents, suggesting the best time for retreatment; and providing opportunities for an "enhanced rechallenge" through additional treatments or combos aimed at overcoming acquired resistance. Besides, we discuss future perspectives concerning the potential role of ctDNA to fine-tune investigational strategies such as immuno-oncology.
C1 [Patelli, Giorgio; Mauri, Gianluca; Pizzutilo, Elio Gregory; Villa, Federica; Calvanese, Gabriele; Agostara, Alberto Giuseppe; Siena, Salvatore; Sartore-Bianchi, Andrea] Univ Milan, Dept Oncol & Hematooncol, Piazza Osped Maggiore 3, I-20162 Milan, Italy.
   [Patelli, Giorgio; Mauri, Gianluca; Tosi, Federica; Amatu, Alessio; Bencardino, Katia; Bonazzina, Erica; Pizzutilo, Elio Gregory; Villa, Federica; Calvanese, Gabriele; Agostara, Alberto Giuseppe; Stabile, Stefano; Ghezzi, Silvia; Siena, Salvatore; Sartore-Bianchi, Andrea] Grande Osped Metropolitano Niguarda, Dept Hematol Oncol & Mol Med, Milan, Italy.
   [Patelli, Giorgio; Mauri, Gianluca; Crisafulli, Giovanni; Marsoni, Silvia] IFOM ETS The AIRC Inst Mol Oncol, Milan, Italy.
   [Di Nicolantonio, Federica; Bardelli, Alberto] Fdn Piemonte Oncol IRCCS, Candiolo Canc Inst, Candiolo, Italy.
   [Di Nicolantonio, Federica; Bardelli, Alberto] Univ Torino, Dept Oncol, Candiolo, Italy.
   [Sartore-Bianchi, Andrea] Grande Osped Metropolitano Niguarda, Div Clin Res & Innovat, Milan, Italy.
   [Sartore-Bianchi, Andrea] Univ Milan, Grande Osped Metropolitano Niguarda, Dept Hematol Oncol & Mol Med, Div Clin Res & Innovat, Piazza Osped Maggiore 3, I-20162 Milan, Italy.
C3 University of Milan; IFOM - FIRC Institute of Molecular Oncology; IRCCS
   Fondazione del Piemonte per l'Oncologia; University of Turin; University
   of Milan
RP Sartore-Bianchi, A (corresponding author), Univ Milan, Dept Oncol & Hematooncol, Piazza Osped Maggiore 3, I-20162 Milan, Italy.; Sartore-Bianchi, A (corresponding author), Univ Milan, Grande Osped Metropolitano Niguarda, Dept Hematol Oncol & Mol Med, Div Clin Res & Innovat, Piazza Osped Maggiore 3, I-20162 Milan, Italy.
EM andrea.sartorebianchi@unimi.it
RI Amatu, Alessio/K-2669-2018; Sartore-Bianchi, Andrea/AAB-9848-2019;
   Giardina, Giorgio/Y-5513-2019; Di Nicolantonio, Federica/A-2503-2011;
   Siena, Salvatore/ACK-2413-2022; TOSI, FEDERICA MARIA/AIA-1174-2022;
   Patelli, Giorgio/GON-8110-2022; Pizzutilo, Elio Gregory/KIG-8873-2024;
   Crisafulli, Giovanni/AAB-6256-2019
OI Patelli, Giorgio/0000-0001-8697-2158; Sartore-Bianchi,
   Andrea/0000-0003-0780-0409; Amatu, Alessio/0000-0001-5396-3378;
   Calvanese, Gabriele/0009-0001-5758-5586; Mauri,
   Gianluca/0000-0002-7646-0973; Agostara, Alberto
   Giuseppe/0000-0001-5646-7150; Crisafulli, Giovanni/0000-0002-5511-1555;
   Pizzutilo, Elio Gregory/0000-0002-1440-1820; Bonazzina,
   Erica/0000-0002-0660-5583
FU Fondazione AIRC per la ricerca sul cancro ETS (AIRC); Fondazione
   Oncologia Niguarda Onlus [21091]; Fondazione AIRC per la ricerca sul
   cancro ETS
FX The authors are supported by Fondazione Oncologia Niguarda Onlus (G.
   Patelli, G. Mauri, A. Sartore-Bianchi) and Fondazione AIRC per la
   ricerca sul cancro ETS (ID 21091 program; S. Marsoni, A. Bardelli, S.
   Siena, A. Sartore-Bianchi). G. Patelli and G. Mauri are PhD students
   within the European School of Molecular Medicine (SEMM).
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NR 102
TC 8
Z9 8
U1 0
U2 2
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1078-0432
EI 1557-3265
J9 CLIN CANCER RES
JI Clin. Cancer Res.
PD NOV 14
PY 2023
VL 29
IS 22
BP 4530
EP 4539
DI 10.1158/1078-0432.CCR-23-0079
PG 10
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA CG6J2
UT WOS:001124136900015
PM 37436743
OA Green Published, hybrid
DA 2025-01-04
ER

PT J
AU Wagner, AD
   Özdemir, BC
   Rüschoff, J
AF Wagner, Anna D.
   Ozdemir, Berna C.
   Rueschoff, Josef
TI Human epidermal growth factor receptor 2-positive digestive tumors
SO CURRENT OPINION IN ONCOLOGY
LA English
DT Review
DE anti-HER2 therapy; digestive cancer; HER2-positive cancer; HER2 testing
ID ADVANCED GASTRIC-CANCER; ANTIBODY-DRUG CONJUGATE; HER2 SCORING SYSTEM;
   TRASTUZUMAB EMTANSINE; EXPRESSION STATUS; ADVANCED BREAST;
   AMPLIFICATION; PATHOLOGISTS; CAPECITABINE; MULTICENTER
AB Purpose of review
   This manuscript aims at providing an update and overview on the role of Human epidermal growth factor receptor 2 (HER2) testing and HER2-directed therapies in digestive tumors.
   Recent findings
   Phase 3 trial data demonstrating a survival benefit of HER2-targeting treatments are limited to gastric cancer. However, HER2 positivity is also found in 5-6% of colorectal, 7% of pancreatic, and 16% of extrahepatic biliary cancers. Although phase 2 trial data support the use of the combination of trastuzumab and lapatinib with chemotherapy in HER2-positive colorectal cancer, the patient's benefit from targeted treatment of HER2-positive biliary or pancreatic neoplasms is currently unclear, and further clinical trials are necessary.
   Summary
   With the exception of gastric cancer, there are currently no defined guidelines for HER2 testing in other digestive tumors. Various HER2-targeting therapies, which are standard of care in HER2-positive breast cancer, failed in HER2-positive gastric cancers. Thus, the predictive value of HER2 overexpression depends on the tumor type, and results of breast cancer trials cannot a priori be extrapolated to digestive cancers. Next-generation sequencing panel diagnostics may furthermore identify targetable activating mutations in gastric, extrahepatic biliary, and colorectal cancer, particularly if traditional testing (immunohistochemistry/in-situ hybridization) is negative. However, their clinical relevance needs to be determined.
C1 [Wagner, Anna D.; Ozdemir, Berna C.] Lausanne Univ Hosp, Dept Oncol, Rue Bugnon 46, CH-1007 Lausanne, Switzerland.
   [Wagner, Anna D.; Ozdemir, Berna C.] Univ Lausanne, Lausanne, Switzerland.
   [Ozdemir, Berna C.] Int Canc Prevent Inst, Lausanne, Switzerland.
   [Rueschoff, Josef] Inst Pathol Nordhessen, Kassel, Germany.
   [Rueschoff, Josef] Targos Mol Pathol GmbH, Kassel, Germany.
C3 University of Lausanne; Centre Hospitalier Universitaire Vaudois (CHUV);
   University of Lausanne; Targos Molecular Pathology GmbH
RP Wagner, AD (corresponding author), Lausanne Univ Hosp, Dept Oncol, Rue Bugnon 46, CH-1007 Lausanne, Switzerland.
EM dorothea.wagner@chuv.ch
RI ; Ozdemir, Berna C./ABY-1073-2022
OI Wagner, Anna Dorothea/0000-0003-4728-7013; Ozdemir, Berna
   C./0000-0002-7380-0055
FU Roche
FX A.D.W. has received consultant or advisory fee from Eli Lilly, Celgene,
   Shire, Servier, Roche, Bristol-Myers Squibb, as well as travel
   fees/accommodation from Merck Sharp & Dohme, AstraZeneca, Ipsen, Pfizer,
   Sanofi. She is coordinating investigator of the EORTC-1203
   'INNOVATION'-trial, which is supported by an educational grant from
   Roche to EORTC. J.R. has acted in an advisory and/or consulting role for
   Roche, MSD, and BMS, and received research funding from Roche.
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NR 58
TC 4
Z9 4
U1 1
U2 11
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 1040-8746
EI 1531-703X
J9 CURR OPIN ONCOL
JI Curr. Opin. Oncol.
PD JUL
PY 2019
VL 31
IS 4
BP 354
EP 361
DI 10.1097/CCO.0000000000000544
PG 8
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA IQ4OX
UT WOS:000480731200018
PM 31170116
DA 2025-01-04
ER

PT J
AU Yu, CJ
   Huang, FQ
   Wang, KS
   Liu, MM
   Chow, WA
   Ling, X
   Li, FZ
   Causey, JL
   Huang, XZ
   Cook-Wiens, G
   Cui, XJ
AF Yu, Changjun
   Huang, Faqing
   Wang, Kinsley
   Liu, Mengmeng
   Chow, Warren A.
   Ling, Xiang
   Li, Fengzhi
   Causey, Jason L.
   Huang, Xiuzhen
   Cook-Wiens, Galen
   Cui, Xiaojiang
TI Single protein encapsulated SN38 for tumor-targeting treatment
SO JOURNAL OF TRANSLATIONAL MEDICINE
LA English
DT Article
DE Single protein encapsulation; SN38; SPESN38-5; SPESN38-8; Colorectal
   cancer; Soft tissue sarcoma; Topoisomerase I inhibitor; FcRn
ID ALBUMIN-BOUND PACLITAXEL; HUMAN TOPOISOMERASE-I; SACITUZUMAB GOVITECAN;
   IRINOTECAN CPT-11; ACTIVE METABOLITE; INHIBITOR SN-38; PHASE-II;
   CAMPTOTHECIN; CANCER; FCRN
AB BackgroundThe alkaloid camptothecin analog SN38 is a potent antineoplastic agent, but cannot be used directly for clinical application due to its poor water solubility. Currently, the prodrug approach on SN38 has resulted in 3 FDA-approved cancer therapeutics, irinotecan, ONIVYDE, and Trodelvy. However, only 2-8% of irinotecan can be transformed enzymatically in vivo into the active metabolite SN38, which severely limits the drug's efficacy. While numerous drug delivery systems have been attempted to achieve effective SN38 delivery, none have produced drug products with antitumor efficacy better than irinotecan in clinical trials. Therefore, novel approaches are urgently needed for effectively delivering SN38 to cancer cells with better efficacy and lower toxicity.MethodsBased on the unique properties of human serum albumin (HSA), we have developed a novel single protein encapsulation (SPE) technology to formulate cancer therapeutics for improving their pharmacokinetics (PK) and antitumor efficacy and reducing their side effects. Previous application of SPE technology to doxorubicin (DOX) formulation has led to a promising drug candidate SPEDOX-6 (FDA IND #, 152154), which will undergo a human phase I clinical trial. Using the same SPE platform on SN38, we have now produced two SPESN38 complexes, SPESN38-5 and SPESN38-8. We conducted their pharmacological evaluations with respect to maximum tolerated dose, PK, and in vivo efficacy against colorectal cancer (CRC) and soft tissue sarcoma (STS) in mouse models.ResultsThe lyophilized SPESN38 complexes can dissolve in aqueous media to form clear and stable solutions. Maximum tolerated dose (MTD) of SPESN38-5 is 250 mg/kg by oral route (PO) and 55 mg/kg by intravenous route (IV) in CD-1 mice. SPESN38-8 has the MTD of 45 mg/kg by IV in the same mouse model. PK of SPESN38-5 by PO at 250 mg/kg gave mouse plasma AUC0-infinity of 0.05 and 4.5 nmol x h/mL for SN38 and SN38 glucuronidate (SN38G), respectively, with a surprisingly high molar ratio of SN38G:SN38 = 90:1. However, PK of SPESN38-5 by IV at 55 mg/kg yielded much higher mouse plasma AUC0-infinity of 19 and 28 nmol x h/mL for SN38 and SN38G, producing a much lower molar ratio of SN38G:SN38 = 1.5:1. Antitumor efficacy of SPESN38-5 and irinotecan (control) was evaluated against HCT-116 CRC xenograft tumors. The data indicates that SPESN38-5 by IV at 55 mg/kg is more effective in suppressing HCT-116 tumor growth with lower systemic toxicity compared to irinotecan at 50 mg/kg. Additionally, SPESN38-8 and DOX (control) by IV were evaluated in the SK-LMS-1 STS mouse model. The results show that SPESN38-8 at 33 mg/kg is highly effective for inhibiting SK-LMS-1 tumor growth with low toxicity, in contrast to DOX's insensitivity to SK-LMS-1 with high toxicity.ConclusionSPESN38 complexes provide a water soluble SN38 formulation. SPESN38-5 and SPESN38-8 demonstrate better PK values, lower toxicity, and superior antitumor efficacy in mouse models, compared with irinotecan and DOX.
C1 [Yu, Changjun] CALTECH, Dept Chem, Pasadena, CA 91125 USA.
   [Yu, Changjun; Wang, Kinsley; Liu, Mengmeng] Sunstate Biosci LLC, 870 S Myrtle Ave, Monrovia, CA 91016 USA.
   [Huang, Faqing] Univ Southern Mississippi, Dept Chem & Biochem, Hattiesburg, MS 39406 USA.
   [Chow, Warren A.] UCI Hlth, Dept Med, Div Hematol Oncol, Orange, CA 92868 USA.
   [Ling, Xiang; Li, Fengzhi] Roswell Park Comprehens Canc Ctr, Dept Pharmacol & Therapeut, Elm & Carlton St, Buffalo, NY 14263 USA.
   [Ling, Xiang] Canget BioTekpharma LLC, 701 Ellicott St, Buffalo, NY 14203 USA.
   [Causey, Jason L.] Arkansas State Univ, Dept Comp Sci, Jonesboro, AR 72467 USA.
   [Huang, Xiuzhen] Cedars Sinai Med Ctr, Dept Computat Med, Los Angeles, CA 90048 USA.
   [Cook-Wiens, Galen] Cedars Sinai Med Ctr, Dept Biomed Sci, Los Angeles, CA 90048 USA.
   [Cui, Xiaojiang] Cedars Sinai Med Ctr, Samuel Oschin Comprehens Canc Inst, Dept Surg, Los Angeles, CA 90048 USA.
C3 California Institute of Technology; University of Southern Mississippi;
   Roswell Park Comprehensive Cancer Center; Arkansas State University;
   Cedars Sinai Medical Center; Cedars Sinai Medical Center; Cedars Sinai
   Medical Center
RP Yu, CJ (corresponding author), CALTECH, Dept Chem, Pasadena, CA 91125 USA.; Yu, CJ (corresponding author), Sunstate Biosci LLC, 870 S Myrtle Ave, Monrovia, CA 91016 USA.; Huang, FQ (corresponding author), Univ Southern Mississippi, Dept Chem & Biochem, Hattiesburg, MS 39406 USA.; Cui, XJ (corresponding author), Cedars Sinai Med Ctr, Samuel Oschin Comprehens Canc Inst, Dept Surg, Los Angeles, CA 90048 USA.
EM cjyu@caltech.edu; faqing.huang@usm.edu; xiaojiang.cui@cshs.org
OI Yu, C. J./0000-0002-5722-6751; Wang, Kinsley/0000-0002-1491-2719
FU Foundation for the National Institutes of Health
FX Not applicable.
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NR 65
TC 1
Z9 1
U1 2
U2 13
PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
EI 1479-5876
J9 J TRANSL MED
JI J. Transl. Med.
PD DEC 10
PY 2023
VL 21
IS 1
AR 897
DI 10.1186/s12967-023-04778-0
PG 16
WC Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine
GA AL9O2
UT WOS:001118739900002
PM 38072965
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Nassani, N
   Alsheikh, M
   Carroll, B
   Nguyen, D
   Carroll, RE
AF Nassani, Najib
   Alsheikh, Mira
   Carroll, Bobby
   Nguyen, Diep
   Carroll, Robert E.
TI Theranostic Gastrointestinal Endoscopy: Bringing Healing Light to the
   Lumen
SO CLINICAL AND TRANSLATIONAL GASTROENTEROLOGY
LA English
DT Review
ID FINE-NEEDLE INJECTION; HEMOSTATIC POWDER TC-325; PHOTODYNAMIC THERAPY;
   PANCREATIC-CANCER; ESOPHAGEAL CANCER; PHASE-I; FLUID COLLECTIONS; GUIDED
   DRAINAGE; DRUG-DELIVERY; ULTRASOUND
AB Current conventional endoscopes have restricted the accuracy of treatment delivery and monitoring. Over the past decade, there have been major developments in nanotechnology and light triggered therapy, potentially allowing a better detection of challenging lesions and targeted treatment of malignancies in the gastrointestinal tract. Theranostics is a developing form of personalized medicine because it combines diagnosis and targeted treatment delivered in one step using advances in nanotechnology. This review describes the light-triggered therapies (including photodynamic, photothermal, and photoimmunotherapies), nanotechnological advances with nanopowder, nanostent, nanogels, and nanoparticles, enhancements brought to endoscopic ultrasound, in addition to experimental endoscopic techniques, combining both enhanced diagnoses and therapies, including a developed prototype of a "smart" multifunctional endoscope for localized colorectal cancer, near-infrared laser endoscope targeting the gastrointestinal stromal tumors, the concept of endocapsule for obscure gastrointestinal bleed, and a proof-of-concept therapeutic capsule using ultrasound-mediated targeted drug delivery. Hence, the following term has been proposed encompassing these technologies: "Theranostic gastrointestinal endoscopy." Future efforts for integration of these technologies into clinical practice would be directed toward translational and clinical trials translating into a more personalized and interdisciplinary diagnosis and treatment, shorter procedural time, higher precision, higher cost-effectiveness, and less need for repetitive procedures.
C1 [Nassani, Najib; Carroll, Robert E.] Univ Illinois, Dept Med, Div Gastroenterol & Hepatol, Chicago, IL 60607 USA.
   [Alsheikh, Mira] Staten Isl Univ Hosp, Dept Med, Zucker SOM Hofstra Northwell, Staten Isl, NY USA.
   [Carroll, Bobby] Syracuse Univ, Dept Phys, Syracuse, NY USA.
   [Nguyen, Diep] Sorbonne Univ, Inst Vis, Dept Visual Informat Proc, INSERM,CNRS, Paris, France.
C3 University of Illinois System; University of Illinois Chicago;
   University of Illinois Chicago Hospital; Northwell Health; Syracuse
   University; Institut National de la Sante et de la Recherche Medicale
   (Inserm); Centre National de la Recherche Scientifique (CNRS); Sorbonne
   Universite
RP Nassani, N (corresponding author), Univ Illinois, Dept Med, Div Gastroenterol & Hepatol, Chicago, IL 60607 USA.
EM najib.nassani@gmail.com
OI Nassani, Najib/0000-0001-8453-9924
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NR 58
TC 4
Z9 5
U1 0
U2 15
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
EI 2155-384X
J9 CLIN TRANSL GASTROEN
JI Clin. Transl. Gastroenterol.
PD MAR
PY 2020
VL 11
DI 10.14309/ctg.0000000000000119
PG 6
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA MO0PI
UT WOS:000551238800001
PM 32352709
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Yildiz, MZ
   Kamanli, AF
   Eskiler, GG
   Tabakoglu, HÖ
   Pala, MA
   Özdemir, AE
AF Yildiz, Mustafa Zahid
   Kamanli, Ali Furkan
   Eskiler, Gamze Gueney
   Tabakoglu, Hasim Ozgur
   Pala, Muhammed Ali
   Ozdemir, Ayla Eren
TI Development of a novel laboratory photodynamic therapy device: automated
   multi-mode LED system for optimum well-plate irradiation
SO LASERS IN MEDICAL SCIENCE
LA English
DT Article
DE Photodynamic therapy; Automated experiment; Dosage control; Dosimetry;
   Embedded systems
ID OPTICAL-PROPERTIES; HUMAN PROSTATE; IN-VIVO; LIGHT; DOSIMETRY; EFFICACY;
   LASER
AB Multi-mode Automated Well-plate PDT LED Laboratory Irradiation System described.Automates and standardizes time-consuming experiments.LED wavelength and temperature stabilized for highly reproducible irradiations.Efficacy demonstrated in 5-aminolevulinic acid (5-ALA) treatments of HT-29 colon cancer cells and WI-38 human lung fibroblasts.
   Photodynamic therapy (PDT) is a targeted treatment method that utilizes a photosensitizer (PS) to induce cytotoxicity in malignant and non-malignant tumors. Optimization of PDT requires investigation of the selectivity of PS for the target tissues, irradiating light source, irradiation wavelengths, fluence rate, fluence, illumination mode, and overall treatment plan. In this study, we developed the Multi-mode Automatized Well-plate PDT LED Laboratory Irradiation System (MAWPLIS), an innovative device that automates time-consuming well plate light dosage/PS dose measurement experiment. The careful control of LED current and temperature stabilization in the LED module allowed the system to achieve high optical output stability. The MAWPLIS was designed by integrating a 3-axis moving system and motion controller, a quick-switching LED controller unit equipped with interchangeable LED modules capable of employing multiple wavelengths, and a TEC system. The proposed system achieved high optical output stability (1 mW) within the range of 0-500 mW, high wavelength stability (5 nm) at 635 nm, and high temperature stability (0.2 degrees C) across all radiation modes. The system's validation involved in vitro analysis using 5-ALA across varying concentrations, incubation periods, light exposures, and wavelengths in HT-29 colon cancer and WI-38 human lung fibroblast cell lines. Specifically, a combination of 405 nm and 635 nm wavelengths was selected to demonstrate enhanced strategies for colon cancer cell eradication and system validation. The MAWPLIS system represents a significant advancement in photodynamic therapy (PDT) research, offering automation and standardization of time-intensive experiments, high stability and precision, and improved PDT efficacy through dual-wavelength integration.
C1 [Yildiz, Mustafa Zahid] Sakarya Univ Appl Sci, Fac Technol Elect & Elect Engn, Serdivan, Turkiye.
   [Kamanli, Ali Furkan] Sakarya Univ Appl Sci, Biomed Technol Applicat & Res Ctr Biyotam, Serdivan, Turkiye.
   [Eskiler, Gamze Gueney] Sakarya Univ, Fac Med, Serdivan, Turkiye.
   [Tabakoglu, Hasim Ozgur] Bakircay Univ, Biomed Engn, Izmir, Turkiye.
   [Pala, Muhammed Ali; Ozdemir, Ayla Eren] Sakarya Univ, Hlth Serv Vocat Sch, Sakarya, Turkiye.
C3 Sakarya University of Applied Science; Sakarya University of Applied
   Science; Sakarya University; Izmir University of Bakircay; Sakarya
   University
RP Kamanli, AF (corresponding author), Sakarya Univ Appl Sci, Biomed Technol Applicat & Res Ctr Biyotam, Serdivan, Turkiye.
EM fkamanli@sakarya.edu.tr
RI PALA, Muhammed Ali/ABG-8198-2021; Yildiz, Mustafa/HJZ-4688-2023; Guney
   Eskiler, Gamze/AAB-6011-2022
OI guney eskiler, gamze/0000-0002-2088-9914; PALA, Muhammed
   Ali/0000-0002-8153-7971
FU Sakarya University of Applied Sciences [118E235]; TUBITAK; Biomedical
   Technologies Application and Research Center (BIYOTAM)
FX This study was supported by TUBITAK 3501 Project no: 118E235 and
   Biomedical Technologies Application and Research Center (BIYOTAM).
   Special thanks to the Muhammed GULER for support.
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NR 40
TC 0
Z9 0
U1 1
U2 4
PU SPRINGER LONDON LTD
PI LONDON
PA 236 GRAYS INN RD, 6TH FLOOR, LONDON WC1X 8HL, ENGLAND
SN 0268-8921
EI 1435-604X
J9 LASER MED SCI
JI Lasers Med. Sci.
PD MAY 16
PY 2024
VL 39
IS 1
AR 131
DI 10.1007/s10103-024-04083-2
PG 12
WC Engineering, Biomedical; Surgery
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Engineering; Surgery
GA QY7T6
UT WOS:001224502000001
PM 38750381
OA hybrid, Green Published
DA 2025-01-04
ER

PT J
AU Cadranel, J
   Liu, SV
   Duruisseaux, M
   Branden, E
   Goto, Y
   Weinberg, BA
   Heining, C
   Schlenk, RF
   Cheema, P
   Jones, MR
   Drilon, A
   Trombetta, D
   Muscarella, LA
   Tolba, K
   Gounant, V
   Cseh, A
   Solca, F
   Laskin, JJ
   Renouf, DJ
AF Cadranel, Jacques
   Liu, Stephen V.
   Duruisseaux, Michael
   Branden, Eva
   Goto, Yasushi
   Weinberg, Benjamin A.
   Heining, Christoph
   Schlenk, Richard F.
   Cheema, Parneet
   Jones, Martin R.
   Drilon, Alexander
   Trombetta, Domenico
   Muscarella, Lucia Anna
   Tolba, Khaled
   Gounant, Valerie
   Cseh, Agnieszka
   Solca, Flavio
   Laskin, Janessa J.
   Renouf, Daniel J.
TI Therapeutic Potential of Afatinib in<i>NRG1</i>Fusion-Driven Solid
   Tumors: A Case Series
SO ONCOLOGIST
LA English
DT Article
DE Gene fusion; NRG1; Afatinib; ErbB-targeted treatment; Case series
ID TARGETING NRG1-FUSIONS; FUSIONS; ADENOCARCINOMA
AB Background Neuregulin 1 (NRG1) fusions, which activate ErbB signaling, are rare oncogenic drivers in multiple tumor types. Afatinib is a pan-ErbB family inhibitor that may be an effective treatment forNRG1fusion-driven tumors. Patients and Methods This report summarizes pertinent details, including best tumor response to treatment, for six patients with metastaticNRG1fusion-positive tumors treated with afatinib. Results The six cases include four female and two male patients who ranged in age from 34 to 69 years. Five of the cases are patients with lung cancer, including two patients with invasive mucinous adenocarcinoma and three patients with nonmucinous adenocarcinoma. The sixth case is a patient with colorectal cancer.NRG1fusion partners for the patients with lung cancer were eitherCD74orSDC4. The patient with colorectal cancer harbored a novelPOMK-NRG1fusion and aKRASmutation. Two patients received afatinib as first- or second-line therapy, three patients received the drug as third- to fifth-line therapy, and one patient received afatinib as fifteenth-line therapy. Best response with afatinib was stable disease in two patients (duration up to 16 months when combined with local therapies) and partial response (PR) of >18 months in three patients, including one with ongoing PR after 27 months. The remaining patient had a PR of 5 months with afatinib 40 mg/day, then another 6 months after an increase to 50 mg/day. Conclusion This report reviews previously published metastaticNRG1fusion-positive tumors treated with afatinib and summarizes six previously unpublished cases. The latter include several with a prolonged response to treatment (>18 months), as well as the first report of efficacy inNRG1fusion-positive colorectal cancer. This adds to the growing body of evidence suggesting that afatinib can be effective in patients withNRG1fusion-positive tumors. Key Points
   NRG1fusions activate ErbB signaling and have been identified as oncogenic drivers in multiple solid tumor types. Afatinib is a pan-ErbB family inhibitor authorized for the treatment of advanced non-small cell lung cancer that may be effective inNRG1fusion-driven tumors. This report summarizes six previously unpublished cases ofNRG1fusion-driven cancers treated with afatinib, including five with metastatic lung cancer and one with metastatic colorectal cancer. Several patients showed a prolonged response of >18 months with afatinib treatment. This case series adds to the evidence suggesting a potential role for afatinib in this area of unmet medical need.
C1 [Cadranel, Jacques] Hop Tenon, AP HP, Paris, France.
   [Cadranel, Jacques] Sorbonne Univ, Grp Rech Clin Theranoscan, Paris, France.
   [Cadranel, Jacques] Sorbonne Univ, Grp Rech Clin Curamus, Paris, France.
   [Liu, Stephen V.; Weinberg, Benjamin A.] Georgetown Univ, Med Ctr, 3800 Reservoir Rd NW, Washington, DC 20007 USA.
   [Duruisseaux, Michael] Hosp Civils Lyon, Louis Pradel Hosp, Resp Dept, Canc Inst, Lyon, France.
   [Duruisseaux, Michael] Canc Res Ctr Lyon, Antcanc Antibodies Lab, Lyon, France.
   [Duruisseaux, Michael] Univ Claude Bernard Lyon 1, Univ Lyon, Lyon, France.
   [Branden, Eva] Gavle Cent Hosp, Gavle, Sweden.
   [Goto, Yasushi] Natl Canc Ctr, Tokyo, Japan.
   [Heining, Christoph] Natl Ctr Tumor Dis NCT Dresden, Dept Translat Med Oncol, Dresden, Germany.
   [Heining, Christoph] German Canc Res Ctr, Dresden, Germany.
   [Heining, Christoph] NCT Dresden, Ctr Personalized Oncol, Dresden, Germany.
   [Heining, Christoph] Tech Univ Dresden, Univ Hosp Carl Gustav Carus Dresden, Dresden, Germany.
   [Heining, Christoph] German Canc Consortium DKTK, Dresden, Germany.
   [Schlenk, Richard F.] Heidelberg Univ Hosp, Natl Ctr Tumor Dis Heidelberg, Heidelberg, Germany.
   [Schlenk, Richard F.] German Canc Res Ctr, Heidelberg, Germany.
   [Cheema, Parneet] Univ Toronto, William Osler Hlth Syst, Toronto, ON, Canada.
   [Jones, Martin R.] QIAGEN Inc, QIAGEN Digital Insights, Redwood City, CA USA.
   [Drilon, Alexander] Mem Sloan Kettering Canc Ctr, 1275 York Ave, New York, NY 10021 USA.
   [Trombetta, Domenico; Muscarella, Lucia Anna] Fdn IRCCS Casa Sollievo Sofferenza Hosp, Foggia, Italy.
   [Tolba, Khaled] Oregon Hlth & Sci Univ, Portland, OR 97201 USA.
   [Gounant, Valerie] Hop Bichat Claude Bernard, AP HP, Paris, France.
   [Gounant, Valerie] Univ Paris 05, Paris, France.
   [Cseh, Agnieszka] Boehringer Ingelheim Int GmbH, Ingelheim, Germany.
   [Solca, Flavio] Boehringer Ingelheim Reg Ctr Vienna GmbH & Co KG, Vienna, Austria.
   [Laskin, Janessa J.; Renouf, Daniel J.] Univ British Columbia, BC Canc, Vancouver, BC, Canada.
C3 Assistance Publique Hopitaux Paris (APHP); Sorbonne Universite; Hopital
   Universitaire Tenon - APHP; Sorbonne Universite; Sorbonne Universite;
   Georgetown University; CHU Lyon; Universite Claude Bernard Lyon 1;
   UNICANCER; Centre Leon Berard; Institut National de la Sante et de la
   Recherche Medicale (Inserm); Universite Claude Bernard Lyon 1; National
   Cancer Center - Japan; Helmholtz Association; German Cancer Research
   Center (DKFZ); Technische Universitat Dresden; Carl Gustav Carus
   University Hospital; Helmholtz Association; German Cancer Research
   Center (DKFZ); Ruprecht Karls University Heidelberg; Helmholtz
   Association; German Cancer Research Center (DKFZ); University of
   Toronto; Memorial Sloan Kettering Cancer Center; Oregon Health & Science
   University; Assistance Publique Hopitaux Paris (APHP); Universite Paris
   Cite; Hopital Universitaire Bichat-Claude Bernard - APHP; Universite
   Paris Cite; Boehringer Ingelheim; Boehringer Ingelheim; University of
   British Columbia
RP Liu, SV (corresponding author), Georgetown Univ, Med Ctr, 3800 Reservoir Rd NW, Washington, DC 20007 USA.
EM stephen.v.liu@gunet.georgetown.edu
RI Schlenk, Richard/AAG-3218-2019; Heining, Christoph/IUO-2974-2023; Liu,
   Stephen/E-5688-2019; Muscarella, Lucia Anna/K-5979-2016; Trombetta,
   Domenico/K-6344-2016
OI Liu, Stephen/0000-0002-4852-3914; Muscarella, Lucia
   Anna/0000-0002-1866-8151; Trombetta, Domenico/0000-0002-6156-8500
FU Boehringer Ingelheim
FX Medical writing assistance, supported financially by Boehringer
   Ingelheim, was provided by Caroline Perry of GeoMed, an Ashfield
   company, part of UDG Healthcare plc, and Toby Allinson, contracted on
   behalf of GeoMed, during the preparation of this article. The authors
   acknowledge Dr. Martine Antoine, Pathologist (Hopital Tenon, Paris,
   France), Pr. Roger Lacave (Hopital Tenon), and Pr. Pierre Laurent Puig
   (Hopital Europeen Georges Pompidou, Paris, France), Molecular
   Biologists, for their contribution in the diagnosis of the NRG1
   fusion-driven patient of Case 4. This work was funded by Boehringer
   Ingelheim.
CR [Anonymous], 2019, J CLIN ONCOL S
   Cheema PK, 2017, J THORAC ONCOL, V12, pE200, DOI 10.1016/j.jtho.2017.07.033
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NR 34
TC 36
Z9 37
U1 0
U2 3
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1083-7159
EI 1549-490X
J9 ONCOLOGIST
JI Oncologist
PD JAN
PY 2021
VL 26
IS 1
BP 7
EP 16
DI 10.1634/theoncologist.2020-0379
EA SEP 2020
PG 10
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA PS1YZ
UT WOS:000571853800001
PM 32852072
OA Bronze, Green Published
DA 2025-01-04
ER

PT J
AU Gu, HT
   Xu, ZQ
   Zhang, JB
   Wei, YB
   Cheng, L
   Wang, JJ
AF Gu, Haitao
   Xu, Zhiquan
   Zhang, Jianbo
   Wei, Yanbing
   Cheng, Ling
   Wang, Jijian
TI circ_0038718 promotes colon cancer cell malignant progression via the
   miR-195-5p/Axin2 signaling axis and also effect Wnt/β-catenin signal
   pathway
SO BMC GENOMICS
LA English
DT Article
DE colon cancer; circ_0038718; Wnt; beta-catenin signaling pathway;
   Proliferation; Migration; Invasion
ID PROLIFERATION; OVEREXPRESSION; METASTASIS; COMPLEXITY; EXPRESSION;
   MIGRATION
AB Objective: Colon cancer (CC) is one of the most common cancers whose progression is regulated by a number of factors, including circular RNAs (circRNAs). Nonetheless, circ_0038718 is a novel circRNA, and its regulatory mechanism in CC remains unclear.
   Methods: Real-time quantitative PCR (qRT-PCR) was performed to detect the expression of circ_0038718, miR-195-5p and Axin2. Western blot was conducted to determine the protein expression of Axin2 and the key proteins on Wnt/beta-catenin signaling pathway. Oligo (dT) (18) primers and RNase R were employed to identify the circular features of circ_0038718, and the location of circ_0038718 in cells was detected via nucleocytoplasmic separation. Dual-luciferase reporter assay and RNA binding protein immunoprecipitation experiment were carried out to investigate the molecular mechanism of circ_0038718/miR-195-5p/Axin2. Additionally, MTT assay was conducted to assess cell proliferation; Transwell assay was performed to evaluate cell migration and invasion, respectively. The effect of circ_0038718 on CC tumor growth was tested through tumor formation in nude mice.
   Results: circ_0038718 was highly expressed in CC and could sponge miR-195-5p in cytoplasm. Silencing circ_0038718 suppressed the proliferative, migratory and invasive abilities of CC cells, while the promoting effect of high circ_0038718 expression on CC cells was reversed upon miR-195-5p over-expression. Axin2 was a downstream target of miR-195-5p and could regulate the Wnt/beta-catenin signaling pathway. Axin2 expression was modulated by circ_0038718/miR-195-5p. Knockdown of Axin2 could also attenuate the promoting effect of high circ_0038718 expression on CC cell malignant progression, thus inhibiting tumor growth.
   Conclusion: circ_0038718 is able to facilitate CC cell malignant progression via the miR-195-5p/Axin2 axis, which will provide a new idea for finding a novel targeted treatment of CC.
C1 [Gu, Haitao; Xu, Zhiquan; Zhang, Jianbo; Wang, Jijian] Chongqing Med Univ, Dept Gastrointestinal Surg, Affiliated Hosp 2, 288 Tianwen Dadao Rd, Chongqing 401336, Peoples R China.
   [Wei, Yanbing; Cheng, Ling] Shanghai Engn Res Ctr Pharmaceut Translat, Shanghai 200231, Peoples R China.
C3 Chongqing Medical University; Shanghai Academy of Science & Technology
RP Wang, JJ (corresponding author), Chongqing Med Univ, Dept Gastrointestinal Surg, Affiliated Hosp 2, 288 Tianwen Dadao Rd, Chongqing 401336, Peoples R China.
EM wangjijian_wjj@163.com
RI Zhang, Jianbo/AAW-4090-2021; Wei, Yan-Bing/JNE-2727-2023
FU Basic and Frontier Research Project of Chongqing Science and Technology
   Commission [cstc2017jcyjAX0224]; Basic and Frontier Research Project of
   Chongqing yuzhong district Science and Technology Commission [20170401];
   Shanghai Research Center Project and Kuanren Talents Program of the
   second affiliated hospital of Chongqing Medical University
   [kryc-yq-2110]
FX This study was supported by the funds from Basic and Frontier Research
   Project of Chongqing Science and Technology Commission (No.
   cstc2017jcyjAX0224), Basic and Frontier Research Project of Chongqing
   yuzhong district Science and Technology Commission (No. 20170401),
   Shanghai Research Center Project and Kuanren Talents Program of the
   second affiliated hospital of Chongqing Medical University(Gand Number:
   kryc-yq-2110). The funders had no role in study design, data collection
   and analysis, decision to publish, or preparation of the manuscript.
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NR 35
TC 20
Z9 22
U1 1
U2 7
PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1471-2164
J9 BMC GENOMICS
JI BMC Genomics
PD OCT 27
PY 2021
VL 22
IS 1
AR 768
DI 10.1186/s12864-021-07880-z
PG 17
WC Biotechnology & Applied Microbiology; Genetics & Heredity
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biotechnology & Applied Microbiology; Genetics & Heredity
GA WN6KZ
UT WOS:000711876800002
PM 34706645
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Jiménez-Fonseca, P
   Sastre, J
   García-Alfonso, P
   Gómez-España, MA
   Salud, A
   Gil, S
   Rivera, F
   Reina, JJ
   Quintero, G
   Valladares-Ayerbes, M
   Safont, MJ
   La Casta, A
   Robles-Díaz, L
   García-Paredes, B
   López, RL
   Guillot, M
   Gallego, J
   Alonso-Orduña, V
   Diaz-Rubio, E
   Aranda, E
AF Jimenez-Fonseca, P.
   Sastre, J.
   Garcia-Alfonso, P.
   Gomez-Espana, M. A.
   Salud, A.
   Gil, S.
   Rivera, F.
   Reina, J. J.
   Quintero, G.
   Valladares-Ayerbes, M.
   Safont, M. J.
   La Casta, A.
   Robles-Diaz, L.
   Garcia-Paredes, B.
   Lopez, R. Lopez
   Guillot, M.
   Gallego, J.
   Alonso-Orduna, V.
   Diaz-Rubio, E.
   Aranda, E.
CA Spanish Cooperative Grp Treatment
TI Association of Circulating Tumor Cells and Tumor Molecular Profile With
   Clinical Outcomes in Patients With Previously Untreated Metastatic
   Colorectal Cancer: A Pooled Analysis of the Phase III VISNu-1 and Phase
   II VISNu-2 Randomized Trials
SO CLINICAL COLORECTAL CANCER
LA English
DT Article
DE Metastatic colorectal cancer; Prognostic factors; Bevacizumab; BRAF; RAS
ID PLUS BEVACIZUMAB; PROGRESSION-FREE; SURVIVAL; CHEMOTHERAPY
AB Baseline circulating tumor cell (bCTC ) enumeration is an established biomarker in metastatic colorectal cancer (mCRC). A total of 589 untreated mCRC patients from 2 randomized clinical trials were included for evaluation of the prognostic/predictive role of the bCTC count ( >3 vs. < 3). Our results confirm the poor prognosis of patients with bCTC >3 but this is not associated with other adverse prognostic factors such as RAS/BRAF mutations. Background: The bCTC count is a well-established prognostic biomarker in mCRC, as well as in other tumor types. The aim of this analysis was to evaluate the prognostic/predictive role of the bCTC count ( >3 vs. < 3) in previously untreated mCRC. Patients and Methods: The study involved 589 untreated mCRC patients included in the intention-to-treat population of 2 randomized clinical trials (phase III VISNU-1 [NCT01640405] and phase II VISNU-2 [NCT01640444] studies). Results: Of the 589 patients, 349 (59.2%) had bCTC >3 and 240 (40.7%) had bCTC < 3. Multivariate analysis showed that the bCTC count is an independent prognostic factor for overall survival (OS) (HR 0.59, 95% CI 0.48-0.72; P = 0.000) and potential for progression-free survival (PFS) ( P = 0.0549). Median OS was 32.9 and 19.5 months in patients with bCTC < 3 and bCTC >3 ( P < 0.001), respectively. This effect was also observed comparing OS in RASwt patients from both studies. Other prognostic factors were: ECOG-PS, primary tumor site, number of metastatic sites and surgery of the primary tumor. Median OS was lower for patients treated with anti-VEGF versus anti-EGFR (22.3 vs. 33.3 months, P < 0.0001) while there were no significant differences in PFS according to the targeted treatment received. Conclusion: This post-hoc analysis of 2 randomized studies confirms the poor prognosis of patients with bCTC >3 but this is not associated with other adverse independent prognostic factors such as RAS/BRAF mutations.
C1 [Jimenez-Fonseca, P.] ISPA, Hosp Univ Cent Asturias, Dept Med Oncol, Oviedo 33011, Spain.
   [Sastre, J.; Garcia-Paredes, B.] Univ Complutense, Hosp Clin San Carlos, Inst Invest Hosp Clin San Carlos IdISSC, Dept Med Oncol, Madrid 28040, Spain.
   [Garcia-Alfonso, P.] Hosp Univ Gregorio Maranon, Dept Med Oncol, Madrid 28007, Spain.
   [Gomez-Espana, M. A.; Aranda, E.] Univ Cordoba, Hosp Univ Reina Sofia, Inst Salud Carlos III, IMIBIC,CIBERONC,Dept Med Oncol, Cordoba 14004, Spain.
   [Salud, A.] Hosp Arnau Vilanova, Dept Med Oncol, Lerida 25198, Spain.
   [Gil, S.] IBIMA, Hosp Univ Reg & Virgen Victoria, Dept Med Oncol, Malaga 29010, Spain.
   [Rivera, F.] Hosp Univ Marques Valdecilla, Dept Med Oncol, IDIVAL, Santander 39008, Spain.
   [Reina, J. J.] Complejo Hosp Virgen Macarena, Dept Med Oncol, Seville 41009, Spain.
   [Quintero, G.] Hosp Univ Lucus Augusti, Dept Med Oncol, Lugo 27003, Spain.
   [Valladares-Ayerbes, M.] Hosp Univ Virgen Rocio, Dept Med Oncol, Seville 41013, Spain.
   [Safont, M. J.] Univ Valencia, Hosp Gen Univ Valencia, Dept Med Oncol, CIBERONC, Valencia 46014, Spain.
   [La Casta, A.] Hosp Donostia, Dept Med Oncol, Donostia San Sebastian 20014, Guipuzcoa, Spain.
   [Robles-Diaz, L.] Hosp Univ 12 Octubre, Dept Med Oncol, Madrid 28041, Spain.
   [Lopez, R. Lopez] Hosp Univ Santiago de Compostela, Dept Med Oncol, Santiago De Compostela 15706, Spain.
   [Lopez, R. Lopez] Hosp Univ Santiago de Compostela, Translat Med Oncol Grp, Santiago De Compostela 15706, Spain.
   [Lopez, R. Lopez] CIBERONC, Hlth Res Inst IDIS, Santiago De Compostela 15706, Spain.
   [Guillot, M.] Hosp Univ Son Espases, Dept Med Oncol, Palma De Mallorca 07120, Spain.
   [Gallego, J.] Hosp Gen Univ Elche, Dept Med Oncol, Alicante 03203, Spain.
   [Alonso-Orduna, V.] Inst Invest Sanitaria Aragon IISA, Hosp Univ Miguel Servet, Dept Med Oncol, Zaragoza 50009, Spain.
C3 Instituto de Investigacion Sanitaria del Principado de Asturias (ISPA);
   Central University Hospital Asturias; Complutense University of Madrid;
   Hospital Clinico San Carlos; General University Gregorio Maranon
   Hospital; CIBER - Centro de Investigacion Biomedica en Red; CIBERONC;
   Universidad de Cordoba; Instituto de Salud Carlos III; Instituto de
   Investigacion Biomedica de Malaga y Plataforma en Nanomedicina (IBIMA);
   Universidad de Malaga; Hospital Universitario Marques de Valdecilla
   (HUMV); Hospital Universitario Lucus Augusti-Lugo; Virgen del Rocio
   University Hospital; CIBER - Centro de Investigacion Biomedica en Red;
   CIBERONC; University of Valencia; University Hospital Donostia; Hospital
   Universitario 12 de Octubre; Complexo Hospitalario Universitario de
   Santiago de Compostela; Complexo Hospitalario Universitario de Santiago
   de Compostela; CIBER - Centro de Investigacion Biomedica en Red;
   CIBERONC; Hospital Universitari Son Espases; Miguel Servet University
   Hospital
RP Jiménez-Fonseca, P (corresponding author), ISPA, Hosp Univ Cent Asturias, Dept Med Oncol, Avda Roma S-N, Oviedo 33011, Asturias, Spain.
EM palucaji@hotmail.com
RI Valladares'Ayerbes, MANUEL/LDG-3881-2024; Salvia, Antonieta/C-6531-2011;
   Jimenez-Fonseca, Paula/AAA-1272-2020; Lacasta, Ana/J-1063-2014
OI Aranda Aguilar, Enrique/0000-0002-5471-2842; Jimenez Fonseca,
   Paula/0000-0003-4592-3813
FU Spanish Cooperative Group for the Treatment of Digestive Tumours (TTD);
   Roche Farma, S.A.
FX The authors would like to thank the medical and nursing staff at all the
   participating institutions, the patients and their families for
   participating in the study. We also thank I. Ruiz de Mena and S.
   Rodriguez at the TTD Data Centre and A. Perez and E. Santiago
   (Statistics and Data Management) . This work was supported by the
   Spanish Cooperative Group for the Treatment of Digestive Tumours (TTD) .
   Financial support for the research trials was provided by Roche Farma,
   S.A. Support for third-party writing assistance for this manuscript was
   provided by Roche Farma, S.A.
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NR 14
TC 1
Z9 1
U1 1
U2 10
PU CIG MEDIA GROUP, LP
PI DALLAS
PA 3500 MAPLE AVENUE, STE 750, DALLAS, TX 75219-3931 USA
SN 1533-0028
EI 1938-0674
J9 CLIN COLORECTAL CANC
JI Clin. Colorectal Canc.
PD JUN
PY 2023
VL 22
IS 2
BP 222
EP 230
DI 10.1016/j.clcc.2023.02.004
EA MAY 2023
PG 9
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA J6KC4
UT WOS:001010673100001
PM 36944559
DA 2025-01-04
ER

PT J
AU Iranpour, S
   Abnous, K
   Taghdisi, SM
   Saljooghi, AS
AF Iranpour, Sonia
   Abnous, Khalil
   Taghdisi, Seyed Mohammad
   Saljooghi, Amir Sh
TI Towards the preparation of smart drug delivery platforms for colorectal
   cancer therapy: Biocompatible and targeted mesoporous silica
   nanoparticles with the deferiprone-copper complex gatekeeper
SO JOURNAL OF DRUG DELIVERY SCIENCE AND TECHNOLOGY
LA English
DT Article
DE Colorectal cancer; Iron-chelating; Controlled release; Gatekeepers;
   Nanotechnology; Mesoporous silica nanoparticle
ID DOXORUBICIN
AB Background: Achieving smart drug release and preventing premature leakage throughout the delivery journey are two crucial factors that are essential to take into account in the design of nanocarriers. Mesoporous silica nanoparticles (MSNs) can be modified with gatekeeper molecules to achieve controlled release behavior, making them highly promising nanocarriers for smart drug delivery purposes. Methods: Herein, we introduced a novel gatekeeper in the form of an inverted umbrella, consisting of a deferiprone (DFP)-copper complex, which was strategically immobilized on the surface of MSNs to facilitate smart and controlled release of doxorubicin (DOX) within tumor cells. Polyethylene glycol (PEG) polymer and aptamer were further added onto the surface of the nanocarrier to enhance its biocompatibility, and targeting capabilities. The physicochemical characteristics of the targeted nanoplatform, Apt-PEG-DOX@GNP, were investigated, and its anti-cancer effect was evaluated against C26 cells and CHO cells to assess its specificity. In order to evaluate the anti-tumor efficacy, possible side effects, and biodistribution of the prepared nanocarriers, the in vivo experiment was carried out on BALB/c mice bearing colorectal tumors. Results: The substantial surface area of MSNs, measuring 339 m(2)/g, facilitated effective encapsulation of DOX with a maximum loading 23 % +/- 2.05. Preparation of Apt-PEG-DOX@GNP yielded uniform particles with an average diameter of 144.73 +/- 11.29 nm. The Apt-PEG-DOX@GNP demonstrated iron-dependent release behaviors, wherein the cleavage of DFP-COOH-Cu(II) bonds decorating the silica nanoparticles occurred asynchronously, leading to the formation of new DFP-COOH-Fe(II) bonds for the subsequent release of DOX. The in vivo experiments revealed that the biocompatible nanocarriers displayed targeted toxicity towards C26 tumor-bearing BALB/c mice, resulting in minimal side effects. Conclusion: Our prepared novel nanoplatforms showed promising potential for targeted treatment of colorectal cancer and precise control over the drug release.
C1 [Iranpour, Sonia; Saljooghi, Amir Sh] Ferdowsi Univ Mashhad, Fac Sci, Dept Chem, Mashhad, Iran.
   [Abnous, Khalil] Mashhad Univ Med Sci, Pharmaceut Technol Inst, Pharmaceut Res Ctr, Mashhad, Iran.
   [Abnous, Khalil] Mashhad Univ Med Sci, Sch Pharm, Dept Med Chem, Mashhad, Iran.
   [Taghdisi, Seyed Mohammad] Mashhad Univ Med Sci, Pharmaceut Technol Inst, Targeted Drug Delivery Res Ctr, Mashhad, Iran.
   [Taghdisi, Seyed Mohammad] Mashhad Univ Med Sci, Sch Pharm, Dept Pharmaceut Biotechnol, Mashhad, Iran.
C3 Ferdowsi University Mashhad; Mashhad University of Medical Sciences;
   Mashhad University of Medical Sciences; Mashhad University of Medical
   Sciences; Mashhad University of Medical Sciences
RP Saljooghi, AS (corresponding author), Ferdowsi Univ Mashhad, Fac Sci, Dept Chem, Mashhad, Iran.
EM Saljooghi@um.ac.ir
RI abnous, Khalil/R-8103-2017; Saljooghi, Amir/AAB-6042-2021; Taghdisi,
   Seyed Mohammad/F-6694-2017
OI Taghdisi, Seyed Mohammad/0000-0001-9836-2189
FU Iran National Science Foundation (INSF) [4015585]
FX This work is based upon research funded by Iran National Science
   Foundation (INSF) under project No. 4015585.
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NR 43
TC 0
Z9 0
U1 1
U2 1
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
SN 1773-2247
EI 2588-8943
J9 J DRUG DELIV SCI TEC
JI J. Drug Deliv. Sci. Technol.
PD OCT
PY 2024
VL 100
AR 106087
DI 10.1016/j.jddst.2024.106087
EA AUG 2024
PG 14
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA F8D4N
UT WOS:001312056700001
DA 2025-01-04
ER

PT J
AU Padua-Bracho, A
   Velázquez-Aragón, JA
   Fragoso-Ontiveros, V
   Nuñez-Martínez, PM
   Aguayo, MDM
   Sánchez-Contreras, Y
   Ramirez-Otero, MA
   De la Fuente-Hernández, MA
   Vidal-Millán, S
   Wegman-Ostrosky, T
   Pedroza-Torres, A
   Arriaga-Canon, C
   Herrera-Montalvo, LA
   Alvarez-Gómez, RM
AF Padua-Bracho, Alejandra
   Velazquez-Aragon, Jose A.
   Fragoso-Ontiveros, Veronica
   Nunez-Martinez, Paulina Maria
   Mejia Aguayo, Maria de la Luz
   Sanchez-Contreras, Yuliana
   Ramirez-Otero, Miguel Angel
   De la Fuente-Hernandez, Marcela Angelica
   Vidal-Millan, Silvia
   Wegman-Ostrosky, Talia
   Pedroza-Torres, Abraham
   Arriaga-Canon, Cristian
   Herrera-Montalvo, Luis A.
   Alvarez-Gomez, Rosa Maria
TI A Previously Unrecognized Molecular Landscape of Lynch Syndrome in the
   Mexican Population
SO INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
LA English
DT Article
DE Lynch syndrome; pathogenic variants; mutations; variants of uncertain
   significance; MSH2; MLH1; MSH6; EPCAM; PMS2
ID SUSCEPTIBILITY GENE-MUTATIONS; MISMATCH REPAIR GENES; COLORECTAL-CANCER;
   SEQUENCE VARIANTS; INDIVIDUALS; PREVALENCE; SPECTRUM
AB Lynch syndrome (LS) is the main hereditary colorectal cancer syndrome. There have been few reports regarding the clinical and molecular characteristics of LS patients in Latin America; this is particularly true in the Mexican population, where no information is available. The present study aims to describe the clinical and molecular spectrum of variants in a cohort of patients diagnosed with LS in Mexico. We present a retrospective analysis of 412 patients with suspected LS, whose main site of cancer diagnosis was the colon (58.25%), followed by the endometrium (18.93%). Next-generation sequencing analysis, with an extensive multigene panel, showed that 27.1% (112/414) had a variant in one of the genes of the mismatch repair pathway (MMR); 30.4% (126/414) had a variant in non-MMR genes such as CHEK2, APC, MUTYH, BRCA1, and BRCA2; and 42.5% (176/414) had no genetic variants. Most of the variants were found in MLH1. Pathogenic variants (PVs) in MMR genes were identified in 65.7% (96/146) of the total PVs, and 34.24% (45/146) were in non-MMR genes. Molecular and clinical characterization of patients with LS in specific populations allowed personalized follow-up, with the option for targeted treatment with immune checkpoint inhibitors and the development of public health policies. Moreover, such characterization allows for family cascade testing and consequent prevention strategies.
C1 [Padua-Bracho, Alejandra; Fragoso-Ontiveros, Veronica; Nunez-Martinez, Paulina Maria; Mejia Aguayo, Maria de la Luz; Sanchez-Contreras, Yuliana; Ramirez-Otero, Miguel Angel; De la Fuente-Hernandez, Marcela Angelica; Vidal-Millan, Silvia; Pedroza-Torres, Abraham; Alvarez-Gomez, Rosa Maria] Natl Canc Inst, Hereditary Canc Clin, Mexico City 14080, DF, Mexico.
   [Padua-Bracho, Alejandra] Natl Polytech Inst, Postgrad Program Doctorate Biomed & Mol Biotechno, Mexico City 11340, DF, Mexico.
   [Velazquez-Aragon, Jose A.] Natl Pediat Inst, Expt Oncol Lab, Mexico City 04530, DF, Mexico.
   [Wegman-Ostrosky, Talia; Arriaga-Canon, Cristian] Natl Canc Inst, Basic Res Sub Direct, Mexico City 14080, DF, Mexico.
   [Herrera-Montalvo, Luis A.] Natl Inst Genom Med, Gen Management, Mexico City 14610, DF, Mexico.
C3 Instituto Politecnico Nacional - Mexico; Instituto Nacional de Medicina
   Genomica
RP Alvarez-Gómez, RM (corresponding author), Natl Canc Inst, Hereditary Canc Clin, Mexico City 14080, DF, Mexico.
EM ralvarezg@incan.edu.mx
RI Herrera, Luis/GOV-3311-2022; Herrera, Luis A./E-6138-2018
OI Velazquez-Aragon, Jose/0000-0002-3617-8148; Pedroza Torres,
   Abraham/0000-0001-7857-3464; Padua Bracho,
   Alejandra/0009-0001-7672-7682; Herrera, Luis A./0000-0003-3998-9306;
   Ramirez Otero, Miguel Angel/0000-0001-8428-1150; Wegman-Ostrosky,
   Talia/0000-0002-3207-6697
FU CONACYT FOSISS SALUD [2018-02-A3-S-39248]; LXV legislature of the
   Mexican Chamber of Deputies; budget allocation for Program "Hereditary
   Cancer Clinic" [309]
FX This research was partly supported by the CONACYT FOSISS
   SALUD-2018-02-A3-S-39248, and the budget allocation for Program 309
   "Hereditary Cancer Clinic", granted by the LXV legislature of the
   Mexican Chamber of Deputies.
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NR 51
TC 2
Z9 2
U1 0
U2 5
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
SN 1661-6596
EI 1422-0067
J9 INT J MOL SCI
JI Int. J. Mol. Sci.
PD OCT
PY 2022
VL 23
IS 19
AR 11549
DI 10.3390/ijms231911549
PG 19
WC Biochemistry & Molecular Biology; Chemistry, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Chemistry
GA 5H5RG
UT WOS:000867735800001
PM 36232851
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Arikan, BA
   Korkmaz, OE
AF Arikan, Burcu Acikalin
   Korkmaz, Ozge Eren
TI Risk factors for mortality in healthcare-associated infections caused by
   Klebsiella pneumoniae
SO ANNALS OF CLINICAL AND ANALYTICAL MEDICINE
LA English
DT Article
DE Carbapenem Resistance; Klebsiella Pneumoniae; Hospital Infections;
   Mortality; Risk Factor
AB Aim: Healthcare-associated infections (HAIs) are a major cause of morbidity and mortality in hospitals. This study aimed to evaluate the antibiotic resistance profiles and mortality risk factors associated with Klebsiella pneumoniae in healthcare-associated infections. Material and Methods: This cross-sectional, retrospective study was conducted between January 1, 2018, and January 1, 2024. Adult individuals who had K. pneumoniae isolated from clinical samples taken 48 hours after hospitalization and who met healthcare-associated infection criteria were included in the study. The risk factors associated with mortality were evaluated. Results: A total of 84 cases of HAIs caused by K. pneumoniae were included in the study, 47 (56%) of whom were male. Among these, 73.8% exhibited carbapenem-resistant Klebsiella pneumoniae (CRC-Kp). Univariate logistic regression identified chronic obstructive pulmonary disease (COPD), absence of fever response on the fifth day, and CRC-Kp growth as significant mortality predictors. Multivariate analysis revealed patients not on hemodialysis (HD) and absence of fever response on the fifth day as significantly associated with mortality, with 23.774 and 121.620 times higher risk, respectively. Discussion: These findings underscore the threat posed by K. pneumoniae infections due to antibiotic resistance and mortality, highlighting the urgent need for effective infection control measures and targeted treatment strategies.
C1 [Arikan, Burcu Acikalin] Buca Seyfi Demirsoy Training & Res Hosp, Dept Infect Dis & Clin Microbiol, Izmir, Turkiye.
   [Korkmaz, Ozge Eren] Dokuz Eylul Univ, Dept Epidemiol, Izmir, Turkiye.
C3 Dokuz Eylul University
RP Arikan, BA (corresponding author), Buca Seyfi Demirsoy Training & Res Hosp, Dept Infect Dis & Clin Microbiol, Izmir, Turkiye.
EM dr.hburcua@gmail.com
RI Korkmaz, Ozge/KIL-7072-2024
OI Korkmaz, Ozge/0000-0002-9476-4938
FX This study was approved by the Non-Interventional Ethics Committee of
   Izmir Katip Celebi University (Date: 2024-01-18, No: 0031)
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NR 18
TC 0
Z9 0
U1 1
U2 1
PU BAYRAKOL MEDICAL PUBLISHER
PI ANKARA
PA EMRAH MAHALLESI, GULGUN CADDESI, NO 62-58, KECIOREN, ANKARA, 06010,
   Turkiye
EI 2667-663X
J9 ANN CLIN ANAL MED
JI Ann. Clin. Anal. Med.
PD SEP
PY 2024
VL 15
IS 9
BP 635
EP 639
DI 10.4328/ACAM.22271
PG 5
WC Medicine, General & Internal
WE Emerging Sources Citation Index (ESCI)
SC General & Internal Medicine
GA E4Y5A
UT WOS:001303075200009
OA gold
DA 2025-01-04
ER

PT J
AU Du, H
   Chen, Y
AF Du, Hui
   Chen, Ying
TI Competing endogenous RNA networks in cervical cancer: function,
   mechanism and perspective
SO JOURNAL OF DRUG TARGETING
LA English
DT Review
DE Competing endogenous RNA; microRNA; long non-coding RNA; cervical cancer
ID LONG NONCODING RNA; PROMOTES CELL-PROLIFERATION; EPITHELIAL-MESENCHYMAL
   TRANSITION; POOR-PROGNOSIS; HUMAN-PAPILLOMAVIRUS; DOWN-REGULATION;
   COLORECTAL-CANCER; SUPPRESS PROLIFERATION; INHIBITS PROLIFERATION;
   INCREASED EXPRESSION
AB In the past several years, competing endogenous RNAs (ceRNAs) have emerged as a potential class of post-transcriptional regulators that alter gene expression through a microRNA (miRNA)-mediated mechanism. An increasing number of studies have found that ceRNAs play important roles in tumorigenesis. Cervical cancer is one of the most common cancers in female malignancies. Despite advances in our understanding of this neoplasm, patients with advanced cervical cancer still have poor prognosis. There is an urgent need to provide a new insight on the mechanism of cervical cancer development and may be acted as new anticancer therapeutic strategies. Here, we review the ceRNA studies and coherent researches in cervical cancer, especially in long non-coding RNA (lncRNA) and miRNAs in order to broaden horizons into mechanisms, selection biomarkers for diagnosis as well as predicting prognosis, and targeting treatment for cervical cancer in the future.
C1 [Du, Hui] Hebei Med Univ, Hosp 2, Dept Obstet & Gynecol, Shijiazhuang 050000, Hebei, Peoples R China.
   [Chen, Ying] Tianjin Med Univ Canc Inst & Hosp, Dept Gynecol Oncol, Tianjin, Peoples R China.
   [Chen, Ying] Key Lab Canc Prevent & Therapy, Tianjin, Peoples R China.
   [Chen, Ying] Natl Clin Res Ctr Canc, Tianjin, Peoples R China.
C3 Hebei Medical University; Tianjin Medical University
RP Du, H (corresponding author), Hebei Med Univ, Hosp 2, Dept Obstet & Gynecol, Shijiazhuang 050000, Hebei, Peoples R China.
EM lychenying2004@126.com
FU National Natural Science Foundation [81302250]; Tianjin Health Bureau of
   Science and Technology Funds [2012KZ073]
FX This work was supported by National Natural Science Foundation.
   [81302250] and Tianjin Health Bureau of Science and Technology Funds
   [2012KZ073].
CR López JA, 2011, BIOCHEM BIOPH RES CO, V409, P513, DOI 10.1016/j.bbrc.2011.05.036
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NR 146
TC 23
Z9 26
U1 0
U2 24
PU TAYLOR & FRANCIS LTD
PI ABINGDON
PA 2-4 PARK SQUARE, MILTON PARK, ABINGDON OR14 4RN, OXON, ENGLAND
SN 1061-186X
EI 1029-2330
J9 J DRUG TARGET
JI J. Drug Target.
PD AUG 9
PY 2019
VL 27
IS 7
BP 709
EP 723
DI 10.1080/1061186X.2018.1505894
PG 15
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA IA0JS
UT WOS:000469243500001
PM 30052083
DA 2025-01-04
ER

PT J
AU Duplaquet, L
   Figeac, M
   Leprêtre, F
   Frandemiche, C
   Villenet, C
   Sebda, S
   Sarafan-Vasseur, N
   Bénozène, M
   Vinchent, A
   Goormachtigh, G
   Wicquart, L
   Rousseau, N
   Beaussire, L
   Truant, S
   Michel, P
   Sabourin, JC
   Galateau-Salle, F
   Copin, MC
   Zalcman, G
   De Launoit, Y
   Fafeur, V
   Tulasne, D
AF Duplaquet, Leslie
   Figeac, Martin
   Lepretre, Frederic
   Frandemiche, Charline
   Villenet, Celine
   Sebda, Sheherazade
   Sarafan-Vasseur, Nasrin
   Benozene, Melanie
   Vinchent, Audrey
   Goormachtigh, Gautier
   Wicquart, Laurence
   Rousseau, Nathalie
   Beaussire, Ludivine
   Truant, Stephanie
   Michel, Pierre
   Sabourin, Jean-Christophe
   Galateau-Salle, Francoise
   Copin, Marie-Christine
   Zalcman, Gerard
   De Launoit, Yvan
   Fafeur, Veronique
   Tulasne, David
TI Functional Analysis of Somatic Mutations Affecting Receptor Tyrosine
   Kinase Family in Metastatic Colorectal Cancer
SO MOLECULAR CANCER THERAPEUTICS
LA English
DT Article
ID GROWTH-FACTOR; LUNG-CANCER; ACTIVATING MUTATIONS; PROTOONCOGENE;
   PROGRESSION; GERMLINE; DOMAIN; BRAF
AB Besides the detection of somatic receptor tyrosine kinases (RTK) mutations in tumor samples, the current challenge is to interpret their biological relevance to give patients effective targeted treatment. By high-throughput sequencing of the 58 RTK exons of healthy tissues, colorectal tumors, and hepatic metastases from 30 patients, 38 different somatic mutations in RTKs were identified. The mutations in the kinase domains and present in both tumors and metastases were reconstituted to perform an unbiased functional study. Among eight variants found in seven RTKs (EPHA4-Met726Ile, EPHB2-Val621Ile, ERBB4-Thr731Met, FGFR4-Ala585Thr, VEGFR3-Leu1014Phe, KIT-Pro875Leu, TRKB-Leu584Val, and NTRK2-Lys618Thr), none displayed significantly increased tyrosine kinase activity. Consistently, none of them induced transformation of NIH3T3 fibroblasts. On the contrary, two RTK variants (FGFR4-Ala585Thr and FLT4-Leu1014Phe) caused drastic inhibition of their kinase activity. These findings indicate that these RTK variants are not suitable targets and highlight the importance of functional studies to validate RTK mutations as potential therapeutic targets.
C1 [Duplaquet, Leslie; Benozene, Melanie; Vinchent, Audrey; Goormachtigh, Gautier; Copin, Marie-Christine; De Launoit, Yvan; Fafeur, Veronique; Tulasne, David] Univ Lille, Inst Pasteur Lille, CNRS, UMR M3T 8161, Lille, France.
   [Figeac, Martin; Lepretre, Frederic; Villenet, Celine; Sebda, Sheherazade] Univ Lille, CHU Lille, Plateau Genom Fonct & Struct, Lille, France.
   [Frandemiche, Charline; Rousseau, Nathalie] TCBN, Caen, France.
   [Frandemiche, Charline] OncoBasseNormandie, Reseau Reg Cancerol, Caen, France.
   [Sarafan-Vasseur, Nasrin; Beaussire, Ludivine] Normandie Univ, UNIROUEN, Normandy Ctr Genom & Personalized Med, Iron Grp,Inserm U1245,Rouen Univ Hosp, Rouen, France.
   [Wicquart, Laurence; Copin, Marie-Christine] Tumorotheque C2RC Lille, Lille, France.
   [Truant, Stephanie] Univ Lille, Dept Digest Surg & Transplantat, CHU Lille, Lille, France.
   [Michel, Pierre] Normandie Univ, Rouen Univ Hosp, Dept Hepatogastroenterol, UNIROUEN,Inserm U1245,Iron Grp, Rouen, France.
   [Sabourin, Jean-Christophe] Normandy Univ, Rouen Univ Hosp, Dept Pathol, INSERM 1245, Rouen, France.
   [Galateau-Salle, Francoise] Ctr Leon Berard, MESOPATH MESOBANK, Dept Pathol, Lyon, France.
   [Zalcman, Gerard] Hop Bichat Claude Bernard, Thorac Oncol Dept, Paris Nord CIC1425 CLIP2, Paris, France.
C3 Pasteur Network; Universite de Lille; Institut Pasteur Lille; Centre
   National de la Recherche Scientifique (CNRS); Universite de Lille; CHU
   Lille; Universite de Rouen Normandie; CHU de Rouen; Institut National de
   la Sante et de la Recherche Medicale (Inserm); Universite de Lille; CHU
   Lille; Universite de Rouen Normandie; CHU de Rouen; Institut National de
   la Sante et de la Recherche Medicale (Inserm); Institut National de la
   Sante et de la Recherche Medicale (Inserm); Universite de Rouen
   Normandie; CHU de Rouen; UNICANCER; Centre Leon Berard; Assistance
   Publique Hopitaux Paris (APHP); Universite Paris Cite; Hopital
   Universitaire Bichat-Claude Bernard - APHP
RP Tulasne, D (corresponding author), French Natl Ctr Sci Res, 1 Rue Pr Calmette, F-59021 Lille, France.
EM david.tulasne@ibl.cnrs.fr
RI ZALCMAN, Gerard/M-8113-2019; Tulasne, David/AAR-5287-2020; truant,
   stéphanie/HOA-5895-2023; Salle, Francoise/J-1530-2015; ZALCMAN,
   Gerard/L-7809-2015
OI Figeac, Martin/0000-0001-8523-3708; Truant,
   Stephanie/0000-0002-2828-4864; Duplaquet, Leslie/0000-0002-6544-0432;
   ZALCMAN, Gerard/0000-0002-0343-9575; Tulasne, David/0000-0002-6764-7242;
   de Launoit, Yvan/0000-0003-1837-9808; lepretre,
   frederic/0000-0002-5249-3930; galateau salle,
   francoise/0000-0002-2814-1644; Goormachtigh, Gautier/0000-0003-1736-8269
FU Centre National de la Recherche Scientifique; Institut Pasteur de Lille
   (Lille, France); INSERM; Canceropole Nord-Ouest; Ligue Contre le Cancer,
   Comite Nord; Institut National du Cancer
FX This work was supported by the Centre National de la Recherche
   Scientifique, the Institut Pasteur de Lille (Lille, France), and INSERM,
   and by grants from the "Canceropole Nord-Ouest" (to V. Fafeur and D.
   Tulasne), the "Ligue Contre le Cancer, Comite Nord" (to D. Tulasne), and
   the "Institut National du Cancer" (to D. Tulasne). We would like to
   thank Dr. Liebl, Dr. Elenius, Dr. Klein, Dr. Kaijalainen, Dr. Lu, Dr.
   Dubreuil, Dr. Alitalo, and Dr. Ittmann for providing the RTK expression
   vectors. We would like to thank the Centre de Traitement des Donnees du
   Canceropole Nord-Ouest for clinical data processing.
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NR 34
TC 1
Z9 1
U1 2
U2 3
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1535-7163
EI 1538-8514
J9 MOL CANCER THER
JI Mol. Cancer Ther.
PD JUN
PY 2019
VL 18
IS 6
BP 1137
EP 1148
DI 10.1158/1535-7163.MCT-18-0582
PG 12
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA IB5ES
UT WOS:000470294700011
PM 30926633
OA Green Submitted, Bronze
DA 2025-01-04
ER

PT J
AU Vasiljeva, O
   Hostetter, DR
   Moore, SJ
   Winter, MB
AF Vasiljeva, Olga
   Hostetter, Daniel R.
   Moore, Stephen J.
   Winter, Michael B.
TI The multifaceted roles of tumor-associated proteases and harnessing
   their activity for prodrug activation
SO BIOLOGICAL CHEMISTRY
LA English
DT Review
DE cancer; prodrug; protease; proteolysis; tumor microenvironment
ID UROKINASE PLASMINOGEN-ACTIVATOR; TRANSMEMBRANE SERINE PROTEASES;
   CYSTEINE PROTEINASE-INHIBITORS; CATHEPSIN-B EXPRESSION; MATRIX
   METALLOPROTEINASES; COLORECTAL-CANCER; ASPARAGINYL ENDOPEPTIDASE;
   DOXORUBICIN PRODRUGS; LEGUMAIN EXPRESSION; BARRIER FUNCTION
AB The role of proteases in cancer was originally thought to be limited to the breakdown of basement membranes and extracellular matrix (ECM), thereby promoting cancer cell invasion into surrounding normal tissues. It is now well understood that proteases play a much more complicated role in all stages of cancer progression and that not only tumor cells, but also stromal cells are an important source of proteases in the tumor microenvironment. Among all the proteolytic enzymes potentially associated with cancer, some proteases have taken on heightened importance due to their significant up-regulation and ability to participate at multiple stages of cancer progression and metastasis. In this review, we discuss some of the advances in understanding of the roles of several key proteases from different classes in the development and progression of cancer and the potential to leverage their upregulated activity for the development of novel targeted treatment strategies.
C1 [Vasiljeva, Olga; Hostetter, Daniel R.; Moore, Stephen J.; Winter, Michael B.] CytomX Therapeut Inc, Platform Biol, 151 Oyster Point Blvd, San Francisco, CA 94080 USA.
RP Vasiljeva, O (corresponding author), CytomX Therapeut Inc, Platform Biol, 151 Oyster Point Blvd, San Francisco, CA 94080 USA.
EM olga@cytomx.com
OI Vasiljeva, Olga/0000-0003-3648-5460
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NR 156
TC 26
Z9 28
U1 2
U2 60
PU WALTER DE GRUYTER GMBH
PI BERLIN
PA GENTHINER STRASSE 13, D-10785 BERLIN, GERMANY
SN 1431-6730
EI 1437-4315
J9 BIOL CHEM
JI Biol. Chem.
PD AUG
PY 2019
VL 400
IS 8
BP 965
EP 977
DI 10.1515/hsz-2018-0451
PG 13
WC Biochemistry & Molecular Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology
GA IH9US
UT WOS:000474852600001
PM 30913028
DA 2025-01-04
ER

PT J
AU Han, MZ
   Zhu, H
   Chen, XP
   Luo, X
AF Han, Mengzhen
   Zhu, He
   Chen, Xiaoping
   Luo, Xin
TI 6-O-endosulfatases in tumor metastasis: heparan sulfate proteoglycans
   modification and potential therapeutic targets
SO AMERICAN JOURNAL OF CANCER RESEARCH
LA English
DT Review
DE SULF1; SULF2; HSPG; metastasis; therapeutic target
ID HEPATOCELLULAR-CARCINOMA; HSULF-1 EXPRESSION; COLORECTAL-CANCER;
   TGF-BETA; EXTRACELLULAR SULFATASE; CELL-PROLIFERATION; SIGNALING
   PATHWAYS; OVARIAN-CANCER; GROWTH; PROMOTES
AB Metastasis is the leading cause of cancer -associated mortality. Although advances in the targeted treatment and immunotherapy have improved the management of some cancers, the prognosis of metastatic cancers remains unsatisfied. Therefore, the specific mechanisms in tumor metastasis need further investigation. 6-O-endosulfatases (SULFs), comprising sulfatase1 (SULF1) and sulfatase 2 (SULF2), play pivotal roles in the postsynthetic modifications of heparan sulfate proteoglycans (HSPGs). Consequently, these extracellular enzymes can regulate a variety of downstream pathways by modulating HSPGs function. During the past decades, researchers have detected the expression of SULF1 and SULF2 in most cancers and revealed their roles in tumor progression and metastasis. Herein we reviewed the metastasis steps which SULFs participated in, elucidated the specific roles and mechanisms of SULFs in metastasis process, and discussed the effects of SULFs in different types of cancers. Moreover, we summarized the role of targeting SULFs in combination therapy to treat metastatic cancers, which provided some novel strategies for cancer therapy.
C1 [Han, Mengzhen; Zhu, He; Chen, Xiaoping; Luo, Xin] Huazhong Univ Sci & Technol, Tongji Hosp, Tongji Med Coll, Hepat Surg Ctr, Wuhan 430030, Hubei, Peoples R China.
   [Han, Mengzhen; Zhu, He; Chen, Xiaoping; Luo, Xin] Hubei Key Lab Hepatopancreatobiliary Dis, Wuhan 430030, Hubei, Peoples R China.
   [Luo, Xin] Huazhong Univ Sci & Technol, Hepat Surg Ctr, Tongji Hosp, Hubei Prov Clin Med Res Ctr Hepat Surg,Tongji Med, 1095 Jiefang Ave, Wuhan 430030, Hubei, Peoples R China.
C3 Huazhong University of Science & Technology; Huazhong University of
   Science & Technology
RP Luo, X (corresponding author), Huazhong Univ Sci & Technol, Hepat Surg Ctr, Tongji Hosp, Hubei Prov Clin Med Res Ctr Hepat Surg,Tongji Med, 1095 Jiefang Ave, Wuhan 430030, Hubei, Peoples R China.
EM lx56960201@outlook.com
FU National Natural Science Foundation of China [82203802]
FX <STRONG> </STRONG>The authors would like to thank Dr. Fei Xiong
   (Biliary-Pancreatic Surgery, Tongji Hospital) for kindly providing
   assistance of AI operation. This study was funded by the National
   Natural Science Foundation of China (No. 82203802) .
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NR 181
TC 0
Z9 0
U1 2
U2 2
PU E-CENTURY PUBLISHING CORP
PI MADISON
PA 40 WHITE OAKS LN, MADISON, WI 53711 USA
SN 2156-6976
J9 AM J CANCER RES
JI Am. J. Cancer Res.
PY 2024
VL 14
IS 2
BP 809
EP 828
PG 20
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA KI8V8
UT WOS:001179431500003
DA 2025-01-04
ER

PT J
AU Flanigan, PM
   Aghi, MK
AF Flanigan, Patrick M.
   Aghi, Manish K.
TI Adaptation to antiangiogenic therapy in neurological tumors
SO CELLULAR AND MOLECULAR LIFE SCIENCES
LA English
DT Review
DE Resistance; Adaptive; Glioblastoma; Bevacizumab; Pericytes; Bone marrow;
   Autophagy
ID ENDOTHELIAL GROWTH-FACTOR; PHASE-II TRIAL; ANTI-ANGIOGENIC THERAPY;
   CELL-SURVIVAL; COLORECTAL-CANCER; PROGENITOR CELLS; BLOOD-VESSELS;
   GLIOMA GROWTH; STEM-CELLS; PDGF-B
AB Because tumors require a vascular supply for their survival and growth, angiogenesis is considered an important therapeutic target in most human cancers including cancer of the central nervous system. Antiangiogenic therapy has focused on inhibitors of the vascular endothelial growth factor (VEGF) signaling pathway. VEGF pathway-targeted drugs have shown therapeutic efficacy in several CNS tumors and have been tried most frequently in glioblastoma. These therapies, however, have been less effective than anticipated as some patients do not respond to therapy and some receive only modest benefit. Underlying this suboptimal response are multiple mechanisms of drug resistance involving changes in both tumor cells and their microenvironment. In this review, we discuss the multiple proposed mechanisms by which neurological tumors evolve to become resistant to antiangiogenic therapies. A better understanding of these mechanisms, their context, and their interplay will likely facilitate improvements in pharmacological strategies for the targeted treatment of neurological tumors.
C1 [Flanigan, Patrick M.] Cleveland Clin, Lerner Coll Med, Cleveland, OH 44106 USA.
   [Aghi, Manish K.] Univ Calif San Francisco, Dept Neurol Surg, Calif Ctr Pituitary Disorders, San Francisco, CA 94143 USA.
C3 University System of Ohio; Case Western Reserve University; Cleveland
   Clinic Foundation; University of California System; University of
   California San Francisco
RP Aghi, MK (corresponding author), Univ Calif San Francisco, Dept Neurol Surg, Calif Ctr Pituitary Disorders, San Francisco, CA 94143 USA.
EM aghim@neurosurg.ucsf.edu
OI Flanigan, Patrick/0000-0002-3611-8575
FU NIH [1 R01 NS079697]; National Institute of Neurological Disorders and
   Stroke [R01NS079697] Funding Source: NIH RePORTER
FX This work was supported by funding to M.K.A.'s laboratory from the NIH
   (1 R01 NS079697).
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NR 103
TC 1
Z9 1
U1 0
U2 13
PU SPRINGER BASEL AG
PI BASEL
PA PICASSOPLATZ 4, BASEL, 4052, SWITZERLAND
SN 1420-682X
EI 1420-9071
J9 CELL MOL LIFE SCI
JI Cell. Mol. Life Sci.
PD AUG
PY 2015
VL 72
IS 16
BP 3069
EP 3082
DI 10.1007/s00018-015-1916-0
PG 14
WC Biochemistry & Molecular Biology; Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Cell Biology
GA CN0EX
UT WOS:000358088000005
PM 25943307
OA Green Accepted
DA 2025-01-04
ER

PT J
AU Jiang, K
   Wang, YP
   Wang, XD
   Hui, XB
   Ding, LS
   Liu, J
   Liu, D
AF Jiang, Kun
   Wang, Yan-Ping
   Wang, Xiao-Dong
   Hui, Xiao-Bo
   Ding, Lian-Shu
   Liu, Ji
   Liu, Dai
TI Fms related tyrosine kinase 1 (Flt1) functions as an oncogene and
   regulates glioblastoma cell metastasis by regulating sonic hedgehog
   signaling
SO AMERICAN JOURNAL OF CANCER RESEARCH
LA English
DT Article
DE Flt1; glioblastoma; metastasis; SHH
ID NEGATIVE BREAST-CANCER; COLORECTAL-CANCER; PANCREATIC-CANCER; GLIOMA;
   PROLIFERATION; ANGIOGENESIS; PATHWAY; GROWTH; BRAIN; INVASIVENESS
AB Studies have shown that the abnormal expression of Fms related tyrosine kinase 1 (Flt1) is associated with multiple malignancies, yet its role in glioblastoma pathology remains to be elucidated. In this study, we investigated the role of Flt1 in regulating proliferation, migration and invasion of glioblastoma cells by establishing glioblastoma cell strains with constitutively silenced or elevated Flt1 expression. We demonstrate that ectopic expression of Flt1 promotes glioblastoma cells migration, invasion through cell scratching and Transwell assays. Further study has indicated that Flt1 knockdown prevents the spread of glioblastoma cells in vivo. Conversely, we also show that suppression of Flt1 expression inhibits migration and invasion of glioblastoma cells. Finally, our findings demonstrate that Flt1 promotes invasion and migration of glioblastoma cells through sonic hedgehog (SHH) signaling pathway. Our study suggests that galectin-1 represents a crucial regulator of glioblastoma cells metastasis. Thus, the detection and targeted treatment of Flt1-expressing cancer serves as a new therapeutic target for glioblastoma.
C1 [Jiang, Kun; Wang, Yan-Ping; Wang, Xiao-Dong; Hui, Xiao-Bo; Ding, Lian-Shu; Liu, Ji; Liu, Dai] Nanjing Med Univ, Huaian Peoples Hosp 1, Dept Neurosurg, Huaian 223300, Peoples R China.
C3 Nanjing Medical University
RP Liu, D (corresponding author), Nanjing Med Univ, Huaian Peoples Hosp 1, Dept Neurosurg, Huaian 223300, Peoples R China.
EM liudailiu@aliyun.com
RI Wang, Yanping/AAN-4402-2021
FU Science and Technology Development Foundation of Huai'an [HAS2015018]
FX The study was supported by the Science and Technology Development
   Foundation of Huai'an to Dr. L.S. Ding (China, No. HAS2015018).
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NR 27
TC 10
Z9 11
U1 0
U2 7
PU E-CENTURY PUBLISHING CORP
PI MADISON
PA 40 WHITE OAKS LN, MADISON, WI 53711 USA
SN 2156-6976
J9 AM J CANCER RES
JI Am. J. Cancer Res.
PY 2017
VL 7
IS 5
BP 1164
EP 1176
PG 13
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA EW1NK
UT WOS:000402257100010
PM 28560064
DA 2025-01-04
ER

PT J
AU Satagopan, JM
   Lasonos, A
   Zhou, Q
AF Satagopan, Jaya M.
   Lasonos, Alexia
   Zhou, Qin
TI Prognostic and Predictive Values and Statistical Interactions in the Era
   of Targeted Treatment
SO GENETIC EPIDEMIOLOGY
LA English
DT Article
DE area under the receiver operating characteristic curve; likelihood ratio
   test; relative excess risk due to interaction (RERI); resampling;
   treatment benefit
ID LIKELIHOOD-RATIO TEST; COLORECTAL-CANCER; RISK; GENE; INDEPENDENCE;
   PERFORMANCE; DISEASES; MARKERS
AB The current era of targeted treatment has accelerated the interest in studying gene-treatment, gene-gene, and gene-environment interactions using statistical models in the health sciences. Interactions are incorporated into models as product terms of risk factors. The statistical significance of interactions is traditionally examined using a likelihood ratio test (LRT). Epidemiological and clinical studies also evaluate interactions in order to understand the prognostic and predictive values of genetic factors. However, it is not clear how different types and magnitudes of interaction effects are related to prognostic and predictive values. The contribution of interaction to prognostic values can be examined via improvements in the area under the receiver operating characteristic curve due to the inclusion of interaction terms in the model (AUC). We develop a resampling based approach to test the significance of this improvement and show that it is equivalent to LRT. Predictive values provide insights into whether carriers of genetic factors benefit from specific treatment or preventive interventions relative to noncarriers, under some definition of treatment benefit. However, there is no unique definition of the term treatment benefit. We show that AUC and relative excess risk due to interaction (RERI) measure predictive values under two specific definitions of treatment benefit. We investigate the properties of LRT, AUC, and RERI using simulations. We illustrate these approaches using published melanoma data to understand the benefits of possible intervention on sun exposure in relation to the MC1R gene. The goal is to evaluate possible interventions on sun exposure in relation to MC1R.
C1 [Satagopan, Jaya M.; Lasonos, Alexia; Zhou, Qin] Mem Sloan Kettering Canc Ctr, Dept Epidemiol & Biostat, New York, NY 10017 USA.
C3 Memorial Sloan Kettering Cancer Center
RP Satagopan, JM (corresponding author), Mem Sloan Kettering Canc Ctr, Dept Epidemiol & Biostat, 485 Lexington Ave, New York, NY 10017 USA.
EM satagopj@mskcc.org
OI Satagopan, Jaya/0000-0001-7102-5633
FU NCATS NIH HHS [UL1 TR000457] Funding Source: Medline; NCI NIH HHS
   [R01CA137420, P30CA008748, P30 CA008748, R01 CA137420] Funding Source:
   Medline; NCRR NIH HHS [UL1 RR024996, UL1RR024996] Funding Source:
   Medline
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NR 24
TC 6
Z9 6
U1 0
U2 2
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0741-0395
EI 1098-2272
J9 GENET EPIDEMIOL
JI Genet. Epidemiol.
PD NOV
PY 2015
VL 39
IS 7
BP 509
EP 517
DI 10.1002/gepi.21917
PG 9
WC Genetics & Heredity; Mathematical & Computational Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Genetics & Heredity; Mathematical & Computational Biology
GA CU2FZ
UT WOS:000363340500002
PM 26349638
OA Green Accepted
DA 2025-01-04
ER

PT J
AU Yao, MN
   Ma, XT
   Zhang, X
   Shi, LQ
   Liu, TY
   Liang, XL
   Zhao, HY
   Li, XD
   Li, LQ
   Gao, HN
   Jia, B
   Wang, F
AF Yao, Meinan
   Ma, Xiaotu
   Zhang, Xin
   Shi, Linqing
   Liu, Tianyu
   Liang, Xiaolong
   Zhao, Huiyun
   Li, Xiaoda
   Li, Liqiang
   Gao, Hannan
   Jia, Bing
   Wang, Fan
TI Lectin-Mediated pH-Sensitive Doxorubicin Prodrug for Pre-Targeted
   Chemotherapy of Colorectal Cancer with Enhanced Efficacy and Reduced
   Side Effects
SO THERANOSTICS
LA English
DT Article
DE pre-targeted strategy; avidin; biotin; doxorubicin prodrug; chemotherapy
ID LIPOSOMAL DOXORUBICIN; BREAST-CANCER; DELIVERY; THERAPY; AVIDIN; TUMOR;
   ANTHRACYCLINES; CONJUGATE; COMPLEX
AB Doxorubicin (DOX) has been clinically used as a broad-spectrum chemotherapeutic agent for decades, but its clinical application is hindered by the lack of tumour specificity, severe cardiotoxicity and haematotoxicity. Pre-targeted strategies are highly tumour-specific, therapeutic approaches. Herein, a novel pre-targeted system was constructed, aiming to enhance anticancer efficacy of DOX and maximally reduce its side effects.
   Methods: The DOX prodrug (bDOX) was first synthesized by conjugating DOX with mini-PEGylated (mPEGylated) biotin through a pH-sensitive bond. During the pre-targeted treatment, avidin was first administrated. After an optimized interval, bDOX was second administrated. The nontoxic prodrug bDOX was eventually transformed into the toxic anticancer form (DOX) by a pH-triggered cleavage specifically in tumour cells. The drug efficacy and side effect of the two-step, pre-targeted treatment were fully compared with free DOX in vitro and in vivo.
   Results: The prodrug bDOX was quite stable under neutral conditions and nearly nontoxic, but was immediately transformed into the toxic anticancer form (DOX) under acidic conditions. Compared to free DOX, the pre-targeted bDOX exhibited a higher cellular uptake by human colorectal tumour cells (LS180 and HT-29 cells). In vivo evaluation performed on LS180 xenograft animal model demonstrated that the pre-targeted bDOX achieved a much more significant tumour inhibition than free DOX. The largely decreased, unwanted bystander toxicity was demonstrated by changes in body weight, cardiomyocyte apoptosis, blood routine examination and splenic pathological changes.
   Conclusion: The high therapeutic efficacy, together with the minimal side effects, of this easily synthesized, pre-targeted system exhibited immense potentiality for the clinical application of DOX delivery.
C1 [Yao, Meinan; Zhang, Xin; Shi, Linqing; Liu, Tianyu; Zhao, Huiyun; Li, Xiaoda; Li, Liqiang; Gao, Hannan; Jia, Bing; Wang, Fan] Peking Univ, Med Isotopes Res Ctr, Beijing 100191, Peoples R China.
   [Yao, Meinan; Zhang, Xin; Shi, Linqing; Liu, Tianyu; Zhao, Huiyun; Li, Xiaoda; Li, Liqiang; Gao, Hannan; Jia, Bing; Wang, Fan] Peking Univ, Sch Basic Med Sci, Dept Radiat Med, Beijing 100191, Peoples R China.
   [Ma, Xiaotu; Wang, Fan] Chinese Acad Sci, Inst Biophys, CAS Ctr Excellence Biomacromol, Key Lab Prot & Peptide Pharmaceut, Beijing 100101, Peoples R China.
   [Zhao, Huiyun; Li, Xiaoda] Peking Univ, Med & Hlth Analyt Ctr, Hlth Sci Ctr, Beijing 100191, Peoples R China.
   [Liang, Xiaolong] Peking Univ, Dept Ultrasonog, Hosp 3, Beijing 100191, Peoples R China.
C3 Peking University; Peking University; Chinese Academy of Sciences;
   Institute of Biophysics, CAS; Peking University; Peking University
RP Jia, B; Wang, F (corresponding author), Peking Univ, Med Isotopes Res Ctr, Beijing 100191, Peoples R China.
EM jiabing@bjmu.edu.cn; wangfan@bjmu.edu.cn
RI Jia, Bing/C-3796-2008; Li, Liqiang/H-9094-2013; Liang,
   Xiaolong/M-1941-2018; Chen, Liú/KWU-4813-2024
FU National Key R&D Program of China [2017YFA0205600]; National Natural
   Science Foundation of China (NSFC) [81371614, 81630045, 81420108019,
   81621063, 81427802]; Strategic Priority Research Program of the Chinese
   Academy of Sciences [XDA12020216]
FX This research was supported by the National Key R&D Program of China
   (2017YFA0205600), National Natural Science Foundation of China (NSFC)
   projects (81371614, 81630045, 81420108019, 81621063, 81427802), and
   Strategic Priority Research Program of the Chinese Academy of Sciences
   (XDA12020216).
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NR 41
TC 26
Z9 26
U1 2
U2 35
PU IVYSPRING INT PUBL
PI LAKE HAVEN
PA PO BOX 4546, LAKE HAVEN, NSW 2263, AUSTRALIA
SN 1838-7640
J9 THERANOSTICS
JI Theranostics
PY 2019
VL 9
IS 3
BP 747
EP 760
DI 10.7150/thno.29989
PG 14
WC Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine
GA HJ5CW
UT WOS:000457196900010
PM 30809306
OA Green Submitted, Green Published, gold
DA 2025-01-04
ER

PT J
AU Machairas, N
   Daskalakis, K
   Felekouras, E
   Alexandraki, KI
   Kaltsas, G
   Sotiropoulos, GC
AF Machairas, Nikolaos
   Daskalakis, Kosmas
   Felekouras, Evangelos
   Alexandraki, Krystallenia, I
   Kaltsas, Gregory
   Sotiropoulos, Georgios C.
TI Currently available treatment options for neuroendocrine liver
   metastases
SO ANNALS OF GASTROENTEROLOGY
LA English
DT Review
DE Neuroendocrine; liver metastasis; surgery; ablation; embolization
ID RECEPTOR RADIONUCLIDE THERAPY; ENETS CONSENSUS GUIDELINES; TRANSARTERIAL
   CHEMOEMBOLIZATION TACE; HEPATIC ARTERIAL CHEMOEMBOLIZATION;
   RADIOFREQUENCY THERMAL ABLATION; SINGLE-CENTER EXPERIENCE;
   HEPATOCELLULAR-CARCINOMA; PROGNOSTIC-FACTORS; COLORECTAL-CANCER;
   ENDOCRINE TUMORS
AB Neuroendocrine neoplasms (NEN) are frequently characterized by a high propensity for metastasis to the liver, which appears to be a dominant site of distant-stage disease, affecting quality of life and overall survival. Liver surgery with the intention to cure is the treatment of choice for resectable neuroendocrine liver metastases (NELM), aiming to potentially prolong survival and ameliorate hormonal symptoms refractory to medical control. Surgical resection is indicated for patients with NELM from well-differentiated NEN, while its feasibility and complexity are largely dictated by the degree of liver involvement. As a result of advances in surgical techniques over the past decades, complex 1- and 2-stage, or repeat liver resections are performed safely and effectively by experienced surgeons. Furthermore, liver transplantation for the treatment of NELM should be anchored in a multimodal and multidisciplinary therapeutic strategy and restricted only to highly selected individual cases. A broad spectrum of interventional radiology treatments for NELM have recently been available, with expanding indications that are more applicable, as they are less limited by patient- and tumor-related parameters, being therefore important adjuncts or alternatives to surgery. Overall, liver-targeted treatment modalities may precede the administration of systemic molecular targeted agents and chemotherapy for patients with liver-dominant metastatic disease; these appear to be a crucial component of multimodal management of patients with NEN. In the present review, we discuss surgical and non-surgical liver-targeted treatment approaches for NELM, each complementing the other, with a view to assisting physicians in optimizing multimodal NEN patient care.
C1 [Machairas, Nikolaos; Sotiropoulos, Georgios C.] Natl & Kapodistrian Univ Athens, Med Sch, Dept Propaedeut Surg 2, Athens, Greece.
   [Daskalakis, Kosmas; Alexandraki, Krystallenia, I; Kaltsas, Gregory] Natl & Kapodistrian Univ Athens, Med Sch, Dept Propaedeut Internal Med 1, Athens, Greece.
   [Felekouras, Evangelos] Natl & Kapodistrian Univ Athens, Med Sch, Dept Surg 1, Athens, Greece.
C3 National & Kapodistrian University of Athens; National & Kapodistrian
   University of Athens; National & Kapodistrian University of Athens
RP Sotiropoulos, GC (corresponding author), Univ Athens, Gen Hosp Laiko, Dept Propaedeut Surg 2, Med Sch, 17 Agiou Thoma St, Athens 11527, Greece.
EM geosotirop@med.uoa.gr
RI Machairas, Nikolaos/AAA-2982-2020; Alexandraki, Krystallenia/S-4058-2019
OI Machairas, Nikolaos/0000-0003-3239-3905
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NR 155
TC 18
Z9 18
U1 0
U2 4
PU HELLENIC SOC GASTROENTEROLOGY
PI ATHENS
PA DEMOKRATIAS AVE 67, ATHENS, 15451, GREECE
SN 1108-7471
EI 1792-7463
J9 ANN GASTROENTEROL
JI Ann. Gastroenterol.
PY 2021
VL 34
IS 2
BP 130
EP +
DI 10.20524/aog.2021.0574
PG 16
WC Gastroenterology & Hepatology
WE Emerging Sources Citation Index (ESCI)
SC Gastroenterology & Hepatology
GA QT7NO
UT WOS:000626776600002
PM 33654350
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Schirripa, M
   Biason, P
   Lonardi, S
   Pella, N
   Pino, MS
   Urbano, F
   Antoniotti, C
   Cremolini, C
   Corallo, S
   Pietrantonio, F
   Gelsomino, F
   Cascinu, S
   Orlandi, A
   Munari, G
   Malapelle, U
   Saggio, S
   Fontanini, G
   Rugge, M
   Mescoli, C
   Lazzi, S
   Bonetti, LR
   Lanza, G
   Dei Tos, AP
   De Maglio, G
   Martini, M
   Bergamo, F
   Zagonel, V
   Loupakis, F
   Fassan, M
AF Schirripa, Marta
   Biason, Paola
   Lonardi, Sara
   Pella, Nicoletta
   Pino, Maria Simona
   Urbano, Federica
   Antoniotti, Carlotta
   Cremolini, Chiara
   Corallo, Salvatore
   Pietrantonio, Filippo
   Gelsomino, Fabio
   Cascinu, Stefano
   Orlandi, Armando
   Munari, Giada
   Malapelle, Umberto
   Saggio, Serena
   Fontanini, Gabriella
   Rugge, Massimo
   Mescoli, Claudia
   Lazzi, Stefano
   Bonetti, Luca Reggiani
   Lanza, Giovanni
   Dei Tos, Angelo P.
   De Maglio, Giovanna
   Martini, Maurizio
   Bergamo, Francesca
   Zagonel, Vittorina
   Loupakis, Fotios
   Fassan, Matteo
TI Class 1, 2, and 3 <i>BRAF</i>-Mutated Metastatic Colorectal Cancer: A
   Detailed Clinical, Pathologic, and Molecular Characterization
SO CLINICAL CANCER RESEARCH
LA English
DT Article
ID TRAMETINIB; CARCINOMA; MUTATIONS; MELANOMA; SUBTYPES; INHIBITION
AB Purpose: BRAF mutations are grouped in activating RAS-independent signaling as monomers (class 1-V600E) or as dimers (class 2-codons 597/601), and RAS-dependent with impaired kinase activity (class 3-codons 594/596). Although clinical, pathologic, and molecular features of (V600E)BRAF-mutated metastatic colorectal cancer (mCRC) are well known, limited data are available from the two other classes.
   Experimental Design: Data from 117 patients with BRAF (92 class 1, 12 class 2, and 13 class 3)-mutated mCRC were collected. A total of 540 BRAF wt mCRCs were included as control. IHC profiling was performed to determine the consensus molecular subtypes (CMS), cytokeratin 7/20 profiles, tumor-infiltrating lymphocyte infiltration, and BM1/BM2 categorization. Overall survival (OS) and progression- free survival were evaluated by Kaplan-Meier and log-rank test.
   Results: Class 3 BRAF-mutated mCRC was more frequently left sided (P = 0.0028), pN0 (P = 0.0159), and without peritoneal metastases (P = 0.0176) compared with class 1, whereas class 2 cases were similar to class 1. Hazard ratio for OS, as compared with BRAF wt, was 2.38 [95% confidence interval (CI), 1.61-3.54] for class 1, 1.90 (95% CI, 0.85-4.26) for class 2, and 0.93 (95% CI, 0.51-1.69) for class 3 (P < 0.0001). Class 2 and 3 tumors were all assigned to CMS2-3. A higher median CD3/CD8-positive lymphocyte infiltration was observed in BRAF-mutated class 2 (P = 0.033) compared with class 3 cases.
   Conclusions: For the first time, different clinical and pathologic features and outcome data were reported according to the three BRAF mutation classes in mCRC. Specific targeted treatment strategies should be identified in the near future for such patients.
C1 [Schirripa, Marta; Biason, Paola; Lonardi, Sara; Munari, Giada; Bergamo, Francesca; Zagonel, Vittorina; Loupakis, Fotios] Veneto Inst Oncol IOV, IRCCS, Dept Oncol, Padua, Italy.
   [Pella, Nicoletta] Univ & Gen Hosp, Dept Oncol, Udine, Italy.
   [Pino, Maria Simona] S Maria Annunziata Hosp, Azienda USL Toscana Ctr, Dept Oncol, Med Oncol Unit, Florence, Italy.
   [Urbano, Federica] Sapienza Univ Rome, Policlin Umberto 1, Dept Radiol Sci Oncol & Pathol, Rome, Italy.
   [Antoniotti, Carlotta; Cremolini, Chiara] Univ Pisa, Dept Translat Res & New Technol Med & Surg, Unit Med Oncol, Pisa, Italy.
   [Corallo, Salvatore; Pietrantonio, Filippo; Saggio, Serena] Ist Nazl Tumori, Fdn IRCCS, Dept Med Oncol, Milan, Italy.
   [Pietrantonio, Filippo] Univ Milan, Dept Oncol & Hematooncol, Milan, Italy.
   [Gelsomino, Fabio; Cascinu, Stefano] Univ Hosp Modena, Dept Oncol & Haematol, Modena, Italy.
   [Orlandi, Armando] Univ Agostino Gemelli IRCCS, Fdn Policlin, UOC Oncol, Rome, Italy.
   [Munari, Giada; Rugge, Massimo; Mescoli, Claudia; Fassan, Matteo] Univ Padua, Dept Med DIMED, Surg Pathol & Cytopathol Unit, Padua, Italy.
   [Malapelle, Umberto] Univ Federico II Naples, Dept Publ Hlth, Naples, Italy.
   [Fontanini, Gabriella] Univ Pisa, Dept Surg Med Mol Pathol & Crit Area, Pisa, Italy.
   [Lazzi, Stefano] Univ Siena, Sect Pathol, Dept Med Biotechnol, Siena, Italy.
   [Bonetti, Luca Reggiani] Univ Modena & Reggio Emilia, Sect Pathol, Policlin Modena, Dept Diagnost Med & Publ Hlth, Modena, Italy.
   [Lanza, Giovanni] Univ Ferrara, Dept Pathol, Ferrara, Italy.
   [Dei Tos, Angelo P.] Treviso Gen Hosp, Dept Pathol & Mol Genet, Treviso, Italy.
   [De Maglio, Giovanna] Univ Hosp Udine, Dept Pathol, Udine, Italy.
   [Martini, Maurizio] Univ A Gemelli IRCCS, Fdn Policlin, Area Anat Patol, Dipartimento Sci Salute Donna Bambino & San Pubbl, Rome, Italy.
   [Martini, Maurizio] Univ Cattolica Sacro Cuore, Ist Anat Patol, Rome, Italy.
C3 IRCCS Istituto Oncologico Veneto (IOV); University of Udine; University
   Hospital of Udine; Sapienza University Rome; University Hospital
   Sapienza Rome; University of Pisa; Fondazione IRCCS Istituto Nazionale
   Tumori Milan; University of Milan; Universita di Modena e Reggio Emilia;
   Universita di Modena e Reggio Emilia Hospital; University of Padua;
   University of Naples Federico II; University of Pisa; University of
   Siena; Universita di Modena e Reggio Emilia; University of Ferrara; ULSS
   2 Marca TV; Ospedale Ca' Foncello Treviso; University of Udine;
   University Hospital of Udine; Catholic University of the Sacred Heart;
   IRCCS Policlinico Gemelli
RP Loupakis, F (corresponding author), IOV, IRCCS, Oncol Med 1, Via Gattamelata 64, I-35128 Padua, Italy.
EM fotios.loupakis@iov.veneto.it
RI Dei Tos, Angelo/AAN-3244-2020; Cascinu, Stefano/AAN-1923-2020;
   Antoniotti, Carlotta/KIC-8096-2024; Martini, Maurizio/AAB-1564-2019;
   Biason, Paola/N-6528-2013; Schirripa, Marta/F-3688-2017; Fontanini,
   Gabriella/O-7636-2015; gelsomino, fabio/AAB-8967-2022; Bonetti,
   Luca/AAE-5488-2019; Loupakis, Fotios/I-7243-2012; Bergamo,
   Francesca/AAB-9010-2019; Cremolini, Chiara/AAC-1889-2019; Cascinu,
   Stefano/G-2399-2017; Reggiani Bonetti, Luca/Q-3946-2017; ORLANDI,
   Armando/A-1517-2015; Pietrantonio, Filippo/C-2180-2017; LANZA,
   GIOVANNI/K-6635-2016; zagonel, vittorina/F-4226-2014; LAZZI,
   STEFANO/P-8265-2018; Lonardi, Sara/F-4228-2014; corallo,
   salvatore/AAA-2884-2019; Fassan, Matteo/F-5152-2012
OI Cascinu, Stefano/0000-0003-2215-0731; Reggiani Bonetti,
   Luca/0000-0002-9917-4080; ORLANDI, Armando/0000-0001-5253-4678;
   Pietrantonio, Filippo/0000-0002-8530-8420; gelsomino,
   fabio/0000-0001-7979-4795; LANZA, GIOVANNI/0000-0002-5362-1236; RUGGE,
   MASSIMO/0000-0002-0679-0563; CREMOLINI, CHIARA/0000-0002-0520-4841;
   zagonel, vittorina/0000-0002-0829-2525; DEI TOS,
   ANGELO/0000-0002-1228-8940; LAZZI, STEFANO/0000-0002-2218-3771; Lonardi,
   Sara/0000-0002-7593-8138; corallo, salvatore/0000-0002-6672-0233;
   urbano, federica/0000-0002-9603-0778; Fassan, Matteo/0000-0001-6515-5482
FU Regione Veneto [RP-2014-00000395]
FX This work was supported by a grant from Regione Veneto
   (RP-2014-00000395).
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NR 31
TC 66
Z9 69
U1 0
U2 6
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1078-0432
EI 1557-3265
J9 CLIN CANCER RES
JI Clin. Cancer Res.
PD JUL 1
PY 2019
VL 25
IS 13
BP 3954
EP 3961
DI 10.1158/1078-0432.CCR-19-0311
PG 8
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA IG1FN
UT WOS:000473536100024
PM 30967421
OA Green Submitted, Bronze, Green Published, Green Accepted
DA 2025-01-04
ER

PT J
AU Paschold, L
   Binder, M
AF Paschold, Lisa
   Binder, Mascha
TI Circulating Tumor DNA in Gastric and Gastroesophageal Junction Cancer
SO CURRENT ONCOLOGY
LA English
DT Article
DE gastric adenocarcinoma; gastroesophageal junction cancer; cell-free DNA
   (cfDNA); liquid biopsy; monitoring; resistance; prognostication
ID CELL-FREE DNA; ESOPHAGEAL ADENOCARCINOMA; ACQUIRED-RESISTANCE;
   COLORECTAL-CANCER; PLUS CHEMOTHERAPY; LIQUID BIOPSIES; LUNG-CANCER; COPY
   NUMBER; TRASTUZUMAB; HETEROGENEITY
AB Tumor cells shed DNA into the plasma. "Liquid biopsy" analysis of mutations or other genomic alterations in circulating cell-free DNA (cfDNA) may provide us with a tool to detect minimal residual cancer, comprehensively profile the genomic tumor landscape in search of druggable targets, and monitor cancers non-invasively over time for treatment failure or emerging treatment-resistant tumor subclones. While liquid biopsies have not yet entered routine clinical management in patients with gastric and gastroesophageal junction cancers, this group of diseases may benefit from such advanced diagnostic tools due to their pronounced genetic spatiotemporal heterogeneity and limitations in imaging sensitivity. Moreover, as the armamentarium of targeted treatment approaches and immunotherapies expands, cfDNA analyses may reveal their utility not only as a biomarker of response but also for precision monitoring. In this review, we discuss the different applications of cfDNA analyses in patients with gastric and gastroesophageal junction cancer and the technical challenges that such liquid biopsies have yet to overcome.
C1 [Paschold, Lisa; Binder, Mascha] Martin Luther Univ Halle Wittenberg, Dept Internal Med 4, Oncol Hematol, D-06120 Halle, Saale, Germany.
C3 Martin Luther University Halle Wittenberg
RP Binder, M (corresponding author), Martin Luther Univ Halle Wittenberg, Dept Internal Med 4, Oncol Hematol, D-06120 Halle, Saale, Germany.
EM lisa.paschold@uk-halle.de; mascha.binder@uk-halle.de
OI Binder, Mascha/0000-0003-0663-3004
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NR 69
TC 8
Z9 8
U1 1
U2 9
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
SN 1198-0052
EI 1718-7729
J9 CURR ONCOL
JI Curr. Oncol.
PD MAR
PY 2022
VL 29
IS 3
BP 1430
EP 1441
DI 10.3390/curroncol29030120
PG 12
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 0C8XY
UT WOS:000775590900001
PM 35323320
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Wang, XX
   Zhang, C
   Song, HQ
   Yuan, JL
   Zhang, L
   He, JF
AF Wang, Xiaoxiao
   Zhang, Chao
   Song, Huangqin
   Yuan, Junlong
   Zhang, Lei
   He, Jiefeng
TI CircCCDC66: Emerging roles and potential clinical values in malignant
   tumors
SO FRONTIERS IN ONCOLOGY
LA English
DT Review
DE circular RNA; circCCDC66; malignant tumors; endogenous competitive RNA;
   regulatory mechanism; cancer progression
ID GASTRIC-CANCER; CELL-PROLIFERATION; CIRCULAR RNAS; PROGRESSION;
   EXPRESSION; CARCINOMA; METASTASIS; MECHANISMS; MIGRATION; INVASION
AB Circular RNAs (circRNAs) are endogenous non-coding RNAs (ncRNAs) with a closed-loop structure. In recent years, circRNAs have become the focus of much research into RNA. CircCCDC66 has been identified as a novel oncogenic circRNA and is up-regulated in a variety of malignant tumors including thyroid cancer, non-small cell carcinoma, gastric cancer, colorectal cancer, renal cancer, cervical cancer, glioma, and osteosarcoma. It mediates cancer progression by regulating epigenetic modifications, variable splicing, transcription, and protein translation. The oncogenicity of circCCDC66 suppresses or promotes the expression of related genes mainly through direct or indirect pathways. This finding suggests that circCCDC66 is a biomarker for cancer diagnosis, prognosis assessment and treatment. However, there is no review on the relationship between circCCDC66 and cancers. Thus, the expression, biological functions, and regulatory mechanisms of circCCDC66 in malignant tumor and non-tumor diseases are summarized. The clinical value and prognostic significance of circCCDC66 are also evaluated, which can provide insights helpful to those exploring new strategies for the early diagnosis and targeted treatment of malignancies.
C1 [Wang, Xiaoxiao; Zhang, Chao; Song, Huangqin; Yuan, Junlong; He, Jiefeng] Tongji Shanxi Hosp, Third Hosp Shanxi Med Univ, Shanxi Bethune Hosp, Shanxi Acad Med Sci, Taiyuan, Peoples R China.
   [Zhang, Lei; He, Jiefeng] Tongji Shanxi Hosp, Shanxi Bethune Hosp, Shanxi Acad Med Sci, Dept Hepatobiliary Surg, Taiyuan, Peoples R China.
   [Zhang, Lei] Huazhong Univ Sci & Technol, Tongji Hosp, Inst Hepato Pancreato Biliary Surg, Tongji Med Coll,Hepat Surg Ctr, Wuhan, Peoples R China.
C3 Shanxi Medical University; Huazhong University of Science & Technology
RP He, JF (corresponding author), Tongji Shanxi Hosp, Third Hosp Shanxi Med Univ, Shanxi Bethune Hosp, Shanxi Acad Med Sci, Taiyuan, Peoples R China.; He, JF (corresponding author), Tongji Shanxi Hosp, Shanxi Bethune Hosp, Shanxi Acad Med Sci, Dept Hepatobiliary Surg, Taiyuan, Peoples R China.
EM hejiefeng2005@163.com
FU National Natural Science Fund [82073090]; Shanxi Provincial Department
   of Human Resources and Social Security [20210001]
FX Funding This article was supported by National Natural Science Fund,
   grant number 82073090; Shanxi Provincial Department of Human Resources
   and Social Security, grant number 20210001.
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NR 110
TC 4
Z9 4
U1 1
U2 3
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 2234-943X
J9 FRONT ONCOL
JI Front. Oncol.
PD JAN 9
PY 2023
VL 12
AR 1061007
DI 10.3389/fonc.2022.1061007
PG 16
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 8B2YD
UT WOS:000916793200001
PM 36698408
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Wang, D
   Tang, L
   Zhang, YJ
   Ge, GL
   Jiang, XJ
   Mo, YZ
   Wu, P
   Deng, XY
   Li, Y
   Zuo, SC
   Yan, QJ
   Zhang, SS
   Wang, FY
   Shi, L
   Li, XY
   Xiang, B
   Zhou, M
   Liao, QJ
   Guo, C
   Zeng, ZY
   Xiong, W
   Gong, ZJ
AF Wang, Dan
   Tang, Le
   Zhang, Yijie
   Ge, Guili
   Jiang, Xianjie
   Mo, Yongzhen
   Wu, Pan
   Deng, Xiangying
   Li, Lvyuan
   Zuo, Sicheng
   Yan, Qijia
   Zhang, Shanshan
   Wang, Fuyan
   Shi, Lei
   Li, Xiayu
   Xiang, Bo
   Zhou, Ming
   Liao, Qianjin
   Guo, Can
   Zeng, Zhaoyang
   Xiong, Wei
   Gong, Zhaojian
TI Regulatory pathways and drugs associated with ferroptosis in tumors
SO CELL DEATH & DISEASE
LA English
DT Review
ID COLORECTAL-CANCER CELLS; NONCODING RNAS; BREAST-CANCER; PROMOTES
   FERROPTOSIS; OXIDATIVE STRESS; LUNG-CANCER; FATTY-ACIDS; DEATH;
   METABOLISM; IRON
AB Ferroptosis is a type of cell death that depends on iron and reactive oxygen species (ROS). The accumulation of iron and lipid peroxidation primarily initiates oxidative membrane damage during ferroptosis. The core molecular mechanism of ferroptosis includes the regulation of oxidation and the balance between damage and antioxidant defense. Tumor cells usually contain a large amount of H2O2, and ferrous/iron ions will react with excessive H2O2 in cells to produce hydroxyl radicals and induce ferroptosis in tumor cells. Here, we reviewed the latest studies on the regulation of ferroptosis in tumor cells and introduced the tumor-related signaling pathways of ferroptosis. We paid particular attention to the role of noncoding RNA, nanomaterials, the role of drugs, and targeted treatment using ferroptosis drugs for mediating the ferroptosis process in tumor cells. Finally, we discussed the currently unresolved problems and future research directions for ferroptosis in tumor cells and the prospects of this emerging field. Therefore, we have attempted to provide a reference for further understanding of the pathogenesis of ferroptosis and proposed new targets for cancer treatment.
C1 [Wang, Dan; Liao, Qianjin; Zeng, Zhaoyang; Xiong, Wei] Cent South Univ, NHC Key Lab Carcinogenesis, Hunan Canc Hosp, Changsha, Peoples R China.
   [Wang, Dan; Liao, Qianjin; Zeng, Zhaoyang; Xiong, Wei] Cent South Univ, Hunan Key Lab Canc Metab, Hunan Canc Hosp, Changsha, Peoples R China.
   [Wang, Dan; Liao, Qianjin; Zeng, Zhaoyang; Xiong, Wei] Cent South Univ, Affiliated Canc Hosp, Xiangya Sch Med, Changsha, Peoples R China.
   [Wang, Dan; Tang, Le; Zhang, Yijie; Ge, Guili; Jiang, Xianjie; Mo, Yongzhen; Wu, Pan; Deng, Xiangying; Li, Lvyuan; Zuo, Sicheng; Wang, Fuyan; Xiang, Bo; Zhou, Ming; Guo, Can; Zeng, Zhaoyang; Xiong, Wei] Cent South Univ, Key Lab Carcinogenesis & Canc Invas, Chinese Minist Educ, Canc Res Inst, Changsha, Peoples R China.
   [Yan, Qijia; Zhang, Shanshan] Cent South Univ, Xiangya Hosp, Dept Stomatol, Changsha, Peoples R China.
   [Shi, Lei; Gong, Zhaojian] Cent South Univ, Xiangya Hosp 2, Dept Oral & Maxillofacial Surg, Changsha, Peoples R China.
   [Li, Xiayu] Cent South Univ, Xiangya Hosp 3, Dis Genome Res Ctr, Hunan Key Lab Nonresolving Inflammat & Canc, Changsha, Peoples R China.
C3 Central South University; Central South University; Central South
   University; Central South University; Central South University; Central
   South University; Central South University
RP Xiong, W (corresponding author), Cent South Univ, NHC Key Lab Carcinogenesis, Hunan Canc Hosp, Changsha, Peoples R China.; Xiong, W (corresponding author), Cent South Univ, Hunan Key Lab Canc Metab, Hunan Canc Hosp, Changsha, Peoples R China.; Xiong, W (corresponding author), Cent South Univ, Affiliated Canc Hosp, Xiangya Sch Med, Changsha, Peoples R China.; Xiong, W (corresponding author), Cent South Univ, Key Lab Carcinogenesis & Canc Invas, Chinese Minist Educ, Canc Res Inst, Changsha, Peoples R China.; Gong, ZJ (corresponding author), Cent South Univ, Xiangya Hosp 2, Dept Oral & Maxillofacial Surg, Changsha, Peoples R China.
EM xiongwei@csu.edu.cn; gongzhaojian4458@csu.edu.cn
RI Zhang, shanshan/HLP-6320-2023; Zeng, Zhaoyang/LLL-3057-2024; li,
   xia/HHZ-7468-2022; xiong, wei/GXZ-9586-2022
FU Natural Science Foundation of Hunan Province of China [2021JJ31127]
FX This study was supported by grants from Natural Science Foundation of
   Hunan Province of China (2021JJ31127) and we thank Editage for their
   assistance with language editing.
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NR 224
TC 69
Z9 70
U1 8
U2 73
PU SPRINGERNATURE
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON, N1 9XW, ENGLAND
SN 2041-4889
J9 CELL DEATH DIS
JI Cell Death Dis.
PD JUN 10
PY 2022
VL 13
IS 6
AR 544
DI 10.1038/s41419-022-04927-1
PG 15
WC Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology
GA 2A2RT
UT WOS:000809355600001
PM 35688814
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Moujaber, T
   Etemadmoghadam, D
   Kennedy, CJ
   Chiew, YE
   Balleine, RL
   Saunders, C
   Wain, GV
   Gao, B
   Hogg, R
   Srirangan, S
   Kan, C
   Fereday, S
   Traficante, N
   Patch, AM
   Pearson, JV
   Waddell, N
   Grimmond, SM
   Dobrovic, A
   Bowtell, DDL
   Harnett, PR
   DeFazio, A
   Bowtell, D
   Chenevix-Trench, G
   Green, A
   Webb, P
   DeFazio, A
   Gertig, D
   Traficante, N
   Fereday, S
   Moore, S
   Harrap, K
   Sadkowsky, T
   Pandeya, N
   Hung, J
   Malt, M
   Alexander, B
   Ashover, E
   Brown, S
   Corrish, T
   Green, L
   Jackman, L
   Ferguson, K
   Martin, K
   Martyn, A
   Ranieri, B
   Mellon, A
   Robertson, R
   Vanden Bergh, T
   Jones, M
   Mackenzie, P
   Maidens, J
   Nattress, K
   Chiew, YE
   Stenlake, A
   Sullivan, H
   White, J
   Jayde, V
   Mamers, P
   Bowes, L
   Galletta, L
   Giles, D
   Hendley, J
   Alsop, K
   Ball, C
   Young, C
   Schmidt, T
   Shirley, H
   Viduka, S
   Brooks, J
   Stuart-Harris, R
   Kirsten, R
   Rutovitz, J
   Clingan, P
   Glasgow, A
   Proietto, A
   Braye, S
   Otton, G
   Shannon, J
   Bonaventura, T
   Stewart, J
   Begbie, S
   Bell, D
   Baron-Hay, S
   Ferrier, A
   Gard, G
   Nevell, D
   Pavialds, N
   Valmadre, S
   Young, B
   Camaris, C
   Crouch, R
   Edwards, L
   Hacker, N
   Marsden, D
   Robertson, G
   Beale, P
   Beith, J
   Carter, J
   Dalrymple, C
   Houghton, R
   Russell, P
   Links, M
   Grygiel, J
   Hill, J
   Brand, A
   Byth, K
   Jaworski, R
   Sharma, R
   Harnett, P
   Wain, G
   Friedlander, M
   Ward, B
   Papadimos, D
   Crandon, A
   Cummings, M
   Horwood, K
   Obermair, A
   Perrin, L
   Wyld, D
   Nicklin, J
   Davy, M
   Oehler, MK
   Hall, C
   Dodd, T
   Healy, T
   Pittman, K
   Henderson, D
   Miller, J
   Pierdes, J
   Blomfield, P
   Challis, D
   McIntosh, R
   Parker, A
   Brown, B
   Rome, R
   Allen, D
   Grant, P
   Hyde, S
   Laurie, R
   Robbie, M
   Healy, D
   Jobling, T
   Manolitsas, T
   McNealage, J
   Rogers, P
   Susil, B
   Sumithran, E
   Simpson, L
   Phillips, K
   Rischin, D
   Fax, S
   Johnson, D
   Lade, S
   Loughrey, M
   O'Callaghan, N
   Murray, W
   Waring, P
   Billson, V
   Pyman, J
   Neesham, D
   Quinn, M
   Underhill, C
   Bell, R
   Ng, LF
   Blum, R
   Ganju, V
   Hammond, L
   Leung, Y
   McCartney, A
   Buck, M
   Haviv, I
   Purdie, D
   Whiteman, D
   Zeps, N
AF Moujaber, Tania
   Etemadmoghadam, Dariush
   Kennedy, Catherine J.
   Chiew, Yoke-Eng
   Balleine, Rosemary L.
   Saunders, Catherine
   Wain, Gerard, V
   Gao, Bo
   Hogg, Russell
   Srirangan, Sivatharsny
   Kan, Casina
   Fereday, Sian
   Traficante, Nadia
   Patch, Ann-Marie
   Pearson, John, V
   Waddell, Nicola
   Grimmond, Sean M.
   Dobrovic, Alexander
   Bowtell, David D. L.
   Harnett, Paul R.
   DeFazio, Anna
   Bowtell, D.
   Chenevix-Trench, G.
   Green, A.
   Webb, P.
   DeFazio, A.
   Gertig, D.
   Traficante, N.
   Fereday, S.
   Moore, S.
   Harrap, K.
   Sadkowsky, T.
   Pandeya, N.
   Hung, J.
   Malt, M.
   Alexander, B.
   Ashover, E.
   Brown, S.
   Corrish, T.
   Green, L.
   Jackman, L.
   Ferguson, K.
   Martin, K.
   Martyn, A.
   Ranieri, B.
   Mellon, A.
   Robertson, R.
   Vanden Bergh, T.
   Jones, M.
   Mackenzie, P.
   Maidens, J.
   Nattress, K.
   Chiew, Y. E.
   Stenlake, A.
   Sullivan, H.
   White, J.
   Jayde, V
   Mamers, P.
   Bowes, L.
   Galletta, L.
   Giles, D.
   Hendley, J.
   Alsop, K.
   Ball, C.
   Young, C.
   Schmidt, T.
   Shirley, H.
   Viduka, S.
   Brooks, Julia
   Stuart-Harris, R.
   Kirsten, R.
   Rutovitz, J.
   Clingan, P.
   Glasgow, A.
   Proietto, A.
   Braye, S.
   Otton, G.
   Shannon, J.
   Bonaventura, T.
   Stewart, J.
   Begbie, S.
   Bell, D.
   Baron-Hay, S.
   Ferrier, A.
   Gard, G.
   Nevell, D.
   Pavialds, N.
   Valmadre, S.
   Young, B.
   Camaris, C.
   Crouch, R.
   Edwards, L.
   Hacker, N.
   Marsden, D.
   Robertson, G.
   Beale, P.
   Beith, J.
   Carter, J.
   Dalrymple, C.
   Houghton, R.
   Russell, P.
   Links, M.
   Grygiel, J.
   Hill, J.
   Brand, A.
   Byth, K.
   Jaworski, R.
   Sharma, R.
   Harnett, P.
   Wain, G.
   Friedlander, M.
   Ward, B.
   Papadimos, D.
   Crandon, A.
   Cummings, M.
   Horwood, K.
   Obermair, A.
   Perrin, L.
   Wyld, D.
   Nicklin, J.
   Davy, M.
   Oehler, M. K.
   Hall, C.
   Dodd, T.
   Healy, T.
   Pittman, K.
   Henderson, D.
   Miller, J.
   Pierdes, J.
   Blomfield, P.
   Challis, D.
   McIntosh, R.
   Parker, A.
   Brown, B.
   Rome, R.
   Allen, D.
   Grant, P.
   Hyde, S.
   Laurie, R.
   Robbie, M.
   Healy, D.
   Jobling, T.
   Manolitsas, T.
   McNealage, J.
   Rogers, P.
   Susil, B.
   Sumithran, E.
   Simpson, L.
   Phillips, K.
   Rischin, D.
   Fax, S.
   Johnson, D.
   Lade, S.
   Loughrey, M.
   O'Callaghan, N.
   Murray, W.
   Waring, P.
   Billson, V
   Pyman, J.
   Neesham, D.
   Quinn, M.
   Underhill, C.
   Bell, R.
   Ng, L. F.
   Blum, R.
   Ganju, V
   Hammond, L.
   Leung, Y.
   McCartney, A.
   Buck, M.
   Haviv, I
   Purdie, D.
   Whiteman, D.
   Zeps, N.
CA Australian Ovarian Canc Study
TI <i>BRAF</i> Mutations in Low-Grade Serous Ovarian Cancer and Response to
   BRAF Inhibition
SO JCO PRECISION ONCOLOGY
LA English
DT Article
ID SOLID TUMORS; COLON-CANCER; OPEN-LABEL; VEMURAFENIB; DABRAFENIB;
   CARCINOMA; MELANOMA; SURVIVAL; NRAS; RESPONSIVENESS
AB Purpose Low-grade serous ovarian carcinoma (LGSC) responds poorly to chemotherapy and is characterized by activating mutations in the Ras sarcoma-mitogen-activated protein kinase (RAS-MAPK) pathway, including oncogenic BRAF. However, response to BRAF inhibitors is tumor-type specific. Significant improvement in survival is seen in patients with BRAF-mutant melanoma, but other cancer types, such as colorectal cancers, are generally less sensitive. We examined the frequency and characteristics of BRAF-mutated LGSC and described the response to treatment with BRAF inhibitors.
   Patients and Methods Mutations were assessed in LGSC (N = 65) by using targeted, exome, and whole-genome sequencing. Patient characteristics, treatment, and clinical outcome were assessed, and the median follow-up time was more than 5 years. BRAF inhibitors were trialed in two patients with a somatic BRAF V600E mutation: one patient received dabrafenib monotherapy and was monitored clinically, biochemically (cancer antigen [CA]-125 levels), and with positron emission tomography (PET) imaging. Expression of the BRAF V600E protein in this patient was assessed by immunohistochemistry.
   Results Among patients with LGSC, nine (13.8%) of 65 had a somatic BRAF mutation. Of the nine patients with BRAF mutation-positive LGSC, four experienced progressive disease that did not respond to conventional chemotherapy. Two of the patients experienced progression quickly and died as a result of disease progression, and two received targeted treatment. Two patients with BRAF V600E mutation received BRAF inhibitors at relapse and both achieved durable responses.
   Conclusion BRAF mutations are not uncommon in patients with LGSC and should be routinely tested, because BRAF inhibitors can be an effective treatment for these patients. The results highlight the need for targeted treatment in this rare tumor type, and a prospective study is needed to formally assess the response rate and clinical benefit. (C) 2018 by American Society of Clinical Oncology
C1 [Moujaber, Tania; Kennedy, Catherine J.; Chiew, Yoke-Eng; Balleine, Rosemary L.; Gao, Bo; Srirangan, Sivatharsny; Kan, Casina; Harnett, Paul R.; DeFazio, Anna] Westmead Inst Med Res, Westmead, NSW, Australia.
   [Moujaber, Tania; Kennedy, Catherine J.; Chiew, Yoke-Eng; Balleine, Rosemary L.; Saunders, Catherine; Hogg, Russell; Harnett, Paul R.; DeFazio, Anna] Univ Sydney, Westmead, NSW, Australia.
   [Moujaber, Tania; Kennedy, Catherine J.; Chiew, Yoke-Eng; Balleine, Rosemary L.; Saunders, Catherine; Wain, Gerard, V; Gao, Bo; Harnett, Paul R.; DeFazio, Anna; Chiew, Y. E.; Stenlake, A.; Sullivan, H.; Brand, A.; Byth, K.; Jaworski, R.; Sharma, R.; Harnett, P.; Wain, G.] Westmead Hosp, Westmead, NSW, Australia.
   [Balleine, Rosemary L.] New South Wales Hlth Pathol, Westmead, NSW, Australia.
   [Etemadmoghadam, Dariush; Fereday, Sian; Traficante, Nadia; Bowtell, David D. L.] Peter MacCallum Canc Ctr, Melbourne, Vic, Australia.
   [Etemadmoghadam, Dariush; Grimmond, Sean M.; Dobrovic, Alexander; Bowtell, David D. L.] Univ Melbourne, Melbourne, Vic, Australia.
   [Dobrovic, Alexander] Olivia Newton John Canc Res Inst, Melbourne, Vic, Australia.
   [Dobrovic, Alexander] La Trobe Univ, Bundoora, Vic, Australia.
   [Patch, Ann-Marie; Pearson, John, V; Waddell, Nicola; Purdie, D.; Whiteman, D.] QIMR Berghofer Med Res Inst, Brisbane, Qld, Australia.
   [Bowtell, David D. L.; Bowtell, D.] Imperial Coll London, London, England.
   [Bowtell, D.; Traficante, N.; Fereday, S.; Bowes, L.; Galletta, L.; Giles, D.; Hendley, J.; Alsop, K.; Phillips, K.; Rischin, D.; Fax, S.; Johnson, D.; Lade, S.; Loughrey, M.; O'Callaghan, N.; Murray, W.] Peter MacCallum Canc Ctr, East Melbourne, Vic, Australia.
   [Bowtell, D.; Gertig, D.; Waring, P.] Univ Melbourne, Parkville, Vic, Australia.
   [Chenevix-Trench, G.; Green, A.; Webb, P.; Moore, S.; Harrap, K.; Sadkowsky, T.; Pandeya, N.; Malt, M.; Alexander, B.; Ashover, E.; Brown, S.; Corrish, T.; Green, L.; Jackman, L.; Ferguson, K.; Martin, K.; Martyn, A.; Ranieri, B.] QIMR Berghoier Med Res Inst, Brisbane, Qld, Australia.
   [DeFazio, A.] Univ Sydney, Westmead Inst Med Res, Sydney, NSW, Australia.
   [DeFazio, A.; Hung, J.] Westmead Hosp, Sydney, NSW, Australia.
   [Traficante, N.; Fereday, S.] Peter MacCallurn Canc Ctr, East Melbourne, Vic, Australia.
   [Mellon, A.; Robertson, R.; Proietto, A.; Braye, S.; Otton, G.] John Hunter Hosp, New Lambton, NSW, Australia.
   [Vanden Bergh, T.; Jones, M.; Mackenzie, P.; Camaris, C.; Crouch, R.; Edwards, L.; Hacker, N.; Marsden, D.; Robertson, G.] Royal Hosp Women, Randwick, NSW, Australia.
   [Maidens, J.; Bell, D.; Baron-Hay, S.; Ferrier, A.; Gard, G.; Nevell, D.; Pavialds, N.; Valmadre, S.; Young, B.] Royal North Shore Hosp, St Leonards, NSW, Australia.
   [Nattress, K.; Beale, P.; Beith, J.; Carter, J.; Dalrymple, C.; Houghton, R.; Russell, P.] Royal Prince Alfred Hosp, Camperdown, NSW, Australia.
   [White, J.; Davy, M.; Oehler, M. K.; Hall, C.; Dodd, T.] Royal Adelaide Hosp, Adelaide, SA, Australia.
   [Jayde, V; Blomfield, P.; Challis, D.; McIntosh, R.; Parker, A.] Royal Hobart Hosp, Hobart, Tas, Australia.
   [Mamers, P.; Healy, D.; Jobling, T.; Manolitsas, T.; McNealage, J.; Rogers, P.; Susil, B.; Sumithran, E.; Simpson, L.] Monash Med Ctr, Clayton, Vic, Australia.
   [Ball, C.; Young, C.; Hammond, L.; Leung, Y.; McCartney, A.] King Edward Mem Hosp, Subiaco, WA, Australia.
   [Schmidt, T.; Shirley, H.; Viduka, S.; Zeps, N.] St John God Pathol, Osborne Pk, WA, Australia.
   [Brooks, Julia] St John God Hosp, Subiaco, WA, Australia.
   [Stuart-Harris, R.] Canberra Hosp, Garran, ACT, Australia.
   [Kirsten, R.] Bankstown Hosp, Bankstown, NSW, Australia.
   [Rutovitz, J.] Integrated Canc Ctr, Wahroonga, NSW, Australia.
   [Clingan, P.; Glasgow, A.] Wollongong Hosp, Wollongong, NSW, Australia.
   [Shannon, J.] Nepean Hosp, Kingswood, NSW, Australia.
   [Bonaventura, T.; Stewart, J.] Newcastle Mater Misericordiae Hosp, Waratah, NSW, Australia.
   [Begbie, S.] Port Macquarie Base Hosp, Port Macquarie, NSW, Australia.
   [Links, M.] St George Hosp, Kogarah, NSW, Australia.
   [Grygiel, J.] St Vincents Hosp, Darlinghurst, NSW, Australia.
   [Hill, J.] Wagga Wagga Base Hosp, Wagga Wagga, NSW, Australia.
   [Friedlander, M.] Prince Wales Hosp, Sydney, NSW, Australia.
   [Ward, B.; Papadimos, D.] Mater Misericordiae Univ Hosp, South Brisbane, Qld, Australia.
   [Crandon, A.; Cummings, M.; Horwood, K.; Obermair, A.; Perrin, L.; Wyld, D.; Nicklin, J.] Royal Brisbane & Womens Hosp, Herston, Qld, Australia.
   [Nicklin, J.] Wesley Hosp, Auchenflower, Qld, Australia.
   [Healy, T.; Pittman, K.] Burnside Hosp, Toorak Gardens, SA, Australia.
   [Henderson, D.] Flinders Med Ctr, Bedford Pk, SA, Australia.
   [Miller, J.; Pierdes, J.] Queen Elizabeth Hosp, Woodville South, SA, Australia.
   [Brown, B.; Rome, R.] Freemasons Hosp, East Melbourne, Vic, Australia.
   [Allen, D.; Grant, P.; Hyde, S.; Laurie, R.; Robbie, M.] Mercy Hosp Women, Heidelberg, Vic, Australia.
   [Billson, V; Pyman, J.; Neesham, D.; Quinn, M.] Royal Womens Hosp, Parkville, Vic, Australia.
   [Underhill, C.] Border Med Oncol, Wodonga, Vic, Australia.
   [Bell, R.] Andrew Love Canc Ctr, Geelong, Vic, Australia.
   [Ng, L. F.] Ballarat Base Hosp, Ballarat, Vic, Australia.
   [Blum, R.] Bendigo Hlth Care Grp, Bendigo, Vic, Australia.
   [Ganju, V] Peninsula Hlth, Frankston, Vic, Australia.
   [Buck, M.] Mt Hosp, Perth, WA, Australia.
   [Haviv, I] Bar Ilan Univ, Safed, Israel.
C3 University of Sydney; Westmead Institute for Medical Research;
   University of Sydney; University of Sydney; NSW Health; Westmead
   Hospital; Peter Maccallum Cancer Center; University of Melbourne; La
   Trobe University; Olivia Newton-John Cancer Research Institute; La Trobe
   University; QIMR Berghofer Medical Research Institute; Imperial College
   London; Peter Maccallum Cancer Center; University of Melbourne;
   University of Sydney; Westmead Institute for Medical Research;
   University of Sydney; NSW Health; Westmead Hospital; John Hunter
   Hospital; NSW Health; South Eastern Sydney Local Health District; The
   Royal Hospital for Women; Royal North Shore Hospital; University of
   Sydney; NSW Health; Royal Prince Alfred Hospital; Royal Adelaide
   Hospital; Royal Hobart Hospital; Monash University; Monash Health;
   Monash Medical Centre; University of Western Australia; King Edward
   Memorial Hospital; St John of God Health Care; St John of God Subiaco
   Hospital; St John of God Health Care; Australian National University;
   Canberra Hospital; NSW Health; Bankstown Lidcombe Hospital; Wollongong
   Hospital; Nepean Hospital; Calvary Mater Newcastle Hospital; NSW Health;
   Port Macquarie Base Hospital; St George Hospital; NSW Health; St
   Vincents Hospital Sydney; NSW Health; Wagga Wagga Base Hospital;
   University of New South Wales Sydney; Prince of Wales Hospital (POWH);
   University College Dublin; Royal Brisbane & Women's Hospital; Wesley
   Hospital; Flinders Medical Centre; The Royal Women's Hospital; Bendigo
   Health; Peninsula Health; Bar Ilan University
RP DeFazio, A (corresponding author), Westmead Inst Med Res, Ctr Canc Res, 176 Hawkesbury Rd, Westmead, NSW 2145, Australia.
EM defazio@sydney.edu.an
RI Pearson, John/AAT-4211-2020; Underhill, Craig/ABB-8092-2020; Carter,
   Jonathan/V-2180-2019; Patch, Ann-Marie/C-4201-2018; Zeps,
   Nikolajs/AAF-3186-2021; Waddell, Nicola/H-4929-2015; Mackenzie,
   Penny/ABF-7822-2021; Gertig, Dorota/Z-1087-2019; Chenevix-Trench,
   Georgia/AAV-2014-2020; Kan, Casina/D-3372-2014; gao, bo/HHC-7855-2022;
   Obermair, Andreas/IZP-8773-2023; NG, MEI/Q-3704-2016; Bowtell,
   David/H-1007-2016; friedlander, michael/G-3490-2013; Challis,
   David/B-9262-2008; Rogers, Peter Adrian/C-2651-2008; Harnett,
   Paul/D-4090-2014; Wyld, David/B-8893-2015; Zeps, Nikolajs/C-4180-2013;
   Whiteman, David/P-2728-2014; Grimmond, Sean/J-5304-2016; DeFazio,
   Anna/D-3939-2013; Webb, Penelope/D-5736-2013
OI Rogers, Peter Adrian/0000-0002-7399-8997; Harnett,
   Paul/0000-0001-7021-0642; Wyld, David/0000-0001-9523-4333; Zeps,
   Nikolajs/0000-0002-6404-6839; Hacker, Neville/0000-0002-1445-2302;
   Whiteman, David/0000-0003-2563-9559; Grimmond, Sean/0000-0002-8102-7998;
   Byth Wilson, Karen/0000-0002-1253-6393; Traficante,
   Nadia/0000-0001-7459-8576; DeFazio, Anna/0000-0003-0057-4744; Underhill,
   Craig/0000-0001-9335-2678; Saunders, Catherine AB/0000-0001-6928-7378;
   Kennedy, Catherine/0000-0002-4465-5784; Beale,
   Philip/0000-0003-3628-4597; Webb, Penelope/0000-0003-0733-5930; Jones,
   Marc/0000-0002-3078-8359; Fereday, Sian/0000-0002-8559-8579
FU Cancer Council New South Wales Grant [RG-15-23]; Cancer Institute New
   South Wales [12/RIG/1-17, 15/RIG/1-16]; NHMRC [ID310670, ID628903,
   ID400413, ID400281]; US Army Medical Research and Materiel Command
   [DAMD17-01-1-0729]; Cancer Council Victoria; Queensland Cancer Fund;
   Cancer Council New South Wales; Cancer Council South Australia; Cancer
   Foundation of Western Australia; Cancer Council Tasmania; Agar family;
   Ovarian Cancer Australia; Ovarian Cancer Action (United Kingdom); Peter
   MacCallum Foundation; Cancer Institute New South Wales through the
   Sydney-West Translational Cancer Research Centre; Westmead Medical
   Research Foundation; Jamel Alagha Ovarian Cancer Scholarship; University
   of Sydney; Sydney-West Translational Cancer Research Centre
FX Supported by Cancer Council New South Wales Grant No. RG-15-23. The
   Westmead Gynaecological Oncology Biobank at Westmead is funded by Cancer
   Institute New South Wales Grants No. 12/RIG/1-17 and 15/RIG/1-16 and is
   a member bank of the Australasian Biospecimens Network-Oncology, funded
   by NHMRC Nos. ID310670 and ID628903. The Australian Ovarian Cancer Study
   was supported by the US Army Medical Research and Materiel Command under
   Grant No. DAMD17-01-1-0729, The Cancer Council Victoria, Queensland
   Cancer Fund, The Cancer Council New South Wales, The Cancer Council
   South Australia, The Cancer Foundation of Western Australia, The Cancer
   Council Tasmania, and the NHMRC Nos. ID400413 and ID400281. Also
   supported by S. Boldeman, the Agar family, Ovarian Cancer Australia,
   Ovarian Cancer Action (United Kingdom), and the Peter MacCallum
   Foundation. R.L.B., A.deF., and P.R.H. were funded by the Cancer
   Institute New South Wales through the Sydney-West Translational Cancer
   Research Centre. T.M. received funding as the recipient of an Early
   Career Research Scholarship from the Westmead Medical Research
   Foundation and The Jamel Alagha Ovarian Cancer Scholarship and is
   currently a recipient of a Research Training Program Scholarship from
   the University of Sydney and top-up scholarship from the Sydney-West
   Translational Cancer Research Centre.
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NR 44
TC 27
Z9 27
U1 0
U2 4
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
EI 2473-4284
J9 JCO PRECIS ONCOL
JI JCO Precis. Oncol.
PD MAY 14
PY 2018
VL 2
BP 1
EP 14
DI 10.1200/PO.17.00221
PG 14
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA HQ0LB
UT WOS:000462085400001
PM 35135122
OA Green Published
DA 2025-01-04
ER

PT J
AU Xu, L
   Zhou, D
   Li, F
   Ji, LJ
AF Xu, Liang
   Zhou, Dong
   Li, Fang
   Ji, Lijiang
TI Glutaminase 2 functions as a tumor suppressor gene in gastric cancer
SO TRANSLATIONAL CANCER RESEARCH
LA English
DT Article
DE Glutaminase 2 (GLS2); gastric cancer; proliferation; metastasis
ID GLS2; EXPRESSION; S-1
AB Background: Glutaminase 2 (GLS2) has been described as a tumor suppressor in hepatocellular carcinoma (HCC) and colon cancer. This study aimed to investigate the expression of GLS2 and its biological role in gastric cancer.
   Methods: The expression of GLS2 was determined by quantitative Real-time PCR (qRT-PCR). Proliferation assay was performed by Cell Counting Kit-8 assay. Cell apoptosis assay was performed by Anrtexin V-fluorescein isothiocyanate (FITC) Apoptosis Detection Kit. Migration capability analysis was performed by Transwell chamber assay. The protein GLS2 and caspase 3 was determined by western blotting.
   Results: Here, we demonstrated that GLS2 displayed a significant downregulation in gastric cancer tissues compared to adjacent non-cancer tissues, which suggested that the downregulation of GLS2 might possibly be associated with the development and progression of gastric cancer. We also found that GLS2 overexpression could significantly suppress gastric cancer cell proliferation and migration and enhance gastric cancer cell apoptosis via upregulating the expression of caspase 3.
   Conclusions: These data taken together show that GLS2 functions as a tumor suppressor gene in gastric cancer. This study not only enriches the molecular mechanism of gastric cancer but also supplies a scientific basis for targeted treatment of gastric cancer.
C1 [Xu, Liang; Zhou, Dong; Li, Fang; Ji, Lijiang] Nanjing Univ Chinese Med, Changshu Tradit Chinese Med Hosp, Dept Gen Surg, Changshu Hosp, Changshu, Jiangsu, Peoples R China.
C3 Nanjing University of Chinese Medicine
RP Ji, LJ (corresponding author), Changshu Tradit Chinese Med Hosp, 6 Huang He Rd, Suzhou 215500, Peoples R China.
EM 715772824@qq.com
RI Xu, Liang/F-6914-2015
FU Science and Technology Project of Changshu Health Committee
   [CSWS201911]; Science and Technology Project of Suzhou Science and
   Technology Bureau [SYS2019004]; Science and Technology Project of
   Changshu Science and Technology Bureau [CS201808]
FX This work was supported by the Science and Technology Project of
   Changshu Health Committee (Grant No. CSWS201911), Science and Technology
   Project of Suzhou Science and Technology Bureau (Grant No. SYS2019004),
   and Science and Technology Project of Changshu Science and Technology
   Bureau (Grant No. CS201808).
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NR 32
TC 7
Z9 8
U1 0
U2 6
PU AME PUBLISHING COMPANY
PI SHATIN
PA FLAT-RM C 16F, KINGS WING PLAZA 1, NO 3 KWAN ST, SHATIN, HONG KONG
   00000, PEOPLES R CHINA
SN 2218-676X
EI 2219-6803
J9 TRANSL CANCER RES
JI Transl. Cancer Res.
PD AUG
PY 2020
VL 9
IS 8
BP 4906
EP 4913
DI 10.21037/tcr-20-2246
PG 8
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA ND8FL
UT WOS:000562138400043
PM 35117852
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Xie, FY
   Xu, WH
   Yin, C
   Zhang, GQ
   Zhong, YQ
   Gao, J
AF Xie, Fang-Yuan
   Xu, Wei-Heng
   Yin, Chuan
   Zhang, Guo-Qing
   Zhong, Yan-Qiang
   Gao, Jie
TI Nanomedicine strategies for sustained, controlled, and targeted
   treatment of cancer stem cells of the digestive system
SO WORLD JOURNAL OF GASTROINTESTINAL ONCOLOGY
LA English
DT Review
DE Nanomedicine; Cancer stem cells; Digestive system; Drug delivery; Gene
   delivery
ID TUMOR-INITIATING CELLS; HUMAN GASTRIC-CANCER; HUMAN LIVER-CANCER;
   HEPATOCELLULAR-CARCINOMA; COLORECTAL-CANCER; SELF-RENEWAL; ANTICANCER
   THERAPEUTICS; DIFFERENTIATION THERAPY; OXIDATIVE STRESS; DRUG-RESISTANCE
AB Cancer stem cells (CSCs) constitute a small proportion of the cancer cells that have self-renewal capacity and tumor-initiating ability. They have been identified in a variety of tumors, including tumors of the digestive system. CSCs exhibit some unique characteristics, which are responsible for cancer metastasis and recurrence. Consequently, the development of effective therapeutic strategies against CSCs plays a key role in increasing the efficacy of cancer therapy. Several potential approaches to target CSCs of the digestive system have been explored, including targeting CSC surface markers and signaling pathways, inducing the differentiation of CSCs, altering the tumor microenvironment or niche, and inhibiting ATP-driven efflux transporters. However, conventional therapies may not successfully eradicate CSCs owing to various problems, including poor solubility, stability, rapid clearance, poor cellular uptake, and unacceptable cytotoxicity. Nanomedicine strategies, which include drug, gene, targeted, and combinational delivery, could solve these problems and significantly improve the therapeutic index. This review briefly summarizes the ongoing development of strategies and nanomedicine-based therapies against CSCs of the digestive system.
C1 [Xie, Fang-Yuan; Zhang, Guo-Qing] Shanghai Eastern Hepatobiliary Surg Hosp, Dept Pharm, Shanghai 200438, Peoples R China.
   [Xie, Fang-Yuan; Zhong, Yan-Qiang; Gao, Jie] Second Mil Med Univ, Sch Pharm, Dept Pharmaceut Sci, 325 Guohe Rd, Shanghai 200433, Peoples R China.
   [Xu, Wei-Heng] Second Mil Med Univ, Sch Pharm, Dept Biochem Pharm, Shanghai 200433, Peoples R China.
   [Yin, Chuan] Second Mil Med Univ, Changzheng Hosp, Dept Gastroenterol, Shanghai 200003, Peoples R China.
C3 Naval Medical University; Naval Medical University; Naval Medical
   University; Naval Medical University
RP Gao, J (corresponding author), Second Mil Med Univ, Sch Pharm, Dept Pharmaceut Sci, 325 Guohe Rd, Shanghai 200433, Peoples R China.
EM gaojie@smmu.edu.cn
RI zhang, guoqing/GXG-4800-2022; Gao, Jie/KMY-7382-2024
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NR 102
TC 22
Z9 23
U1 2
U2 10
PU BAISHIDENG PUBLISHING GROUP INC
PI PLEASANTON
PA 8226 REGENCY DR, PLEASANTON, CA 94588 USA
SN 1948-5204
J9 WORLD J GASTRO ONCOL
JI World J. Gastrointest. Oncol.
PD OCT 15
PY 2016
VL 8
IS 10
BP 735
EP 744
DI 10.4251/wjgo.v8.i10.735
PG 10
WC Oncology; Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Gastroenterology & Hepatology
GA FE9TP
UT WOS:000408546400003
PM 27795813
OA Green Submitted, hybrid, Green Published
DA 2025-01-04
ER

PT J
AU Hashimoto, Y
   Yagi, K
   Kondoh, M
AF Hashimoto, Yosuke
   Yagi, Kiyohito
   Kondoh, Masuo
TI Roles of the first-generation claudin binder, <i>Clostridium
   perfringens</i> enterotoxin, in the diagnosis and claudin-targeted
   treatment of epithelium-derived cancers
SO PFLUGERS ARCHIV-EUROPEAN JOURNAL OF PHYSIOLOGY
LA English
DT Review
DE Clostridium perfringens enterotoxin; Claudin; Tumor therapy; Tumor
   diagnosis
ID TIGHT JUNCTION PROTEINS; C-TERMINAL FRAGMENT; PROSTATE-SPECIFIC ANTIGEN;
   GENE-EXPRESSION PROFILES; RESISTANT OVARIAN-CANCER; OPENER JO-1
   IMPROVES; PANCREATIC-CANCER; COLORECTAL-CANCER; IN-VIVO;
   HEPATOCELLULAR-CARCINOMA
AB Given that most malignant tumors are derived from epithelium, developing a strategy for treatment of epithelium-derived cancers (i.e., carcinomas) is a pivotal issue in cancer therapy. Carcinomas, including ovarian, breast, prostate, and pancreatic cancers, are known to overexpress various claudins (CLDNs); in particular, CLDN-3 and -4 are frequently overexpressed in malignant case. The generation of CLDN binders is a key for expanding CLDN-targeted cancer therapy but has been delayed due to the small size of CLDN extracellular domains (approximately 50 amino acids for the first domain and 15 amino acids for the second) and their high homology among species. Interestingly, however, the receptors for Clostridium perfringens enterotoxin (CPE), a foodborne toxin in humans, happen to be identical to CLDN-3 and -4. Thus, the first CLDN binder, CPE, has provided us CLDN-targeted cancer therapy from a concept into a potential reality. In this review, we describe roles of CPE technology in cancer therapy and discuss future directions in the CLDN-targeting concept-to-therapy process.
C1 [Hashimoto, Yosuke; Yagi, Kiyohito; Kondoh, Masuo] Osaka Univ, Grad Sch Pharmaceut Sci, Suita, Osaka 5650871, Japan.
C3 Osaka University
RP Kondoh, M (corresponding author), Osaka Univ, Grad Sch Pharmaceut Sci, Suita, Osaka 5650871, Japan.
EM masuo@phs.osaka-u.ac.jp
RI Hashimoto, Yosuke/ABA-3807-2022
OI Hashimoto, Yosuke/0000-0003-3008-9563
FU Ministry of Health, Labour, and Welfare of Japan; Japan Agency for
   Medical Research and Development (AMED); Ministry of Education, Culture,
   Sports, Science, and Technology of Japan [24390042]; Adaptable and
   Seamless Technology Transfer Program through Target-driven RD Agency;
   Ministry of Education, Culture, Sports, Science and Technology, Japan;
   Takeda Science Foundation; Japan Society for the Promotion of Science;
   Grants-in-Aid for Scientific Research [24390042, 15J10065] Funding
   Source: KAKEN
FX We thank all of the members of our laboratory for their useful comments.
   This work was supported by a Health and Labour Sciences Research Grant
   from the Ministry of Health, Labour, and Welfare of Japan; a research
   grant from the Japan Agency for Medical Research and Development (AMED);
   a Grant-in-Aid for Scientific Research from the Ministry of Education,
   Culture, Sports, Science, and Technology of Japan [grant number
   24390042]; and funds from the Adaptable and Seamless Technology Transfer
   Program through Target-driven R&D Agency; Platform for Drug Discovery,
   Informatics, and Structural Life Science from the Ministry of Education,
   Culture, Sports, Science and Technology, Japan; and the Takeda Science
   Foundation. Y.H. is supported by a Research Fellowship for Young
   Scientists from the Japan Society for the Promotion of Science.
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NR 96
TC 25
Z9 27
U1 0
U2 14
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0031-6768
EI 1432-2013
J9 PFLUG ARCH EUR J PHY
JI Pflugers Arch.
PD JAN
PY 2017
VL 469
IS 1
BP 45
EP 53
DI 10.1007/s00424-016-1878-6
PG 9
WC Physiology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Physiology
GA EG9JC
UT WOS:000391373900006
PM 27629072
DA 2025-01-04
ER

PT J
AU Vural, OA
   Yaman, YT
   Abaci, S
AF Vural, Oznur Akbal
   Yaman, Yesim Tugce
   Abaci, Serdar
TI Secondary metabolite-entrapped, anti-GPA33 targeted poly-dopamine
   nanoparticles and their effectiveness in cancer treatment
SO JOURNAL OF APPLIED POLYMER SCIENCE
LA English
DT Article
DE anti-GPA33; cellular uptake; polydopamine nanoparticles; saponin;
   targeted treatment
ID DRUG-DELIVERY; POLYDOPAMINE NANOPARTICLES; COLORECTAL-CANCER; CELLULAR
   UPTAKE; PARTICLE-SIZE; SURFACE; A33; FLUORESCENT; NANOCOMPOSITES;
   THERAPY
AB In this study, the development of polydopamine nanoparticle (p-Dop NP) as a drug carrier system for saponin (Sap) and its use in in vitro targeted cancer therapy was investigated. The average diameter of p-Dop NP was found as 130 nm with a zeta potential of -18 mV and demonstrated high stability even after 6 weeks. The Sap release and cytotoxicity studies were carried out to reveal the effectiveness of the proposed carrier system. The offered approach demonstrated a high loading capacity of Sap as 81% with a sustainable and controlled release of 75%. To prevent the interaction of the anti-cancer Sap with other healthy tissue and to enhance the targeting of DLD-1 cells, anti-GPA33 was immobilized onto the nanoparticle surface via carbodiimide strategy. The anti-GPA33 and Sap loaded p-Dop NPs demonstrated enhanced toxicity and cellular uptake compared to untargeted Sap loaded NPs as expected. The offered carrier system revealed simple and efficient targeted cancer therapy ability in vitro and may provide new ideas for the design of targeted delivery systems in the future.
C1 [Vural, Oznur Akbal; Yaman, Yesim Tugce] Hacettepe Univ, Adv Technol Applicat & Res Ctr, Ankara, Turkey.
   [Yaman, Yesim Tugce; Abaci, Serdar] Hacettepe Univ, Dept Chem, Analyt Chem Div, Ankara, Turkey.
C3 Hacettepe University; Hacettepe University
RP Abaci, S (corresponding author), Hacettepe Univ, Dept Chem, Analyt Chem Div, Ankara, Turkey.
EM sabaci@hacettepe.edu.tr
RI ; AKBAL, OZNUR/Z-4784-2019
OI ABACI, Serdar/0000-0003-2302-0779; AKBAL, OZNUR/0000-0003-1972-5987
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NR 67
TC 2
Z9 2
U1 4
U2 15
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0021-8995
EI 1097-4628
J9 J APPL POLYM SCI
JI J. Appl. Polym. Sci.
PD JUN 10
PY 2022
VL 139
IS 22
AR e52274
DI 10.1002/app.52274
EA FEB 2022
PG 11
WC Polymer Science
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Polymer Science
GA 0I4RR
UT WOS:000759639200001
DA 2025-01-04
ER

PT J
AU Pataky, RE
   Peacock, S
   Bryan, S
   Sadatsafavi, M
   Regier, DA
AF Pataky, Reka E.
   Peacock, Stuart
   Bryan, Stirling
   Sadatsafavi, Mohsen
   Regier, Dean A.
TI Using Genomic Heterogeneity to Inform Therapeutic Decisions for
   Metastatic Colorectal Cancer: An Application of the Value of
   Heterogeneity Framework
SO APPLIED HEALTH ECONOMICS AND HEALTH POLICY
LA English
DT Article; Early Access
ID COST-EFFECTIVENESS ANALYSIS; PROPENSITY SCORE ESTIMATION; CETUXIMAB PLUS
   IRINOTECAN; PHASE-III TRIAL; RAS MUTATIONS; PANITUMUMAB; KRAS; BENEFIT
AB Background and ObjectiveMutations in KRAS and NRAS are predictive of poor response to cetuximab and panitumumab, two anti-epidermal growth factor receptor (EGFR) monoclonal antibodies used in metastatic colorectal cancer (mCRC). Our objective was to explore the value of using KRAS and NRAS mutation status to inform third-line anti-EGFR therapy for mCRC using the value of heterogeneity (VOH) framework.MethodsWe used administrative data to identify mCRC patients who were potentially eligible for third-line therapy in 2006-2019 in British Columbia (BC), Canada. We compared three alternative stratification policies in place during the study period: the unstratified policy where anti-EGFR therapy was not offered (2006-2009), stratification by KRAS mutation (2009-2016), and stratification by KRAS+NRAS mutation (2016-2019). We used inverse-probability-of-treatment weighting to balance covariates across the three groups. Cost and survival time were calculated using a 3-year time horizon and adjusted for censoring, with bootstrapping to characterize uncertainty. Mean net monetary benefit (NMB) was calculated at a range of threshold values. The VOH of using KRAS and NRAS mutation status to inform treatment selection was calculated as the change in NMB with increasing stratification, under current (static VOH) or perfect (dynamic VOH) information.ResultsWe included 2664 patients in the analysis. At a willingness-to-pay of CA$100,000/ life-year gained (LYG), stratification on KRAS mutation status provided a static VOH of CA$1565 per patient; further stratification on KRAS+NRAS provided additional static VOH of CA$594. The static VOH exceeded the marginal cost of genomic testing under both policies.ConclusionsStratification of anti-EGFR therapy by KRAS and NRAS mutation status can provide additional value at a threshold of CA$100,000/LYG. There is diminishing marginal value and increasing marginal costs as the policy becomes more stratified. The VOH framework can illustrate the value of subgroup-specific decisions in a comprehensive way, to better inform targeted treatment policies.
C1 [Pataky, Reka E.; Peacock, Stuart; Regier, Dean A.] Canadian Ctr Appl Res Canc Control, BC Canc, Vancouver, BC, Canada.
   [Peacock, Stuart] Simon Fraser Univ, Fac Hlth Sci, Vancouver, BC, Canada.
   [Bryan, Stirling] Vancouver Coastal Hlth Res Inst, Ctr Clin Epidemiol & Evaluat, Vancouver, BC, Canada.
   [Bryan, Stirling; Regier, Dean A.] Univ British Columbia, Sch Populat & Publ Hlth, Vancouver, BC, Canada.
   [Sadatsafavi, Mohsen] Univ British Columbia, Fac Pharmaceut Sci, Collaborat Outcomes Res & Evaluat, Vancouver, BC, Canada.
   [Pataky, Reka E.] BC Canc Res Ctr, 675 W 10th Ave, Vancouver, BC V5Z 1L3, Canada.
C3 Simon Fraser University; Vancouver Coastal Health Research Institute;
   University of British Columbia; University of British Columbia; British
   Columbia Cancer Agency
RP Pataky, RE (corresponding author), Canadian Ctr Appl Res Canc Control, BC Canc, Vancouver, BC, Canada.; Pataky, RE (corresponding author), BC Canc Res Ctr, 675 W 10th Ave, Vancouver, BC V5Z 1L3, Canada.
EM rpataky@bccrc.ca
RI Sadatsafayi, Mohsen/AAZ-1593-2020
OI Pataky, Reka/0000-0003-0159-582X; Sadatsafavi,
   Mohsen/0000-0002-0419-7862
FU Canadian Institutes of Health Research Doctoral Research Award; Genome
   BC/Genome Canada [G05CHS]
FX REP was supported by a Canadian Institutes of Health Research Doctoral
   Research Award. The Canadian Network for Learn-ing Healthcare Systems
   and Cost-effective 'Omics Innovation (CLEO) is supported by Genome
   BC/Genome Canada [G05CHS]. The funders were not involved in the writing
   of the manuscript or the decision to submit it for publication.
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NR 53
TC 0
Z9 0
U1 0
U2 0
PU SPRINGER INT PUBL AG
PI CHAM
PA GEWERBESTRASSE 11, CHAM, CH-6330, SWITZERLAND
SN 1175-5652
EI 1179-1896
J9 APPL HEALTH ECON HEA
JI Appl. Health Econ. Health Policy
PD 2024 NOV 9
PY 2024
DI 10.1007/s40258-024-00926-9
EA NOV 2024
PG 12
WC Economics; Health Care Sciences & Services; Health Policy & Services
WE Science Citation Index Expanded (SCI-EXPANDED); Social Science Citation Index (SSCI)
SC Business & Economics; Health Care Sciences & Services
GA L4L7S
UT WOS:001350456500001
PM 39520611
DA 2025-01-04
ER

PT J
AU Mao, L
   Yin, MF
   Ji, CF
   Ma, QX
   Xia, DL
   Yang, L
AF Mao, Ling
   Yin, Mengfei
   Ji, Congfei
   Ma, Qingxia
   Xia, Donglin
   Yang, Lei
TI Targeted delivery of T-cell agonists for enhancing immunotherapy
SO JOURNAL OF DRUG DELIVERY SCIENCE AND TECHNOLOGY
LA English
DT Article
DE Immunotherapy; L-arginine; Platelet; Colon cancer; PD-1
ID DRUG-DELIVERY; L-ARGININE; PLATELET
AB The T-cell agonist, L-arginine (L-arg), can act as an efficient antitumor T-cell response and improve antitumor immune activity. However, the low L-arg concentration in the tumor markedly inhibits the antitumor responses of immune checkpoint inhibitors. Furthermore, no method is currently available for increasing tumor L-arg levels locally. To overcome this challenge, we engineered a platelet (PLTs)-based drug carrier system (L-arg@PLTs) for tumor-targeted delivery and intratumoral release for locally increasing intratumoral L-arg levels. The PLTs drug delivery system can circulate freely in the blood until they are activated by the tumor, and recruit more L-arg@PLTs for targeted release of their content, which could increase the local L-arg concentration in the tumor. L-arg promotes T lymphocyte proliferation in tumor tissues, and T lymphocytes can inhibit tumor cell growth. L-arg acts synergistically with PD-1 inhibitors to inhibit tumor proliferation. Although this method cannot currently be used in clinics because of the limited source of human L-arg and safety-related issues in humans, this study provides a novel insight for tumor treatment. When combined with immunotherapy, this drug delivery system has produced a significant synergistic effect on malignant tumor treatment and offers a new strategy for targeted treatment in immunotherapy.
C1 [Mao, Ling; Yin, Mengfei; Ji, Congfei; Ma, Qingxia; Yang, Lei] Nantong Tumor Hosp, Dept Oncol, Nantong, Peoples R China.
   [Mao, Ling; Yin, Mengfei; Ji, Congfei; Ma, Qingxia; Yang, Lei] Nantong Univ, Affiliated Tumor Hosp, Nantong, Peoples R China.
   [Mao, Ling; Yin, Mengfei] Nantong Univ, Med Sch, Nantong, Peoples R China.
   [Xia, Donglin] Nantong Univ, Sch Publ Hlth, Nantong, Peoples R China.
C3 Nantong University; Nantong University; Nantong University
RP Yang, L (corresponding author), Nantong Tumor Hosp, Dept Oncol, Nantong, Peoples R China.; Yang, L (corresponding author), Nantong Univ, Affiliated Tumor Hosp, Nantong, Peoples R China.; Xia, DL (corresponding author), Nantong Univ, Sch Publ Hlth, Nantong, Peoples R China.
EM xiadonglin@ntu.edu.cn; leiyang.53@163.com
RI Xia, Donglin/GQI-1897-2022
FU Science and Technology Bureau of Nantong [MS22021035]; Science and
   Technol-ogy R & D Found of Nantong City [MS22022037, MS22022096];
   Nantong Health Commission Project [MSZ2023040]
FX The present study was supported by the Science and Technology Bureau of
   Nantong (grant No. MS22021035) , the Science and Technology R & D Found
   of Nantong City (No. MS22022037, MS22022096) , and Nantong Health
   Commission Project (No. MSZ2023040) .
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NR 45
TC 0
Z9 0
U1 2
U2 14
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
SN 1773-2247
EI 2588-8943
J9 J DRUG DELIV SCI TEC
JI J. Drug Deliv. Sci. Technol.
PD NOV
PY 2023
VL 89
AR 105074
DI 10.1016/j.jddst.2023.105074
EA OCT 2023
PG 10
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA Y5VS4
UT WOS:001105939800001
DA 2025-01-04
ER

PT J
AU Cai, ZL
   Wei, Y
   Chen, S
   Gong, Y
   Fu, Y
   Dai, XH
   Zhou, Y
   Yang, HJ
   Tang, LM
   Liu, HY
AF Cai, Zeling
   Wei, Yi
   Chen, Shuai
   Gong, Yu
   Fu, Yue
   Dai, Xianghua
   Zhou, Yan
   Yang, Haojun
   Tang, Liming
   Liu, Hanyang
TI Screening and identification of key biomarkers in alimentary tract
   cancers: A bioinformatic analysis
SO CANCER BIOMARKERS
LA English
DT Article
DE Alimentary tract cancers; differentially expressed genes; microarray
   datasets; enrichment analysis; survival analysis
ID HIGH EXPRESSION; POOR-PROGNOSIS; KIF14; COL10A1; MUTATION; FEATURES;
   RISK
AB BACKGROUND: Alimentary tract cancers (ATCs) are the most malignant cancers in the world. Numerous studies have revealed the tumorigenesis, diagnosis and treatment of ATCs, but many mechanisms remain to be explored.
   METHODS: To identify the key genes of ATCs, microarray datasets of oesophageal cancer, gastric cancer and colorectal cancer were obtained from the Gene Expression Omnibus (GEO) database. In total, 207 differentially expressed genes (DEGs) were screened. KEGG and GO function enrichment analyses were conducted, and a protein-protein interaction (PPI) network was generated and gene modules analysis was performed using STRING and Cytoscape.
   RESULTS: Five hub genes were screened, and the associated biological processes indicated that these genes were mainly enriched in cellular processes, protein binding and metabolic processes. Clinical survival analysis showed that COL10A1 and KIF14 may be significantly associated with the tumorigenesis or pathology grade of ATCs. In addition, relative human ATC cell lines along with blood samples and tumour tissues of ATC patients were obtained. The data proved that high expression of COL10A1 and KIF14 was associated with tumorigenesis and could be detected in blood.
   CONCLUSION: In conclusion, the identification of hub genes in the present study helped us to elucidate the molecular mechanisms of tumorigenesis and identify potential diagnostic indicators and targeted treatment for ATCs.
C1 [Cai, Zeling; Dai, Xianghua] Nantong Univ, Affiliated Haimen Peoples Hosp, Genter Gen Surg, Nantong, Jiangsu, Peoples R China.
   [Wei, Yi; Chen, Shuai; Gong, Yu; Fu, Yue; Zhou, Yan; Yang, Haojun; Tang, Liming; Liu, Hanyang] Nanjing Med Univ, Ctr Gastrointestinal Dis, Affiliated Changzhou Peoples Hosp 2, 68 Gehu Rd, Changzhou, Jiangsu, Peoples R China.
C3 Nantong University; Nanjing Medical University
RP Tang, LM; Liu, HY (corresponding author), Nanjing Med Univ, Ctr Gastrointestinal Dis, Affiliated Changzhou Peoples Hosp 2, 68 Gehu Rd, Changzhou, Jiangsu, Peoples R China.
EM drtangliming@163.com; brandenliu@live.com
RI Liu, Hanyang/ACN-2818-2022
OI Liu, Hanyang/0000-0002-1035-4895
FU Jiangsu Natural Science Foundation [BK20181155]; Nanjing Medical
   University [2017NJMU043]; Changzhou Department of Health [QN201711];
   Changzhou NO. 2 People's Hospital [2018K003]
FX The expenditure of this whole study was funded by research grants from
   the Jiangsu Natural Science Foundation (grant no. BK20181155), the
   Nanjing Medical University (grant no. 2017NJMU043), the Changzhou
   Department of Health (grant no. QN201711) and the Changzhou NO. 2
   People's Hospital (grant no. 2018K003).
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NR 55
TC 3
Z9 3
U1 0
U2 5
PU IOS PRESS
PI AMSTERDAM
PA NIEUWE HEMWEG 6B, 1013 BG AMSTERDAM, NETHERLANDS
SN 1574-0153
EI 1875-8592
J9 CANCER BIOMARK
JI Cancer Biomark.
PY 2020
VL 29
IS 2
BP 221
EP 233
DI 10.3233/CBM-201580
PG 13
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA OH6TL
UT WOS:000582728300006
PM 32623389
DA 2025-01-04
ER

PT J
AU Heby, M
   Karnevi, E
   Elebro, J
   Nodin, B
   Eberhard, J
   Saukkonen, K
   Hagström, J
   Mustonen, H
   Seppänen, H
   Haglund, C
   Jirström, K
   Larsson, AH
AF Heby, Margareta
   Karnevi, Emelie
   Elebro, Jacob
   Nodin, Bjorn
   Eberhard, Jakob
   Saukkonen, Kapo
   Hagstrom, Jaana
   Mustonen, Harri
   Seppanen, Hanna
   Haglund, Caj
   Jirstrom, Karin
   Larsson, Anna H.
TI Additive clinical impact of epidermal growth factor receptor and
   podocalyxin-like protein expression in pancreatic and periampullary
   adenocarcinomas
SO SCIENTIFIC REPORTS
LA English
DT Article
ID EPITHELIAL-MESENCHYMAL TRANSITION; POOR-PROGNOSIS; TGF-BETA; MAJOR
   SIALOPROTEIN; INDEPENDENT FACTOR; CANCER; OVEREXPRESSION; CELLS
AB The outcome of periampullary adenocarcinomas remains poor with few treatment options. Podocalyxin-like protein (PODXL) is an anti-adhesive protein, the high expression of which has been shown to confer a poor prognosis in numerous malignancies. A correlation and adverse prognostic synergy between PODXL and the epidermal growth factor receptor (EGFR) has been observed in colorectal cancer. Here, we investigated whether this also applies to periampullary adenocarcinomas. We analyzed the immunohistochemical expression of PODXL and EGFR in tissue microarrays with tumors from two patient cohorts; (Cohort 1, n=175) and (Cohort 2, n=189). The effect of TGF-beta -induced expression and siRNA-mediated knockdown of PODXL and EGFR, were investigated in pancreatic cancer cells (PANC-1) in vitro. We found a correlation between PODXL and EGFR in these cancers, and a synergistic adverse effect on survival. Furthermore, silencing PODXL in pancreatic cancer cells resulted in the down-regulation of EGFR, but not vice versa. Consequently, these findings suggest a functional link between PODXL and EGFR, and the potential combined utility as biomarkers possibly improving patient stratification. Further studies examining the mechanistic basis underlying these observations may open new avenues of targeted treatment options for subsets of patients affected by these particularly aggressive cancers.
C1 [Heby, Margareta; Karnevi, Emelie; Elebro, Jacob; Nodin, Bjorn; Eberhard, Jakob; Jirstrom, Karin; Larsson, Anna H.] Lund Univ, Skane Univ Hosp, Dept Clin Sci Lund, Div Oncol & Pathol, S-22185 Lund, Sweden.
   [Saukkonen, Kapo; Mustonen, Harri; Seppanen, Hanna; Haglund, Caj] Univ Helsinki, Dept Surg, POB 440, FIN-00029 Helsinki, Finland.
   [Saukkonen, Kapo; Mustonen, Harri; Seppanen, Hanna; Haglund, Caj] Helsinki Univ Hosp, POB 440, FIN-00029 Helsinki, Finland.
   [Saukkonen, Kapo; Hagstrom, Jaana; Haglund, Caj] Univ Helsinki, Res Programmes Unit, Translat Canc Biol, POB 63, FIN-00014 Helsinki, Finland.
   [Hagstrom, Jaana] Univ Helsinki, Haartman Inst, Dept Pathol, FIN-00014 Helsinki, Finland.
   [Hagstrom, Jaana] Univ Helsinki, HUSLAB, FIN-00014 Helsinki, Finland.
   [Hagstrom, Jaana] Univ Helsinki, Helsinki Univ Hosp, FIN-00014 Helsinki, Finland.
C3 Lund University; Skane University Hospital; University of Helsinki;
   University of Helsinki; Helsinki University Central Hospital; University
   of Helsinki; University of Helsinki; University of Helsinki; University
   of Helsinki; Helsinki University Central Hospital
RP Heby, M (corresponding author), Lund Univ, Skane Univ Hosp, Dept Clin Sci Lund, Div Oncol & Pathol, S-22185 Lund, Sweden.
EM margareta.heby@med.lu.se
RI Seppänen, Hanna/AER-1337-2022; Hagstrom, jaana/G-1468-2018
OI Mustonen, Harri Kalevi/0000-0001-5632-6796; , Hanna/0000-0002-2529-651X;
   Jirstrom, Karin/0000-0003-2257-5000; Hagstrom, jaana/0000-0001-6079-7881
FU Swedish Research Council; Swedish Cancer Society; Mrs Berta Kamprad
   Foundation; Region Skane Regional research grants; Governmental Funding
   for Clinical Research within the National Health Service (ALF); Lund
   University Faculty of Medicine; Skane University Hospital Funds and
   Donations; Helsinki University Hospital Research Grants; Sigrid Juselius
   Foundation; Lund University
FX This study was supported by grants from the Swedish Research Council,
   the Swedish Cancer Society, the Mrs Berta Kamprad Foundation, Region
   Skane Regional research grants, Governmental Funding for Clinical
   Research within the National Health Service (ALF), Lund University
   Faculty of Medicine, Skane University Hospital Funds and Donations,
   Helsinki University Hospital Research Grants and the Sigrid Juselius
   Foundation. Open access funding provided by Lund University.
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NR 50
TC 3
Z9 3
U1 0
U2 6
PU NATURE PORTFOLIO
PI BERLIN
PA HEIDELBERGER PLATZ 3, BERLIN, 14197, GERMANY
SN 2045-2322
J9 SCI REP-UK
JI Sci Rep
PD JUN 25
PY 2020
VL 10
IS 1
AR 10373
DI 10.1038/s41598-020-67187-z
PG 10
WC Multidisciplinary Sciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Science & Technology - Other Topics
GA MH2PL
UT WOS:000546573500015
PM 32587323
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Bosman, FT
AF Bosman, Fredrik T.
TI Tumor Heterogeneity: Will It Change What Pathologists Do?
SO PATHOBIOLOGY
LA English
DT Article
DE Tumor heterogeneity; Molecular heterogeneity; Morphological
   heterogeneity; Differentiation; Clonal evolution; Sampling
ID COLORECTAL-CANCER; INTRATUMOR HETEROGENEITY; GENETIC-HETEROGENEITY;
   CLONAL EVOLUTION; CELL CARCINOMA; LUNG-CANCER; IMMUNOHISTOCHEMISTRY;
   GENERATION; MODEL
AB Although the notion that tumors are heterogeneous is well rooted in diagnostic pathology, the extent of this heterogeneity at the molecular level and its impact on (targeted) treatment choice will certainly influence the practice of pathology. Even though the consequences of tumor heterogeneity for cancer care are as yet incompletely understood, pathologists can contribute to solving major scientific and clinical problems related to tumor heterogeneity by rethinking guidelines for tumor sampling, to have a more comprehensive covering of intratumor heterogeneity in the available tumor tissue samples. They should develop guidelines and/or technology to adequately document sample characteristics such as percentage of tumor cells in a sample. They need to contribute to training of bioinformaticians in the field of cancer pathobiology and integrate such well-trained bioinformaticians in the workflow leading to a final pathology report. They also need to redefine postgraduate training programs in diagnostic pathology to address the need for in-depth training in molecular cancer pathobiology Pathologists might contribute more to making the public at large aware of the importance of data sharing. Finally, pathologists should support the creation of consortia in which clinical and molecular data are shared with the translational research community. (C) 2017 S. Karger AG, Basel.
C1 [Bosman, Fredrik T.] Univ Inst Pathol, Rue Bugnon 25, CH-1011 Lausanne, Switzerland.
RP Bosman, FT (corresponding author), Univ Inst Pathol, Rue Bugnon 25, CH-1011 Lausanne, Switzerland.
EM Fred.bosman@chuv.ch
OI Bosman, Fred/0000-0002-1652-6977
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NR 32
TC 6
Z9 7
U1 1
U2 4
PU KARGER
PI BASEL
PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND
SN 1015-2008
EI 1423-0291
J9 PATHOBIOLOGY
JI Pathobiology
PY 2018
VL 85
IS 1-2
BP 18
EP 22
DI 10.1159/000469664
PG 5
WC Cell Biology; Pathology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology; Pathology
GA GF1QI
UT WOS:000431709300003
PM 28482346
OA Bronze
DA 2025-01-04
ER

PT J
AU Woodward, ER
   Green, K
   Burghel, GJ
   Bulman, M
   Clancy, T
   Lalloo, F
   Schlecht, H
   Wallace, AJ
   Evans, DG
AF Woodward, Emma R.
   Green, Kate
   Burghel, George J.
   Bulman, Michael
   Clancy, Tara
   Lalloo, Fiona
   Schlecht, Helene
   Wallace, Andrew J.
   Evans, D. Gareth
TI 30 year experience of index case identification and outcomes of cascade
   testing in high-risk breast and colorectal cancer predisposition genes
SO EUROPEAN JOURNAL OF HUMAN GENETICS
LA English
DT Article
ID SCORING SYSTEM; MUTATIONS; VARIANTS; FAMILIES; GENETICS; CRITERIA
AB It is 30 years since the first diagnostic cancer predisposition gene (CPG) test in the Manchester Centre for Genomic Medicine (MCGM), providing opportunities for cancer prevention, early detection and targeted treatments in index cases and at-risk family members. Here, we present time trends (1990-2020) of identification of index cases with a germline CPG variant and numbers of subsequent cascade tests, for 15 high-risk breast and gastro-intestinal tract cancer-associated CPGs: BRCA1, BRCA2, PALB2, PTEN, TP53, APC, BMPR1a, CDH1, MLH1, MSH2, MSH6, PMS2, SMAD4, STK11 and MUTYH. We recorded 2082 positive index case diagnostic screening tests, generating 3216 positive and 3140 negative family cascade (non-index) tests. This is equivalent to an average of 3.05 subsequent cascade tests per positive diagnostic index test, with 1.54 positive and 1.51 negative non-index tests per family. The CPGs with the highest numbers of non-index positive cases identified on cascade testing were BRCA1/2 (n = 1999) and the mismatch repair CPGs associated with Lynch Syndrome (n = 731). These data are important for service provision and health economic assessment of CPG diagnostic testing, in terms of cancer prevention and early detection strategies, and identifying those likely to benefit from targeted treatment strategies.
C1 [Woodward, Emma R.; Green, Kate; Burghel, George J.; Bulman, Michael; Lalloo, Fiona; Schlecht, Helene; Wallace, Andrew J.; Evans, D. Gareth] Manchester Univ Hosp NHS Fdn Trust, Manchester Ctr Genom Med, Manchester M13 9WL, Lancs, England.
   [Woodward, Emma R.; Clancy, Tara; Evans, D. Gareth] Univ Manchester, Manchester Acad Hlth Sci Ctr, Fac Biol Med & Hlth, Div Evolut & Genom Sci,Sch Biol Sci, Manchester M13 9PL, Lancs, England.
C3 Wythenshawe Hospital NHS Foundation Trust; University of Manchester
RP Evans, DG (corresponding author), Manchester Univ Hosp NHS Fdn Trust, Manchester Ctr Genom Med, Manchester M13 9WL, Lancs, England.; Evans, DG (corresponding author), Univ Manchester, Manchester Acad Hlth Sci Ctr, Fac Biol Med & Hlth, Div Evolut & Genom Sci,Sch Biol Sci, Manchester M13 9PL, Lancs, England.
EM gareth.evans@mft.nhs.uk
RI Evans, D/AAB-4308-2022; Woodward, Emma/U-1282-2019; Woodward,
   Emma/G-9684-2016
OI Evans, Gareth/0000-0002-8482-5784; Woodward, Emma/0000-0002-6297-2855
FU Manchester NIHR Biomedical Research Centre [IS-BRC-1215-200074]
FX E.R.W. and D.G.E. are supported by the Manchester NIHR Biomedical
   Research Centre (IS-BRC-1215-200074). No specific funding was associated
   with this study.
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NR 34
TC 17
Z9 17
U1 0
U2 0
PU SPRINGERNATURE
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON, N1 9XW, ENGLAND
SN 1018-4813
EI 1476-5438
J9 EUR J HUM GENET
JI Eur. J. Hum. Genet.
PD APR
PY 2022
VL 30
IS 4
BP 413
EP 419
DI 10.1038/s41431-021-01011-8
EA DEC 2021
PG 7
WC Biochemistry & Molecular Biology; Genetics & Heredity
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Genetics & Heredity
GA 0I4BY
UT WOS:000726522100001
PM 34866136
OA Green Published, hybrid
DA 2025-01-04
ER

PT J
AU Bignell, M
   Carr, NJ
   Mohamed, F
AF Bignell, Mark
   Carr, Norman J.
   Mohamed, Faheez
TI Pathophysiology and classification of pseudomyxoma peritonei
SO PLEURA AND PERITONEUM
LA English
DT Review
DE appendiceal mucinous neoplasm; cytoreductive surgery; HIPEC; oncogenes;
   pseudomyxoma peritonei (PMP); tumour markers
ID HYPERTHERMIC INTRAPERITONEAL CHEMOTHERAPY; METASTATIC COLORECTAL-CANCER;
   COMPLETE TUMOR REMOVAL; CLINICOPATHOLOGICAL ANALYSIS; MUCINOUS
   CARCINOMATOSIS; COMPLETE CYTOREDUCTION; P53 OVEREXPRESSION; APPENDICEAL
   ORIGIN; EPITHELIAL NEOPLASMS; 1ST-LINE TREATMENT
AB Background: The term pseudomyxoma peritonei (PMP) was first described in 1884 and there has been much debate since then over the term. A recent consensus of world experts agreed that PMP should be thought of as a clinical entity characterised by the presence of mucinous ascites, omental cake, peritoneal implants and possibly ovarian involvement. It generally originates from mucinous appendiceal tumours.
   Content: This review details the clinical presentation of this unusual condition, presents the new classification system and how this relates to outcome. The pathophysiology of this disease is also explored with a special reference to the relationship of the disease to tumour markers.
   Summary: A classification system has been agreed upon by the leading experts in PMP which is now divided into low and high grade mucinous carcinomatosis peritonei. This distinction correlates with clinical outcome as does the presence of raised tumour markers preoperatively.
   Outlook: Research needs to be focused on understanding the factors associated with poor prognosis through well designed multi-centred prospective studies. This will allow us to identify patients with bad tumour biology so that targeted treatment based on likely prognosis may then become a reality.
C1 [Bignell, Mark; Carr, Norman J.; Mohamed, Faheez] Peritoneal Malignancy Inst, Basingstoke, Hants, England.
   [Mohamed, Faheez] North Hamsphire Hosp, Aldermaston Rd, Basingstoke RG24 9NA, Hants, England.
   [Carr, Norman J.] Univ Southampton, Cellular Pathol, Southampton, Hants, England.
C3 University of Southampton
RP Mohamed, F (corresponding author), Peritoneal Malignancy Inst, Basingstoke, Hants, England.; Mohamed, F (corresponding author), North Hamsphire Hosp, Aldermaston Rd, Basingstoke RG24 9NA, Hants, England.
EM faheez.mohamed@hhft.nhs.uk
RI Carr, Nicholas/ABD-2360-2021
OI Carr, Norman/0000-0002-5087-6874
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NR 61
TC 13
Z9 14
U1 0
U2 2
PU DE GRUYTER OPEN LTD
PI WARSAW
PA BOGUMILA ZUGA 32A ST, 01-811 WARSAW, POLAND
SN 2364-7671
EI 2364-768X
J9 PLEURA PERITONEUM
JI Pleura Peritoneum
PD MAR
PY 2016
VL 1
IS 1
BP 3
EP 13
DI 10.1515/pap-2016-0008
PG 11
WC Oncology; Surgery
WE Emerging Sources Citation Index (ESCI)
SC Oncology; Surgery
GA FF4BX
UT WOS:000408874200002
PM 30911604
DA 2025-01-04
ER

PT J
AU Xue, DD
   Zheng, Y
   Wen, JY
   Han, JZ
   Tuo, HF
   Liu, YF
   Peng, YH
AF Xue, Dongdong
   Zheng, Ya
   Wen, Junye
   Han, Jingzhao
   Tuo, Hongfang
   Liu, Yifan
   Peng, Yanhui
TI Role of chemokines in hepatocellular carcinoma
SO ONCOLOGY REPORTS
LA English
DT Review
DE hepatocellular carcinoma; metastasis; chemokine; exosomes; targeted
   treatment
ID MESENCHYMAL STEM-CELLS; SUPPRESSES LIVER METASTASIS; EXTRACELLULAR
   VESICLES; POOR-PROGNOSIS; UP-REGULATION; CANCER-CELLS; NEUTROPHIL
   INFILTRATION; TUMOR MICROENVIRONMENT; RECEPTOR EXPRESSION;
   COLORECTAL-CANCER
AB Hepatocellular carcinoma (HCC) is a prevalent malignant tumor worldwide, with an unsatisfactory prognosis, although treatments are improving. One of the main challenges for the treatment of HCC is the prevention or management of recurrence and metastasis of HCC. It has been found that chemokines and their receptors serve a pivotal role in HCC progression. In the present review, the literature on the multifactorial roles of exosomes in HCC from PubMed, Cochrane library and Embase were obtained, with a specific focus on the functions and mechanisms of chemokines in HCC. To date, >50 chemokines have been found, which can be divided into four families: CXC, CX3C, CC and XC, according to the different positions of the conserved N-terminal cysteine residues. Chemokines are involved in the inflammatory response, tumor immune response, proliferation, invasion and metastasis via modulation of various signaling pathways. Thus, chemokines and their receptors directly or indirectly shape the tumor cell microenvironment, and regulate the biological behavior of the tumor. In addition, the potential application of chemokines in chemotaxis of exosomes as drug vehicles is discussed. Exosomes containing chemokines or expressing receptors for chemokines may improve chemotaxis to HCC and may thus be exploited for targeted drug delivery.
C1 [Xue, Dongdong; Wen, Junye; Han, Jingzhao; Tuo, Hongfang; Liu, Yifan; Peng, Yanhui] Hebei Gen Hosp, Dept Hepatobiliary Surg, 348 West He Ping Rd, Shijiazhuang 050051, Hebei, Peoples R China.
   [Zheng, Ya] Tongji Univ, Med Ctr Lab, Sch Med, Tongji Hosp, Shanghai 200065, Peoples R China.
C3 Tongji University
RP Peng, YH (corresponding author), Hebei Gen Hosp, Dept Hepatobiliary Surg, 348 West He Ping Rd, Shijiazhuang 050051, Hebei, Peoples R China.
EM yhpeng@hebmu.edu.cn
FU Hebei Provincial Government Clinical Medicine Talents Training and Basic
   Research Project [361003]
FX The present review was supported by the Hebei Provincial Government
   Clinical Medicine Talents Training and Basic Research Project (grant no.
   361003).
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NR 161
TC 31
Z9 32
U1 3
U2 27
PU SPANDIDOS PUBL LTD
PI ATHENS
PA POB 18179, ATHENS, 116 10, GREECE
SN 1021-335X
EI 1791-2431
J9 ONCOL REP
JI Oncol. Rep.
PD MAR
PY 2021
VL 45
IS 3
BP 809
EP 823
DI 10.3892/or.2020.7906
PG 15
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA QC5AL
UT WOS:000614844300001
PM 33650640
OA hybrid, Green Published
DA 2025-01-04
ER

PT J
AU Leth, JM
   Newcombe, EA
   Gronnemose, AL
   Jorgensen, JT
   Qvist, K
   Clausen, AS
   Knudsen, LBS
   Kjaer, A
   Kragelund, BB
   Jorgensen, TJD
   Ploug, M
AF Leth, Julie Maja
   Newcombe, Estella Anne
   Gronnemose, Anne Louise
   Jorgensen, Jesper Tranekjaer
   Qvist, Katrine
   Clausen, Anne Skovsbo
   Knudsen, Line Bruhn Schneider
   Kjaer, Andreas
   Kragelund, Birthe Brandt
   Jorgensen, Thomas Jorgen Dyreborg
   Ploug, Michael
TI Targeted imaging of uPAR expression in vivo with cyclic AE105 variants
SO SCIENTIFIC REPORTS
LA English
DT Article
ID PLASMINOGEN-ACTIVATOR RECEPTOR; HELIX DIPOLE MODEL; UROKINASE RECEPTOR;
   RADIONUCLIDE THERAPY; COLORECTAL-CANCER; NMR-SPECTROSCOPY;
   CELL-ADHESION; BINDING-SITE; PEPTIDE; PET
AB A comprehensive literature reports on the correlation between elevated levels of urokinase-type plasminogen activator receptor (uPAR) and the severity of diseases with chronic inflammation including solid cancers. Molecular imaging is widely used as a non-invasive method to locate disease dissemination via full body scans and to stratify patients for targeted treatment. To date, the only imaging probe targeting uPAR that has reached clinical phase-II testing relies on a high-affinity 9-mer peptide (AE105), and several studies by positron emission tomography (PET) scanning or near-infra red (NIR) fluorescence imaging have validated its utility and specificity in vivo. While our previous studies focused on applying various reporter groups, the current study aims to improve uPAR-targeting properties of AE105. We successfully stabilized the small uPAR-targeting core of AE105 by constraining its conformational landscape by disulfide-mediated cyclization. Importantly, this modification mitigated the penalty on uPAR-affinity typically observed after conjugation to macrocyclic chelators. Cyclization did not impair tumor targeting efficiency of AE105 in vivo as assessed by PET imaging and a trend towards increased tracer uptake was observed. In future studies, we predict that this knowledge will aid development of new fluorescent AE105 derivatives with a view to optical imaging of uPAR to assist precision guided cancer surgery.
C1 [Leth, Julie Maja; Gronnemose, Anne Louise; Ploug, Michael] Copenhagen Univ Hosp, Rigshosp, Finsen Lab, DK-2200 Copenhagen N, Denmark.
   [Leth, Julie Maja; Gronnemose, Anne Louise; Ploug, Michael] Univ Copenhagen, Biotech Res & Innovat Ctr BRIC, DK-2200 Copenhagen N, Denmark.
   [Newcombe, Estella Anne; Kragelund, Birthe Brandt] Struct Biol & NMR Lab, Copenhagen N, Denmark.
   [Newcombe, Estella Anne; Kragelund, Birthe Brandt] REPIN, Copenhagen N, Denmark.
   [Newcombe, Estella Anne; Kragelund, Birthe Brandt] Univ Copenhagen, Dept Biol, Linderstrom Lang Ctr Prot Sci, Ole Maaloes Vej 5, DK-2200 Copenhagen N, Denmark.
   [Gronnemose, Anne Louise; Jorgensen, Thomas Jorgen Dyreborg] Univ Southern Denmark, Dept Biochem & Mol Biol, DK-5230 Odense M, Denmark.
   [Jorgensen, Jesper Tranekjaer; Qvist, Katrine; Clausen, Anne Skovsbo; Knudsen, Line Bruhn Schneider; Kjaer, Andreas] Copenhagen Univ Hosp, Rigshosp, Dept Clin Physiol & Nucl Med, Copenhagen N, Denmark.
   [Jorgensen, Jesper Tranekjaer; Qvist, Katrine; Clausen, Anne Skovsbo; Knudsen, Line Bruhn Schneider; Kjaer, Andreas] Copenhagen Univ Hosp, Rigshosp, Cluster Mol Imaging, Copenhagen N, Denmark.
   [Jorgensen, Jesper Tranekjaer; Qvist, Katrine; Clausen, Anne Skovsbo; Knudsen, Line Bruhn Schneider; Kjaer, Andreas] Univ Copenhagen, Dept Biomed Sci, Copenhagen N, Denmark.
C3 Rigshospitalet; University of Copenhagen; University of Copenhagen;
   University of Copenhagen; University of Southern Denmark; University of
   Copenhagen; Rigshospitalet; University of Copenhagen; Rigshospitalet;
   University of Copenhagen
RP Ploug, M (corresponding author), Copenhagen Univ Hosp, Rigshosp, Finsen Lab, DK-2200 Copenhagen N, Denmark.; Ploug, M (corresponding author), Univ Copenhagen, Biotech Res & Innovat Ctr BRIC, DK-2200 Copenhagen N, Denmark.
EM m-ploug@finsenlab.dk
RI Newcombe, Estella/R-4817-2017; Jørgensen, Thomas/JHU-4703-2023;
   Jørgensen, Jesper/AAY-3085-2020; Kragelund, Birthe/M-3927-2014; Kjaer,
   Andreas/E-8932-2015
OI Kjaer, Andreas/0000-0002-2706-5547; Newcombe,
   Estella/0000-0001-6132-6168; Gronnemose, Anne
   Louise/0000-0003-4583-8010; Ploug, Michael/0000-0003-2215-4265;
   Jorgensen, Thomas J.D./0000-0002-7149-316X
FU Novo Nordisk foundation [NNF18OC0033926, NNF18OC0032996]; European Union
   [670261, 668532]; Lundbeck Foundation; Innovation Fund Denmark; Danish
   Cancer Society; Neye Foundation; Research Foundation of Rigshospitalet;
   Danish National Research Foundation [(126)-PERSIMUNE]; Research Council
   of the Capital Region of Denmark; Danish Health Authority; John and
   Birthe Meyer Foundation; Research Council for Independent Research;
   Sygeforsikringen Danmark
FX We thank Gry E. Rasmussen and Eva C. Osterlund for technical assistance.
   This work was supported by grants from the Novo Nordisk foundation
   (NNF18OC0033926 to B.B.K.). NMR spectra were recorded at cOpenNMR, an
   infrastructure facility funded by the Novo Nordisk Foundation
   (NNF18OC0032996), the European Union's Horizon 2020 research and
   innovation programme under grant agreements no. 670261 (ERC Advanced
   Grant) and 668532 (Click-It), the Lundbeck Foundation, the Innovation
   Fund Denmark, the Danish Cancer Society, the Neye Foundation, the
   Sygeforsikringen Danmark, the Research Foundation of Rigshospitalet, the
   Danish National Research Foundation (grant 126)-PERSIMUNE, the Research
   Council of the Capital Region of Denmark, the Danish Health Authority,
   the John and Birthe Meyer Foundation, and Research Council for
   Independent Research. Andreas Kjaer is a Lundbeck Foundation Professor.
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NR 83
TC 0
Z9 0
U1 6
U2 12
PU NATURE PORTFOLIO
PI BERLIN
PA HEIDELBERGER PLATZ 3, BERLIN, 14197, GERMANY
SN 2045-2322
J9 SCI REP-UK
JI Sci Rep
PD OCT 11
PY 2023
VL 13
IS 1
AR 17248
DI 10.1038/s41598-023-43934-w
PG 17
WC Multidisciplinary Sciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Science & Technology - Other Topics
GA AD7J4
UT WOS:001116585900026
PM 37821532
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Babincák, M
   Jendzelovsky, R
   Kosuth, J
   Majerník, M
   Vargová, J
   Mikulásek, K
   Zdráhal, Z
   Fedorocko, P
AF Babincak, Marian
   Jendzelovsky, Rastislav
   Kosuth, Jan
   Majernik, Martin
   Vargova, Jana
   Mikulasek, Kamil
   Zdrahal, Zbynek
   Fedorocko, Peter
TI Death Receptor 5 (TNFRSF10B) Is Upregulated and TRAIL Resistance Is
   Reversed in Hypoxia and Normoxia in Colorectal Cancer Cell Lines after
   Treatment with Skyrin, the Active Metabolite of <i>Hypericum</i> spp.
SO CANCERS
LA English
DT Article
DE skyrin; hypoxia; colorectal cancer; proteomics; Death receptor 5; TRAIL;
   TRAIL resistance; Hypericum
ID LIGAND-INDUCED APOPTOSIS; PHOTODYNAMIC THERAPY; DOWN-REGULATION;
   SECONDARY METABOLITES; MEDIATED APOPTOSIS; P-GLYCOPROTEIN; CYTOSKYRIN-A;
   TUMOR; PROTEIN; DR5
AB Simple Summary
   Hypoxic conditions are common in solid tumors and are very often connected with the poor prognosis of cancer patients. The lack of oxygen often causes the failure of therapy due to multiple mechanisms increasing cancer survival. Skyrin (SKR) is a secondary plant metabolite from the genus Hypericum spp., with a potential anticancer effects but still unknown mechanism of action. Based on our comprehensive analysis of SKR action, SKR shows significant efficiency against cancer, but not healthy cells, induces apoptosis, and upregulates Death receptor 5 in cancer cells in normoxic, as well as hypoxic conditions. SKR reverses TRAIL resistance even in TRAIL-resistant cancer cell lines in hypoxia. To sum up, SKR can be possibly used as a natural antitumor drug per se or as an adjuvant to TRAIL treatment in hypoxic and therapy-resistant tumors.
   Skyrin (SKR) is a plant bisanthraquinone secondary metabolite from the Hypericum genus with potential use in anticancer therapy. However, its effect and mechanism of action are still unknown. The negative effect of SKR on HCT 116 and HT-29 cancer cell lines in hypoxic and normoxic conditions was observed. HCT 116 cells were more responsive to SKR treatment as demonstrated by decreased metabolic activity, cellularity and accumulation of cells in the G1 phase. Moreover, an increasing number of apoptotic cells was observed after treatment with SKR. Based on the LC-MS comparative proteomic data from hypoxia and normoxia (data are available via ProteomeXchange with the identifier PXD019995), SKR significantly upregulated Death receptor 5 (DR5), which was confirmed by real-time qualitative PCR (RT-qPCR). Furthermore, multiple changes in the Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-activated cascade were observed. Moreover, the reversion of TRAIL resistance was observed in HCT 116, HT-29 and SW620 cell lines, even in hypoxia, which was linked to the upregulation of DR5. In conclusion, our results propose the use of SKR as a prospective anticancer drug, particularly as an adjuvant to TRAIL-targeting treatment to reverse TRAIL resistance in hypoxia.
C1 [Babincak, Marian; Jendzelovsky, Rastislav; Kosuth, Jan; Majernik, Martin; Vargova, Jana; Fedorocko, Peter] Pavol Jozef Safarik Univ Kosice, Fac Sci, Inst Biol & Ecol, Srobarova 2, Kosice 04154, Slovakia.
   [Mikulasek, Kamil; Zdrahal, Zbynek] Masaryk Univ, Cent European Inst Technol, Kamenice 5, Brno 62500, Czech Republic.
   [Mikulasek, Kamil; Zdrahal, Zbynek] Masaryk Univ, Fac Sci, Natl Ctr Biomol Res, Kamenice 5, Brno 62500, Czech Republic.
C3 University of Pavol Jozef Safarik Kosice; Masaryk University Brno;
   Masaryk University Brno
RP Fedorocko, P (corresponding author), Pavol Jozef Safarik Univ Kosice, Fac Sci, Inst Biol & Ecol, Srobarova 2, Kosice 04154, Slovakia.
EM marian.babincak@upjs.sk; rastislav.jendzelovsky@upjs.sk;
   jan.kosuth@upjs.sk; martin.majernik@upjs.sk; jana.vargova@upjs.sk;
   357352@mail.muni.cz; zdrahal@sci.muni.cz; peter.fedorocko@upjs.sk
RI Babincak, Marian/AAB-4264-2019; Majerník, Martin/AAQ-9799-2020;
   Jendželovský, Rastislav/R-5992-2016; Zdrahal, Zbynek/D-9491-2012;
   Vargova, Jana/S-2863-2016; Kosuth, Jan/R-5972-2016; Fedorocko,
   Peter/R-2433-2016
OI Vargova, Jana/0000-0002-4066-3453; Jendzelovsky,
   Rastislav/0000-0001-6338-0723; Kosuth, Jan/0000-0001-5584-8728;
   Fedorocko, Peter/0000-0002-1138-6282; Majernik,
   Martin/0000-0002-0479-7059; Zdrahal, Zbynek/0000-0003-3044-5548;
   Babincak, Marian/0000-0002-2540-5608
FU Slovak Research and Development Agency [APVV-18-0125]; Scientific Grant
   Agency of the Ministry of Education of the Slovak Republic [VEGA
   1/0022/19]; Medical University Science Park in Kosice (MediPark, Kosice)
   [ITMS 26220220185]; MediPark, Kosice-Phase II - Operational Program
   Research and Development Program - ERDF [ITMS2014+: 313011D103]; MEYS CR
   [LM2018127, LM2015043]; project "e-Infrastruktura CZ" within the program
   Projects of Large Research, Development and Innovations Infrastructures
   [e-INFRA LM2018140]; projects CEITEC 2020 [LQ1601]
FX This research was supported by the Slovak Research and Development
   Agency (APVV-18-0125), the Scientific Grant Agency of the Ministry of
   Education of the Slovak Republic (VEGA 1/0022/19), the Medical
   University Science Park in Kosice (MediPark, Kosice, ITMS 26220220185)
   and MediPark, Kosice-Phase II (ITMS2014+: 313011D103) supported by the
   Operational Program Research and Development Program, funded by the
   ERDF. Measurements at Proteomics Core Facility CEITEC MU Brno, Czech
   Republic were supported by the projects CEITEC 2020 (LQ1601) and CIISB
   research infrastructure project LM2018127 and LM2015043 funded by MEYS
   CR. Computational resources were supplied by the project
   "e-Infrastruktura CZ" (e-INFRA LM2018140) provided within the program
   Projects of Large Research, Development and Innovations Infrastructures.
   The APC was funded by the Slovak Research and Development Agency
   (APVV-18-0125).
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NR 108
TC 5
Z9 5
U1 1
U2 17
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2072-6694
J9 CANCERS
JI Cancers
PD APR
PY 2021
VL 13
IS 7
AR 1646
DI 10.3390/cancers13071646
PG 30
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA RK5FB
UT WOS:000638320900001
PM 33916015
OA Green Published, gold
DA 2025-01-04
ER

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   Bensi, M.
   Rossini, D.
   Passardi, A.
   Tamberi, S.
   Giampieri, R.
   Antonuzzo, L.
   Noto, L.
   Roviello, G.
   Zichi, C.
   Salati, M.
   Puccini, A.
   Noto, C.
   Parisi, A.
   Rihawi, K.
   Persano, M.
   Crespi, V
   Libertini, M.
   Giordano, M.
   Moretto, R.
   Lonardi, S.
   Cremolini, C.
TI Encorafenib plus cetuximab with or without binimetinib in patients with
   BRAF V600E-mutated metastatic colorectal cancer: real-life data from an
   Italian multicenter experience
SO ESMO OPEN
LA English
DT Article
DE BRAF V600E mutation; BEACON trial; real-life studies; encorafenib;
   binimetinib; adjusted MAF
AB Background: Encorafenib plus cetuximab with or without binimetinib showed increased objective response rate (ORR), progression-free survival (PFS), and overall survival (OS) compared with chemotherapy plus anti-EGFR in previously treated patients with BRAF V600E-mutated (mut) metastatic colorectal cancer (mCRC). Although no formal comparison was planned, addition of binimetinib to encorafenib plus cetuximab did not provide significant efficacy advantage.
   Patients and methods: This real-life study was aimed at evaluating safety, activity, and efficacy of encorafenib plus cetuximab with or without binimetinib in patients with BRAF V600E-mut mCRC treated at 21 Italian centers within a nominal use program launched in May 2019.
   Results: Out of 133 patients included, 97 (73%) received encorafenib plus cetuximab (targeted doublet) and 36 (27%) the same therapy plus binimetinib (targeted triplet). Most patients had Eastern Cooperative Group Performance Status (ECOG-PS) of 0 or 1 (86%), right-sided primary tumor (69%), and synchronous disease (66%). Twenty (15%) tumors were DNA mismatch repair deficiency (dMMR)/microsatellite instability (MSI)-high. As many as 44 (34%) patients had received two or more prior lines of therapy, 122 (92%) were previously exposed to oxaliplatin, and 109 (82%) to anti-vascular endothelial growth factor (anti-VEGF). Most frequent adverse events were asthenia (62%) and anti- EGFR-related skin rash (52%). Any grade nausea (P = 0.03), vomiting (P = 0.04), and diarrhea (P = 0.07) were more frequent with the triplet therapy, while melanocytic nevi were less common (P = 0.06). Overall, ORR and disease control rate (DCR) were 23% and 69%, respectively, with numerically higher rates in the triplet group (ORR 31% versus 17%, P = 0.12; DCR 78% versus 65%, P = 0.23). Median PFS and OS were 4.5 and 7.2 months, respectively. Worse ECOG-PS, peritoneal metastases, and more than one prior treatment were independent poor prognostic factors for PFS and OS. Clonality of BRAF mutation measured as adjusted mutant allele fraction in tumor tissue was not associated with clinical outcome.
   Conclusions: Our real-life data are consistent with those from the BEACON trial in terms of safety, activity, and efficacy. Patients in good general condition and not heavily pretreated are those more likely to derive benefit from the targeted treatment.
C1 [Boccaccino, A.; Borelli, B.; Rossini, D.; Giordano, M.; Cremolini, C.] Azienda Osped Univ Pisana, Dept Translat Res & New Technol Med & Surg, Unit Med Oncol 2, Pisa, Italy.
   [Intini, R.] Veneto Inst Oncol IOV IRCCS, Dept Oncol, Med Oncol Unit 1, Padua, Italy.
   [Antista, M.] Fdn IRCCS Ist Nazl Tumori, ENETS Ctr Excellence, Med Oncol Dept, Milan, Italy.
   [Bensi, M.] Fdn Policlin Univ Agostino Gemelli IRCCS, Comprehens Canc Ctr, Oncol Med, Rome, Italy.
   [Bensi, M.] Univ Cattolica Sacro Cuore, Rome, Italy.
   [Passardi, A.] IRCCS Ist Romagnolo Studio Tumori IRST Dino Amado, Dept Med Oncol, Meldola, Italy.
   [Tamberi, S.] AUSL Romagna, UOC Oncol Ravenna, Ravenna, Italy.
   [Giampieri, R.] Univ Politecn Marche, Dipartimento Sci Clin & Mol, Clin Oncol, Ancona, Italy.
   [Antonuzzo, L.] Careggi Univ Hosp, Clin Oncol Unit, Florence, Italy.
   [Antonuzzo, L.] Univ Florence, Dept Expt & Clin Med, Florence, Italy.
   [Noto, L.] Policlin G Rodolico, UOC Oncol Med, Catania, Italy.
   [Noto, L.] AOU Policlin San Marco, Catania, Italy.
   [Roviello, G.] Univ Florence, Dept Hlth Sci, Florence, Italy.
   [Zichi, C.] AO Ordine Mauriziano Umberto I, Oncol Med, Turin, Italy.
   [Salati, M.] Univ Hosp Modena, Dept Oncol & Hematol, Div Oncol, Modena, Italy.
   [Salati, M.] Univ Modena & Reggio Emilia, PhD Program Clin & Expt Med, Modena, Italy.
   [Puccini, A.] Univ Genoa, Osped Policlin San Martino IRCCS, Genoa, Italy.
   [Noto, C.] Univ Udine, Dipartimento Area Med, Udine, Italy.
   [Noto, C.] Azienda Sanitaria Univ Friuli Cent, Dipartimento Oncol Med, Udine, Italy.
   [Parisi, A.] St Salvatore Hosp, Med Oncol, Laquila, Italy.
   [Parisi, A.] Univ Aquila, Dept Life Hlth & Environm Sci, Laquila, Italy.
   [Rihawi, K.] IRCSS Azienda Osped Univ Bologna, Bologna, Italy.
   [Persano, M.] Univ Cagliari, Med Oncol, Cagliari, Italy.
   [Crespi, V] Univ Turin, Dept Oncol, Turin, Italy.
   [Libertini, M.] Poliambulanza Fdn, Oncol Unit, Brescia, Italy.
   [Moretto, R.] Azienda Osped Univ Pisana, Unit Med Oncol 2, Pisa, Italy.
   [Lonardi, S.] Veneto Inst Oncol IOV IRCCS, Med Oncol 3, Via Gattamelata 64, I-35128 Padua, Italy.
C3 University of Pisa; Azienda Ospedaliero Universitaria Pisana; IRCCS
   Istituto Oncologico Veneto (IOV); Fondazione IRCCS Istituto Nazionale
   Tumori Milan; Catholic University of the Sacred Heart; IRCCS Policlinico
   Gemelli; Catholic University of the Sacred Heart; IRCCS Policlinico
   Gemelli; AUSL della Romagna; Marche Polytechnic University; University
   of Florence; Azienda Ospedaliero Universitaria Careggi; University of
   Florence; University of Florence; Mauritian Umberto I Hospital; A.O.U.
   Citta della Salute e della Scienza di Torino; AOU San Giovanni
   Battista-Molinette; Universita di Modena e Reggio Emilia; Universita di
   Modena e Reggio Emilia Hospital; Universita di Modena e Reggio Emilia;
   University of Genoa; University of Udine; University of L'Aquila;
   University of Cagliari; University of Turin; University of Pisa; Azienda
   Ospedaliero Universitaria Pisana; IRCCS Istituto Oncologico Veneto (IOV)
RP Lonardi, S (corresponding author), Veneto Inst Oncol IOV IRCCS, Med Oncol 3, Via Gattamelata 64, I-35128 Padua, Italy.
EM sara.lonardi@iov.veneto.it
RI Salati, Massimiliano/LRH-1437-2024; Parisi, Alessandro/AAB-9728-2019;
   Puccini, Alberto/F-3255-2018; Rossini, Daniele/GPW-8241-2022; Passardi,
   Alessandro/AAH-4786-2019; Cremolini, Chiara/AAC-1889-2019; Antista,
   Maria/AAC-2415-2020; Roviello, Giandomenico/AAA-5310-2019; Intini,
   Rossana/F-9492-2018; Bensi, Maria/AAC-5711-2022; Lonardi,
   Sara/F-4228-2014
OI Bensi, Maria/0000-0002-5647-0525; Antonuzzo,
   Lorenzo/0000-0003-3349-5604; Lonardi, Sara/0000-0002-7593-8138; Rossini,
   Daniele/0009-0000-3777-8471; Puccini, Alberto/0000-0002-2492-4043;
   Roviello, Giandomenico/0000-0001-5504-8237
FU Italian Ministry of Health [GR-2019-12368903]
FX Partially funded by the Italian Ministry of Health grant "Ricerca
   Finalizzata Giovani Ricercatori" [grant number GR-2019-12368903].
CR André T, 2020, NEW ENGL J MED, V383, P2207, DOI 10.1056/NEJMoa2017699
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NR 22
TC 17
Z9 18
U1 1
U2 1
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
EI 2059-7029
J9 ESMO OPEN
JI ESMO Open
PD JUN
PY 2022
VL 7
IS 3
DI 10.1016/j.esmoop.2022.100506
PG 8
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 6I7BR
UT WOS:000886288700003
PM 35696748
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Adams, R
   Brown, E
   Brown, L
   Butler, R
   Falk, S
   Fisher, D
   Kaplan, R
   Quirke, P
   Richman, S
   Samuel, L
   Seligmann, J
   Seymour, M
   Shiu, KK
   Wasan, H
   Wilson, R
   Maughan, T
AF Adams, Richard
   Brown, Ewan
   Brown, Louise
   Butler, Rachel
   Falk, Stephen
   Fisher, David
   Kaplan, Richard
   Quirke, Phil
   Richman, Susan
   Samuel, Leslie
   Seligmann, Jenny
   Seymour, Matt
   Shiu, Kai Keen
   Wasan, Harpreet
   Wilson, Richard
   Maughan, Tim
CA FOCUS4 Trial Investigators
TI Inhibition of EGFR, HER2, and HER3 signalling in patients with
   colorectal cancer wild-type for <i>BRAF</i>, <i>PIK3CA</i>, <i>KRAS</i>,
   and <i>NRAS</i> (FOCUS4-D): a phase 2-3 randomised trial
SO LANCET GASTROENTEROLOGY & HEPATOLOGY
LA English
DT Article
ID COMBINATION CHEMOTHERAPY; 1ST-LINE TREATMENT; CETUXIMAB; OXALIPLATIN;
   SURVIVAL; THERAPY; INTERMITTENT; EXPRESSION; MUTATION; AZD8931
AB Background A substantial change in trial methodology for solid tumours has taken place, in response to increased understanding of cancer biology. FOCUS4 is a phase 2-3 trial programme testing targeted agents in patients with advanced colorectal cancer in molecularly stratified cohorts. Here, we aimed to test the hypothesis that combined inhibition of EGFR, HER2, and HER3 signalling with the tyrosine kinase inhibitor AZD8931 will control growth of all wild-type tumours.
   Methods In FOCUS4-D, we included patients from 18 hospitals in the UK with newly diagnosed advanced or metastatic colorectal cancer whose tumour was wild-type for BRAF, PIK3CA, KRAS, and NRAS. After 16 weeks of first-line therapy, patients with stable or responding tumours were randomised to oral AZD8931 (40 mg twice a day) or placebo. Randomisation was done by minimisation with a random element of 20%, minimisation by hospital site, site of primary tumour, WHO performance status, 16-week CT scan result, number of metastatic sites, and first-line chemotherapy regimen. The primary outcome was progression-free-survival. CT scans were assessed by local radiologists according to Response Evaluation Criteria in Solid Tumors (RECIST), version 1.1. Preplanned interim analyses were assessed per protocol and were agreed using multiarm multistage (MAMS) trial design methodology triggered by occurrence of progression-free survival events in the placebo group. The final analysis was assessed by intention to treat. This trial is registered at controlled-trials. com, ISRCTN 90061546.
   Findings Between July 7, 2014, and March 7, 2016, 32 patients were randomised to study treatment, 16 to AZD8931 and 16 to placebo. At the first preplanned interim analysis (March, 2016), the independent data monitoring committee (IDMC) recommended closure of FOCUS4-D because of a lack of activity. At the final analysis (Aug 1, 2016), 31 patients had had a progression-free survival event (15 with AZD8931 and 16 with placebo). Median progression-free survival was 3.48 months (95% CI 1.51-5.09) in the placebo group and 2.96 months (1.94-5.62) in the AZD8931 group. No progression-free survival benefit of AZD8931 compared with placebo was noted (hazard ratio [HR] 1.10, 95% CI 0.47-3.57; p=0.95). The most common grade 3 adverse event in the AZD8931 group was skin rash (three [20%] of 15 patients with available data vs none of 16 patients in the placebo group), and in the placebo group it was diarrhoea (one [7%] vs one [6%]). No grade 4 adverse events were recorded and no treatment-related deaths were reported.
   Interpretation The MAMS trial design for FOCUS4 has shown efficiency and effectiveness in trial outcome delivery, informing the decision to proceed or stop clinical evaluation of a targeted treatment within a molecularly defined cohort of patients. The overarching FOCUS4 trial is now aiming to open a replacement arm in the cohort with all wild-type tumours. Copyright (C) The Author(s). Published by Elsevier Ltd.
C1 [Adams, Richard] Cardiff Univ, Cardiff, S Glam, Wales.
   [Adams, Richard] Velindre Canc Ctr, Cardiff, S Glam, Wales.
   [Brown, Ewan] Edinburgh Canc Ctr NHS Lothian, Edinburgh, Midlothian, Scotland.
   [Brown, Louise; Fisher, David; Kaplan, Richard] UCL, MRC, Clin Trials Unit, London, England.
   [Butler, Rachel] Univ Wales Hosp, All Wales Genet Lab, Cardiff, S Glam, Wales.
   [Falk, Stephen] Univ Hosp Bristol NHS Fdn Trust, Bristol, Avon, England.
   [Quirke, Phil; Richman, Susan; Seligmann, Jenny; Seymour, Matt] Univ Leeds, Leeds Inst Canc & Pathol, Leeds, W Yorkshire, England.
   [Samuel, Leslie] Aberdeen Royal Infirm, Aberdeen, Scotland.
   [Shiu, Kai Keen] UCL, London, England.
   [Wasan, Harpreet] Imperial Coll London, London, England.
   [Wilson, Richard] Queens Univ Belfast, Ctr Canc Res & Cell Biol, Belfast, Antrim, North Ireland.
   [Maughan, Tim] Univ Oxford, MRC Oxford Inst Radiat Oncol, Canc Res UK, Oxford, England.
C3 Cardiff University; Velindre Cancer Centre; Medical Research Council
   Clinical Trials Unit; University of London; University College London;
   Cardiff University; University of Bristol; University of Leeds;
   University of Aberdeen; University of London; University College London;
   Imperial College London; Queens University Belfast; University of
   Oxford; Cancer Research UK
RP Adams, R (corresponding author), Cardiff Univ, Ctr Trials Res, Velindre Canc Ctr, Cardiff CF14 2TL, S Glam, Wales.; Brown, L (corresponding author), UCL, MRC Clin Trials Unit, London WC1V 6LJ, England.
EM adamsra3@cf.ac.uk; l.brown@ucl.ac.uk
RI Seligmann, Jenny/AAC-2030-2022; Quirke, Philip/AAI-1362-2019; Fisher,
   David/KLC-7622-2024; Maughan, Tim/AAV-7636-2021
OI Seymour, Matthew/0000-0002-2441-9629; Wilson,
   Richard/0000-0001-8018-7730; Samuel, Leslie/0000-0002-8402-8670;
   Richman, Susan/0000-0003-3993-5041; Fisher, David/0000-0002-2512-2296;
   Brown, Louise/0000-0003-2827-6634; Wasan, Harpreet/0000-0002-6268-2030;
   Adams, Richard/0000-0003-3915-7243; Quirke, Philip/0000-0002-3597-5444;
   Kaplan, Richard S./0000-0002-0189-8348
FU Medical Research Council (MRC) Efficacy and Mechanism Evaluation
   programme; National Institute for Health Research (NIHR) Efficacy and
   Mechanism Evaluation programme; Cancer Research UK; NIHR Clinical Trials
   Research Network; Health and Care Research Wales; AstraZeneca; MRC
   [G0701770, MC_UU_12023/3, MC_EX_UU_G0800814, MC_EX_G0800814] Funding
   Source: UKRI
FX Medical Research Council (MRC) and National Institute for Health
   Research (NIHR) Efficacy and Mechanism Evaluation programme, Cancer
   Research UK, NIHR Clinical Trials Research Network, Health and Care
   Research Wales, and AstraZeneca.
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NR 25
TC 39
Z9 40
U1 0
U2 10
PU ELSEVIER INC
PI SAN DIEGO
PA 525 B STREET, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 2468-1253
J9 LANCET GASTROENTEROL
JI Lancet Gastroenterol. Hepatol.
PD MAR
PY 2018
VL 3
IS 3
BP 162
EP 171
DI 10.1016/S2468-1253(17)30394-1
PG 10
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA FY6UF
UT WOS:000426997700016
PM 29254887
OA Green Published, hybrid, Green Accepted
DA 2025-01-04
ER

PT J
AU Shrestha, S
   Shrestha, A
   Kim, J
   Thapa, RK
   Kim, JO
AF Shrestha, Smala
   Shrestha, Amit
   Kim, Jeonghwan
   Thapa, Raj Kumar
   Kim, Jong Oh
TI Recent advances in albumin nanoparticle-based cancer therapies
SO JOURNAL OF PHARMACEUTICAL INVESTIGATION
LA English
DT Review; Early Access
DE Albumin; Cancer; Drug delivery; Nanoparticles; Targeting
ID BOVINE SERUM-ALBUMIN; CELL LUNG-CANCER; DRUG-DELIVERY; TARGETED
   TREATMENT; NAB-PACLITAXEL; COLON-CANCER; HALF-LIFE; DOXORUBICIN;
   CHEMOTHERAPY; STRATEGY
AB BackgroundNanotechnology is increasingly utilized in treating complex and challenging diseases, notably cancer. Among the emerging strategies, albumin, a versatile biomaterial, demonstrates promising potential in forming nanoparticles with exceptional tumor-targeting capabilities and enhanced accumulation properties. Albumin nanoplatform presents a myriad of advantages including superior biocompatibility, biodegradability, and a favorable toxicological profile, culminating in improved anti-tumor efficacy.Area CoveredThis comprehensive review focuses on recent advancements of albumin nanoparticles for the treatment of various types of cancers, various techniques employed during their preparations, alongside the associated challenges and future avenues.Expert OpinionAlbumin nanoparticles emerge as both safe and efficacious nanoplatforms for diagnosing and treating diverse cancer types. Nonetheless, there exist challenges that necessitate attention. The utilization of various organic solvents in albumin nanoparticle synthesis poses potential safety hazards. Exploring alternative methodologies devoid of organic solvents holds promise for safer production in the future. Moreover, the structural alterations of human serum albumin (HSA) and its cellular transport pathways during reactions in the organic phase further complicate the development of HSA-based delivery systems. Additionally, the inherent structural characteristics of albumin couples with the presence of diverse enzymes and proteins within the body pose hurdles in maintaining its stability. Consequently, further investigations aimed at refining the preparation techniques of albumin nanoparticles are imperative to bolster their safety, stability, and therapeutic efficacy in cancer treatment.
C1 [Shrestha, Smala; Shrestha, Amit; Kim, Jeonghwan; Kim, Jong Oh] Yeungnam Univ, Coll Pharm, 280 Daehak Ro, Gyongsan 712749, South Korea.
   [Thapa, Raj Kumar] Gandaki Univ, Pharm Program, Pokhara 32, Pokhara, Nepal.
   [Thapa, Raj Kumar] Gandaki Univ, Res Ctr, Invent & Innovat Ctr, Pokhara, Nepal.
C3 Yeungnam University
RP Kim, JO (corresponding author), Yeungnam Univ, Coll Pharm, 280 Daehak Ro, Gyongsan 712749, South Korea.; Thapa, RK (corresponding author), Gandaki Univ, Pharm Program, Pokhara 32, Pokhara, Nepal.; Thapa, RK (corresponding author), Gandaki Univ, Res Ctr, Invent & Innovat Ctr, Pokhara, Nepal.
EM rkthapa@gandakiuniversity.edu.np; jongohkim@yu.ac.kr
RI Thapa, Raj/ABF-5467-2020
FU The 2024 Yeungnam University Research Grant
FX This work was supported by the 2024 Yeungnam University Research Grant.
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NR 101
TC 3
Z9 3
U1 33
U2 33
PU SPRINGERNATURE
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON, N1 9XW, ENGLAND
SN 2093-5552
EI 2093-6214
J9 J PHARM INVEST
JI J. Pharm. Investig.
PD 2024 JUL 5
PY 2024
DI 10.1007/s40005-024-00687-6
EA JUL 2024
PG 14
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA XP5H8
UT WOS:001262893900002
DA 2025-01-04
ER

PT J
AU Tan, DSP
   Tan, DSW
   Tan, IBH
   Yan, BE
   Choo, SP
   Chng, WJ
   Hwang, WYK
AF Tan, David Shao-Peng
   Tan, Daniel Shao-Weng
   Tan, Iain Bee Huat
   Yan, Benedict
   Choo, Su Pin
   Chng, Wee Joo
   Hwang, William Ying Khee
TI Recommendations to improve the clinical adoption of NGS-based cancer
   diagnostics in Singapore
SO ASIA-PACIFIC JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Review
DE cancer genetics; group 1; major specialty; molecular genetics; group 3;
   other specific research areas; tumor markers; group 3; other specific
   research areas
ID MODIFYING ANTIRHEUMATIC AGENTS; TUMOR MUTATIONAL BURDEN; MAINTENANCE
   THERAPY; PRECISION MEDICINE; OVARIAN-CARCINOMA; DOUBLE-BLIND;
   ASSOCIATION; ELIGIBILITY; RUCAPARIB; DECISION
AB Next-generation sequencing (NGS)-based diagnostics have demonstrated clinical utility in predicting improved survival benefits with targeted treatment in certain cancer types, and positive cost-benefit in several healthcare systems. However, clinical adoption in Singapore remains low despite commercial availability of these diagnostics. This expert opinion review examines the key challenges to the clinical adoption of NGS-based diagnostics in Singapore, provides recommendations on impactful initiatives to improve adoption, and also offers practical guidance on specific cancer types in which NGS-based diagnostics are appropriate for use in Singapore. Limited patient affordability is one major challenge to clinical adoption of NGS-based diagnostics, which could be improved by enabling patient access to more funds for specific cancer types with clear benefits. Expert opinion based on current evidence and clinical experience supports the upfront use of hotspot panels in advanced non-small cell lung cancer (NSCLC), metastatic colorectal cancer, advanced and recurrent ovarian cancer, and acute myeloid leukemia. Comprehensive genomic profiling could be considered for upfront use in select patients with NSCLC and ovarian cancer, or in refractory patients with the four cancer types. Wider adoption of NGS-based diagnostics will improve the delivery of cancer care in Singapore and Asia-Pacific, and thus lead to better patient outcomes.
C1 [Tan, David Shao-Peng; Chng, Wee Joo] Natl Univ Hlth Syst, Natl Univ Canc Inst Singapore, Dept Haematol Oncol, Singapore, Singapore.
   [Tan, David Shao-Peng; Chng, Wee Joo] Natl Univ Singapore, Yong Loo Lin Sch Med, Dept Med, Singapore, Singapore.
   [Tan, David Shao-Peng; Chng, Wee Joo] Natl Univ Singapore, Canc Sci Inst Singapore, Singapore, Singapore.
   [Tan, Daniel Shao-Weng; Tan, Iain Bee Huat; Hwang, William Ying Khee] Natl Canc Ctr Singapore, Dept Med Oncol, Singapore, Singapore.
   [Yan, Benedict] Natl Univ Hlth Syst, Mol Diag Ctr, Dept Lab Med, Singapore, Singapore.
   [Choo, Su Pin] Mt Elizabeth Novena Specialist Ctr, Curie Oncol, Singapore, Singapore.
   [Choo, Su Pin] Singapore Soc Oncol, Singapore, Singapore.
   [Hwang, William Ying Khee] Singapore Gen Hosp, Dept Haematol, Singapore, Singapore.
   [Hwang, William Ying Khee] Duke NUS Med Sch, Canc & Stem Cell Biol, Singapore, Singapore.
C3 National University of Singapore; National University of Singapore;
   National University of Singapore; National Cancer Centre Singapore
   (NCCS); National University of Singapore; Singapore General Hospital;
   National University of Singapore
RP Hwang, WYK (corresponding author), Natl Canc Ctr Singapore, Dept Med Oncol, Singapore, Singapore.
EM william.hwang.y.k@singhealth.com.sg
RI Hwang, William/AAT-3079-2021; CHOO, Su/ABB-3892-2020; Tan,
   David/HIR-2214-2022
OI Hwang, William Ying Khee/0000-0003-0143-6263; Tan,
   David/0000-0001-9087-5262
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NR 61
TC 10
Z9 10
U1 0
U2 5
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1743-7555
EI 1743-7563
J9 ASIA-PAC J CLIN ONCO
JI Asia-Pac. J. Clin. Oncol.
PD AUG
PY 2020
VL 16
IS 4
BP 222
EP 231
DI 10.1111/ajco.13339
PG 10
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA MM3JV
UT WOS:000550052000004
PM 32301274
OA Green Published, hybrid
DA 2025-01-04
ER

PT J
AU Pahwa, R
   Saini, S
   Chhabra, J
   Goyal, R
   Kumar, S
   Awasthi, R
   Dureja, H
AF Pahwa, Rakesh
   Saini, Swati
   Chhabra, Jatin
   Goyal, Rajat
   Kumar, Shobhit
   Awasthi, Rajendra
   Dureja, Harish
TI Harnessing nanotechnology for enhanced delivery of erlotinib: a dynamic
   duo in cancer treatment
SO BENI-SUEF UNIVERSITY JOURNAL OF BASIC AND APPLIED SCIENCES
LA English
DT Review
DE Nanotechnology; Erlotinib; Anticancer; EGFR; Drug delivery
ID GROWTH-FACTOR RECEPTOR; CELL LUNG-CANCER; TYROSINE KINASE INHIBITOR;
   PHASE-II TRIAL; LOADED PLGA NANOPARTICLES; SOLID LIPID NANOPARTICLES;
   IN-VITRO EVALUATION; CO-DELIVERY; THERAPEUTIC-EFFICACY; BREAST-CANCER
AB Erlotinib is a reversible epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor that acts by inhibiting signaling pathways, resulting in the disruption of cancerous cell proliferation. Erlotinib is a promising anticancer agent mainly utilized in the mitigation of non-small cell lung cancer cells (NSCLC) and pancreatic tumor. Apart from NSCLC and pancreatic tumor, erlotinib has also been employed in different malignancies, including metastatic colorectal cancer, malignant glioma, breast cancer, gastrointestinal cancers, etc. Despite erlotinib's distinctive qualities as a targeted drug, its applications are still limited by poor solubility, variable oral bioavailability, a high daily dose requirement, large protein binding, and primitive or acquired therapeutic resistance. Nanotechnology is a favorable approach to increase therapeutic effectiveness of erlotinib. It is one of the newest scientific field directed toward the diagnosis and targeted treatment of cancer. This technology aids in the distinction between normal and malignant cells, which overlays the strategy for targeted delivery. This manuscript discussed the advances of erlotinib nanoformulations in the management of different cancers. Moreover, the manuscript also comprises various research outcomes of erlotinib nanoformulations with other therapeutic agents as combinational therapy. Erlotinib can be delivered to a precise target in the body utilizing different polymers, lipids, and metals.
C1 [Pahwa, Rakesh; Saini, Swati; Chhabra, Jatin] Kurukshetra Univ, Inst Pharmaceut Sci, Kurukshetra 136119, Haryana, India.
   [Goyal, Rajat] Maharishi Markandeshwar Univ, MM Coll Pharm, Ambala 133207, Haryana, India.
   [Kumar, Shobhit] Meerut Inst Engn & Technol MIET, Dept Pharmaceut Technol, Meerut 250005, Uttar Pradesh, India.
   [Awasthi, Rajendra] UPES, Sch Hlth Sci & Technol, Dept Pharmaceut Sci, Dehra Dun 248007, Uttarakhad, India.
   [Dureja, Harish] Maharshi Dayanand Univ, Dept Pharmaceut Sci, Rohtak 124001, Haryana, India.
   [Dureja, Harish] Chitkara Univ, Chitkara Coll Pharm, Ctr Res Impact & Outcome, Chandigarh 140401, Punjab, India.
   [Dureja, Harish] Univ Technol Sydney, Australian Res Ctr Complementary & Integrat Med, Fac Hlth, Ultimo, Australia.
C3 Kurukshetra University; Maharishi Markandeshwar University; Meerut
   Institute of Engineering & Technology; University of Petroleum & Energy
   Studies (UPES); Maharshi Dayanand University; Chitkara University,
   Punjab; University of Technology Sydney
RP Awasthi, R (corresponding author), UPES, Sch Hlth Sci & Technol, Dept Pharmaceut Sci, Dehra Dun 248007, Uttarakhad, India.; Dureja, H (corresponding author), Maharshi Dayanand Univ, Dept Pharmaceut Sci, Rohtak 124001, Haryana, India.; Dureja, H (corresponding author), Chitkara Univ, Chitkara Coll Pharm, Ctr Res Impact & Outcome, Chandigarh 140401, Punjab, India.; Dureja, H (corresponding author), Univ Technol Sydney, Australian Res Ctr Complementary & Integrat Med, Fac Hlth, Ultimo, Australia.
EM awasthi02@gmail.com; harishdureja@gmail.com
RI DUREJA, HARISH/D-7653-2018; Awasthi, Rajendra/O-7514-2019; GOYAL,
   RAJAT/GON-9827-2022
OI GOYAL, RAJAT/0000-0001-5702-0932; Awasthi, Rajendra/0000-0002-1286-1874
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NR 122
TC 0
Z9 0
U1 2
U2 2
PU SPRINGERNATURE
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON, N1 9XW, ENGLAND
EI 2314-8543
J9 BENI-SUEF U J BASIC
JI Beni-Suef Univ. J. Basic Appl. Sci.
PD JUL 26
PY 2024
VL 13
IS 1
AR 69
DI 10.1186/s43088-024-00528-3
PG 19
WC Multidisciplinary Sciences
WE Emerging Sources Citation Index (ESCI)
SC Science & Technology - Other Topics
GA ZU3T1
UT WOS:001277769100001
OA gold
DA 2025-01-04
ER

PT J
AU Liu, JR
   Ke, F
   Cheng, HB
   Zhou, JR
AF Liu, Jianrong
   Ke, Fei
   Cheng, Haibo
   Zhou, Jinrong
TI Traditional Chinese medicine as targeted treatment for
   epithelial-mesenchymal transition-induced cancer progression
SO JOURNAL OF CELLULAR BIOCHEMISTRY
LA English
DT Article
DE cancer stem cells (CSCs); epithelial-mesenchymal transition (EMT);
   traditional Chinese medicine (TCM); tumor-related immune
   microenvironment; vasculogenic mimicry (VM)
ID NF-KAPPA-B; HUMAN COLORECTAL-CANCER; VASCULOGENIC MIMICRY FORMATION;
   GROWTH-FACTOR-BETA; STEM-CELLS; E-CADHERIN; HEPATOCELLULAR-CARCINOMA;
   SIGNALING PATHWAYS; PANCREATIC-CANCER; TUMOR-METASTASIS
AB The epithelial-mesenchymal transition (EMT) program, which loosens cell-cell adhesion complexes, endows cells with enhanced migratory and invasive properties. Furthermore, this process facilitates both the development of drug resistance and immunosuppression by tumor cells, which preclude the successful treatment of cancer. Recent research has demonstrated that many signaling pathways are involved in EMT progression. In addition, cancer stem cells (CSCs), vasculogenic mimicry (VM) and the tumor-related immune microenvironment all play important roles in tumor formation. However, there are few reports on the relationships between EMT and these factors. In addition, in recent years, traditional Chinese medicine (TCM) has developed a unique system for treating cancer. In this review, we summarize the crucial signaling pathways associated with the EMT process in cancer patients and discuss the interconnections between EMT and other molecular factors (such as CSCs, VM, and the tumor-related immune microenvironment). We attempt to identify common regulators that might be potential therapeutic targets to thereby optimize tumor treatment. In addition, we outline recent research on TCM approaches that target EMT and thereby provide a foundation for further research on the exact mechanisms by which TCMs affect EMT in cancer.
C1 [Liu, Jianrong; Zhou, Jinrong] Nanjing Univ Chinese Med, Sch Med & Life Sci, 138 Xianlin Ave, Nanjing 210046, Jiangsu, Peoples R China.
   [Ke, Fei] Nanjing Univ Chinese Med, Jiangsu Prov Hosp TCM, Affiliated Hosp, Dept Pathol, 155 Hanzhong Rd, Nanjing 210029, Jiangsu, Peoples R China.
   [Cheng, Haibo] Nanjing Univ Chinese Med, Clin Med Coll 1, Jiangsu Collaborat Innovat Ctr Tradit Chinese Med, 138 Xianlin Ave, Nanjing 210046, Jiangsu, Peoples R China.
C3 Nanjing University of Chinese Medicine; Nanjing University of Chinese
   Medicine; Nanjing University of Chinese Medicine
RP Zhou, JR (corresponding author), Nanjing Univ Chinese Med, Sch Med & Life Sci, 138 Xianlin Ave, Nanjing 210046, Jiangsu, Peoples R China.; Ke, F (corresponding author), Nanjing Univ Chinese Med, Jiangsu Prov Hosp TCM, Affiliated Hosp, Dept Pathol, 155 Hanzhong Rd, Nanjing 210029, Jiangsu, Peoples R China.; Cheng, HB (corresponding author), Nanjing Univ Chinese Med, Clin Med Coll 1, Jiangsu Collaborat Innovat Ctr Tradit Chinese Med, 138 Xianlin Ave, Nanjing 210046, Jiangsu, Peoples R China.
EM kfljr2014@163.com; chbnzy_nj@163.com; jrzhoubidmdharvard@yeah.net
OI Liu, Jian-rong/0000-0002-8168-8139
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NR 104
TC 7
Z9 7
U1 0
U2 24
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0730-2312
EI 1097-4644
J9 J CELL BIOCHEM
JI J. Cell. Biochem.
PD FEB
PY 2019
VL 120
IS 2
BP 1068
EP 1079
DI 10.1002/jcb.27588
PG 12
WC Biochemistry & Molecular Biology; Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Cell Biology
GA HL6CW
UT WOS:000458822400004
PM 30431663
DA 2025-01-04
ER

PT J
AU Tewari, D
   Priya, A
   Bishayee, A
   Bishayee, A
AF Tewari, Devesh
   Priya, Anu
   Bishayee, Anusha
   Bishayee, Anupam
TI Targeting transforming growth factor-β signalling for cancer prevention
   and intervention: Recent advances in developing small molecules of
   natural origin
SO CLINICAL AND TRANSLATIONAL MEDICINE
LA English
DT Review
DE apoptosis; cancer; in vitro; in vivo; natural products; proliferation;
   TGF-beta signalling; treatment
ID EPITHELIAL-MESENCHYMAL TRANSITION; TGF-BETA; INHIBITS METASTASIS;
   TRANSCRIPTION FACTORS; CURCUMIN REVERSES; STEROIDAL SAPONIN;
   COLORECTAL-CANCER; CARCINOMA CELLS; DOWN-REGULATION; ARJUNOLIC ACID
AB Background: Cancer is the world's second leading cause of death, but a significant advancement in cancer treatment has been achieved within the last few decades. However, major adverse effects and drug resistance associated with standard chemotherapy have led towards targeted treatment options.
   Objectives: Transforming growth factor-beta (TGF-beta) signaling plays a key role in cell proliferation, differentiation, morphogenesis, regeneration, and tissue homeostasis. The prime objective of this review is to decipher the role of TGF-beta in oncogenesis and to evaluate the potential of various natural and synthetic agents to target this dysregulated pathway to confer cancer preventive and anticancer therapeutic effects.
   Methods: Various authentic and scholarly databases were explored to search and obtain primary literature for this study. The Preferred Reporting Items for Systematic Reviews and Meta-Analysis (PRISMA) criteria was followed for the review.
   Results: Here we provide a comprehensive and critical review of recent advances on our understanding of the effect of various bioactive natural molecules on the TGF-beta signaling pathway to evaluate their full potential for cancer prevention and therapy.
   Conclusion: Based on emerging evidence as presented in this work, TGF-beta-targeting bioactive compounds from natural sources can serve as potential therapeutic agents for prevention and treatment of various human malignancies.
C1 [Tewari, Devesh] Lovely Profess Univ, Sch Pharmaceut Sci, Dept Pharmacognosy, Phagwara 144411, Punjab, India.
   [Priya, Anu] Lovely Profess Univ, Sch Pharmaceut Sci, Dept Pharmacol, Phagwara, Punjab, India.
   [Bishayee, Anusha] Pine View Sch, Osprey, FL USA.
   [Bishayee, Anupam] Lake Erie Coll Osteopath Med, Coll Osteopath Med, Bradenton, FL USA.
C3 Lovely Professional University; Lovely Professional University
RP Tewari, D (corresponding author), Lovely Profess Univ, Sch Pharmaceut Sci, Dept Pharmacognosy, Phagwara 144411, Punjab, India.; Bishayee, A (corresponding author), Lake Erie Coll Osteopath Med, 5000 Lakewood Ranch Blvd, Bradenton, FL 34211 USA.
EM devesh.24531@lpu.co.in; abishayee@lecom.edu
RI Tewari, Devesh/P-9954-2019; A, Priya/AAH-4231-2019; Bishayee,
   Anupam/G-4290-2012
OI Tewari, Dr. Devesh/0000-0002-5125-3791
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NR 258
TC 24
Z9 24
U1 1
U2 13
PU JOHN WILEY & SONS LTD
PI CHICHESTER
PA THE ATRIUM, SOUTHERN GATE, CHICHESTER PO19 8SQ, W SUSSEX, ENGLAND
SN 2001-1326
J9 CLIN TRANSL MED
JI Clin. Transl. Med.
PD APR
PY 2022
VL 12
IS 4
AR e795
DI 10.1002/ctm2.795
PG 34
WC Oncology; Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Research & Experimental Medicine
GA 0G6CQ
UT WOS:000778131300001
PM 35384373
OA Green Published
DA 2025-01-04
ER

PT J
AU Shukla, S
   Karbhari, A
   Rastogi, S
   Agarwal, U
   Rai, P
   Mahajan, A
AF Shukla, S.
   Karbhari, A.
   Rastogi, S.
   Agarwal, U.
   Rai, P.
   Mahajan, A.
TI Bench-to-bedside imaging in brain metastases: a road to precision
   oncology
SO CLINICAL RADIOLOGY
LA English
DT Review
ID MAGNETIC-RESONANCE-SPECTROSCOPY; CONTRAST-ENHANCED MRI; BREAST-CANCER
   PATIENTS; HIGH-DOSE GADOTERIDOL; HIGH-GRADE GLIOMAS; LEPTOMENINGEAL
   METASTASES; MALIGNANT-MELANOMA; SOLITARY METASTASES; IMPROVES DETECTION;
   PERFUSION MRI
AB Radiology has seen tremendous evolution in the last few decades. At the same time, oncology has made great strides in diagnosing and treating cancer. Distant metastases of neoplasms are being encountered more often in light of longer patient survival due to better therapeutic strategies and diagnostic methods. Brain metastasis (BM) is a dismal manifestation of systemic cancer. In the present scenario, magnetic resonance imaging (MRI), computed tomography (CT) and positron emission tomography (PET) are playing a big role in providing molecular information about cancer. Lately, molecular imaging has emerged as a stirring arena of dynamic imaging techniques that have enabled clinicians and scientists to noninvasively visualize and understand biological processes at the cellular and molecular levels. This knowledge has impacted etiopathogenesis, detection, personalized treatment, drug development, and our understanding of carcinogenesis. This article offers insight into the molecular biology underlying brain metastasis, its pathogenesis, imaging protocols, and algorithms. It also discusses disease-specific molecular imaging features, focusing on common tumors that spread to the brain, such as lung, breast, colorectal cancer, melanoma, and renal cell carcinoma. Additionally, it covers various targeted treatment options, criteria for assessing treatment response, and the role of artificial intelligence in diagnosing, managing, and predicting prognosis for patients with brain metastases. (c) 2024 The Royal College of Radiologists. Published by Elsevier Ltd. All rights reserved.
C1 [Shukla, S.] Tata Mem Hosp, Mahamana Pandit Madan Mohan Malaviya Canc Ctr, Dept Radiodiag & Imaging, Varanasi 221005, Maharashtra, India.
   [Shukla, S.] Tata Mem Hosp, Homi Bhabha Canc Hosp, Varanasi 221005, Maharashtra, India.
   [Shukla, S.; Karbhari, A.; Rastogi, S.; Agarwal, U.; Rai, P.] Tata Mem Hosp, Homi Bhabha Natl Inst, Dept Radiodiag & Imaging, Mumbai 400012, Maharashtra, India.
   [Mahajan, A.] Clatterbridge Canc Ctr NHS Fdn Trust, Dept Imaging, 65 Pembroke Pl, Liverpool L7 8YA, England.
   [Mahajan, A.] Univ Liverpool, Fac Hlth & Life Sci, Liverpool L7 8TX, England.
C3 Tata Memorial Centre (TMC); Tata Memorial Hospital; Mahamana Pandit
   Madan Mohan Malaviya Cancer Centre, Varanasi; Tata Memorial Centre
   (TMC); Tata Memorial Hospital; Homi Bhabha Cancer Hospital Varanasi;
   Homi Bhabha National Institute; Tata Memorial Centre (TMC); Tata
   Memorial Hospital; University of Liverpool
RP Mahajan, A (corresponding author), Clatterbridge Canc Ctr NHS Fdn Trust, Dept Imaging, 65 Pembroke Pl, Liverpool L7 8YA, England.
EM abhishek.mahajan@nhs.net
RI SHUKLA, SHREYA/ABE-3074-2021; Mahajan, Abhishek/AAO-1329-2021
OI Rastogi, Shivam/0000-0002-2067-1691; Mahajan,
   Abhishek/0000-0001-6606-6537; Shukla, Shreya/0000-0002-7815-9252
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NR 98
TC 1
Z9 1
U1 4
U2 4
PU W B SAUNDERS CO LTD
PI LONDON
PA 32 JAMESTOWN RD, LONDON NW1 7BY, ENGLAND
SN 0009-9260
EI 1365-229X
J9 CLIN RADIOL
JI Clin. Radiol.
PD JUL
PY 2024
VL 79
IS 7
BP 485
EP 500
DI 10.1016/j.crad.2024.02.015
EA MAY 2024
PG 16
WC Radiology, Nuclear Medicine & Medical Imaging
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Radiology, Nuclear Medicine & Medical Imaging
GA US6J3
UT WOS:001250083100004
PM 38637186
DA 2025-01-04
ER

PT J
AU Gild, ML
   Bullock, M
   Pon, CK
   Robinson, BG
   Clifton-Bligh, RJ
AF Gild, M. L.
   Bullock, M.
   Pon, C. K.
   Robinson, B. G.
   Clifton-Bligh, R. J.
TI Destabilizing RET in targeted treatment of thyroid cancers
SO ENDOCRINE CONNECTIONS
LA English
DT Article
DE thyroid cancer; HSP90; AUY922; RET; MAPK; mTOR
ID SHOCK-PROTEIN 90; CARCINOMA CELL-PROLIFERATION; TYROSINE KINASE
   INHIBITORS; DEOXYRIBONUCLEIC-ACID; HSP90 INHIBITORS; NVP-AUY922;
   MEDULLARY; GROWTH; HEAT-SHOCK-PROTEIN-90; LINES
AB Metastatic differentiated thyroid cancers (DTC) are resistant to traditional chemotherapy. Kinase inhibitors have shown promise in patients with progressive DTC, but dose-limiting toxicity is commonplace. HSP90 regulates protein degradation of several growth-mediating kinases such as RET, and we hypothesized that HSP90 inhibitor (AUY922) could inhibit RET-mediated medullary thyroid cancer (MTC) as well as papillary thyroid cancer (PTC) cell growth and also radioactive iodine uptake by PTC cells. Studies utilized MTC cell lines TT (C634W) and MZ-CRC-1 (M918T) and the PTC cell line TPC-1 (RET/PTC1). Cell viability was assessed with MTS assays and apoptosis by flow cytometry. Signaling target expression was determined by western blot and radioiodine uptake measured with a gamma counter. Prolonged treatment of both MTC cell lines with AUY922 simultaneously inhibited both MAPK and mTOR pathways and significantly induced apoptosis (58.7 and 78.7% reduction in MZ-CRC-1 and TT live cells respectively, following 1 mu M AUY922; P < 0.02). Similarly in the PTC cell line, growth and signaling targets were inhibited, and also a 2.84-fold increase in radioiodine uptake was observed following AUY922 administration (P=0.015). AUY922 demonstrates in vitro activity against MTC and PTC cell lines. We observed a potent dose-dependent increase in apoptosis in MTC cell lines following drug administration confirming its anti-tumorigenic effects. Western blots confirm inhibition of pro-survival proteins including AKT suggesting this as the mechanism of cell death. In a functional study, we observed an increase in radioiodine uptake in the PTC cell line following AUY922 treatment. We believe HSP90 inhibition could be a viable alternative for treatment of RET-driven chemo-resistant thyroid cancers.
C1 [Gild, M. L.; Bullock, M.; Pon, C. K.; Robinson, B. G.; Clifton-Bligh, R. J.] Kolling Inst Med Res, Canc Genet Lab, Sydney, NSW, Australia.
   [Robinson, B. G.; Clifton-Bligh, R. J.] Univ Sydney, Royal North Shore Hosp, Dept Endocrinol, Sydney, NSW 2065, Australia.
C3 University of Sydney; Kolling Institute of Medical Research; University
   of Sydney; Royal North Shore Hospital
RP Clifton-Bligh, RJ (corresponding author), Kolling Inst Med Res, Canc Genet Lab, Sydney, NSW, Australia.; Clifton-Bligh, RJ (corresponding author), Univ Sydney, Royal North Shore Hosp, Dept Endocrinol, Sydney, NSW 2065, Australia.
EM jclifton@med.usyd.edu.au
RI Robinson, B/LBH-2242-2024; Gild, Matti/AAH-2367-2021; Bullock,
   Martyn/D-2868-2015
OI Bullock, Martyn/0000-0002-3740-5509; Clifton-Bligh,
   Roderick/0000-0002-1545-0368; Gild, Matti/0000-0002-6670-2254
FU Australian Postgraduate Award; NHMRC project grant [1061941]; National
   Health and Medical Research Council of Australia [1061941] Funding
   Source: NHMRC
FX M L Gild was awarded the Australian Postgraduate Award. M Bullock and R
   J Clifton-Bligh were supported by an NHMRC project grant (1061941).
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NR 32
TC 4
Z9 4
U1 0
U2 2
PU BIOSCIENTIFICA LTD
PI BRISTOL
PA EURO HOUSE, 22 APEX COURT WOODLANDS, BRADLEY STOKE, BRISTOL BS32 4JT,
   ENGLAND
EI 2049-3614
J9 ENDOCR CONNECT
JI Endocr. Connect.
PD JAN 1
PY 2016
VL 5
IS 1
BP 10
EP 19
DI 10.1530/EC-15-0098
PG 10
WC Endocrinology & Metabolism
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Endocrinology & Metabolism
GA DV9MD
UT WOS:000383263700002
PM 26574568
OA Green Published, gold, Green Submitted
DA 2025-01-04
ER

PT J
AU Reeves, KM
   Song, PN
   Angermeier, A
   Della Manna, D
   Li, YF
   Wang, JB
   Yang, ES
   Sorace, AG
   Larimer, BM
AF Reeves, Kirsten M.
   Song, Patrick N.
   Angermeier, Allyson
   Della Manna, Deborah
   Li, Yufeng
   Wang, Jianbo
   Yang, Eddy S.
   Sorace, Anna G.
   Larimer, Benjamin M.
TI 18F-FMISO PET Imaging Identifies Hypoxia and Immunosuppressive Tumor
   Microenvironments and Guides Targeted Evofosfamide Therapy in Tumors
   Refractory to PD-1 and CTLA-4 Inhibition
SO CLINICAL CANCER RESEARCH
LA English
DT Article
ID CANCER
AB Purpose: Hypoxia is a common characteristic of many tumor microenvironments, and it has been shown to promote suppression of antitumor immunity. Despite strong biological rationale, longitudinal correlation of hypoxia and response to immunotherapy has Experimental Design: In this study, we probed the tumor and its surrounding microenvironment with 18F-FMISO PET imaging to noninvasively quantify tumor hypoxia in vivo prior to and during PD-1 and CTLA-4 checkpoint blockade in preclinical models of breast and colon cancer. Results: Longitudinal imaging identified hypoxia as an early predictive biomarker of therapeutic response (prior to anatomic changes in tumor volume) with a decreasing standard uptake value (SUV) ratio in tumors that effectively respond to therapy. PET signal correlated with ex vivo markers of tumor immune response including cytokines (IFNg, GZMB, and TNF), damage-associated molecular pattern receptors (TLR2/4), and immune cell popula-tions (macrophages, dendritic cells, and cytotoxic T cells). Respond-ing tumors were marked by increased inflammation that were spatially distinct from hypoxic regions, providing a mechanistic understanding of the immune signaling pathways activated. To exploit image-guided combination therapy, hypoxia signal from PET imaging was used to guide the addition of a hypoxia targeted treatment to nonresponsive tumors, which ultimately provided therapeutic synergy and rescued response as determined by longi-tudinal changes in tumor volume. Conclusions: The results generated from this work provide an immediately translatable paradigm for measuring and targeting hypoxia to increase response to immune checkpoint therapy and using hypoxia imaging to guide combinatory therapies.
C1 [Reeves, Kirsten M.; Song, Patrick N.; Li, Yufeng; Sorace, Anna G.; Larimer, Benjamin M.] Univ Alabama Birmingham, Dept Radiol, Birmingham, AL 35233 USA.
   [Reeves, Kirsten M.; Angermeier, Allyson; Della Manna, Deborah; Li, Yufeng; Wang, Jianbo; Yang, Eddy S.; Sorace, Anna G.; Larimer, Benjamin M.] Univ Alabama Birmingham, ONeal Comprehens Canc Ctr, Birmingham, AL 35233 USA.
   [Reeves, Kirsten M.; Song, Patrick N.] Univ Alabama Birmingham, Grad Biomed Sci Program, Birmingham, AL 35233 USA.
   [Angermeier, Allyson; Wang, Jianbo; Yang, Eddy S.] Univ Alabama Birmingham, Cell Dev & Integrat Biol, Birmingham, AL 35233 USA.
   [Della Manna, Deborah; Yang, Eddy S.] Univ Alabama Birmingham, Radiat Oncol, Birmingham, AL 35233 USA.
   [Li, Yufeng] Univ Alabama Birmingham, Dept Med, Div Preventat Med, Birmingham, AL 35233 USA.
   [Sorace, Anna G.] Univ Alabama Birmingham, Dept Biomed Engn, Birmingham, AL 35233 USA.
C3 University of Alabama System; University of Alabama Birmingham;
   University of Alabama System; University of Alabama Birmingham;
   University of Alabama System; University of Alabama Birmingham;
   University of Alabama System; University of Alabama Birmingham;
   University of Alabama System; University of Alabama Birmingham;
   University of Alabama System; University of Alabama Birmingham;
   University of Alabama System; University of Alabama Birmingham
RP Larimer, BM (corresponding author), Univ Alabama Birmingham, ONeal Comprehens Canc Ctr, Dept Radiol, 1824 6th Ave S,Wallace Tumor Inst 310G, Birmingham, AL 35233 USA.; Sorace, AG (corresponding author), Univ Alabama Birmingham, ONeal Comprehens Canc Ctr, Dept Radiol, 1670 Univ Blvd, Birmingham, AL 35233 USA.
EM agsorace@uab.edu; blarimer@uab.edu
OI Song, Patrick/0000-0002-1545-0886; Reeves, Kirsten/0000-0001-9199-1580;
   Angermeier, Allyson/0000-0002-2212-8414; Larimer,
   Benjamin/0000-0002-1288-7206
FU UAB O'Neal Preclinical Imaging Shared Facility Grant (National Cancer
   Institute) [P30CA013148]; NIH Directors' New Innovator Award [NCI
   DP2CA261453]; NIH Pathway to Independence award [NCI R00CA215604]; NIH
   [NCI R01CA240589]; American Cancer Society Research Scholar Grant
   [RSG-18-006-01-CCE]; O'Neal Comprehensive Cancer Center Mary Ann Harvard
   Award
FX The authors thank the UAB Cyclotron Facility, UAB NanoString Core, UAB
   Pathology Core for technical assistance. Funding was provided by the UAB
   O'Neal Preclinical Imaging Shared Facility Grant (National Cancer
   Institute P30CA013148), a NIH Directors' New Innovator Award (NCI
   DP2CA261453) to B. Larimer, a NIH Pathway to Independence award (NCI
   R00CA215604) to B. Larimer, NIH research funding (NCI R01CA240589) to A.
   Sorace, an American Cancer Society Research Scholar Grant
   (RSG-18-006-01-CCE) to A. Sorace, and an O'Neal Comprehensive Cancer
   Center Mary Ann Harvard Award to B. Larimer.
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NR 37
TC 25
Z9 29
U1 1
U2 1
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1078-0432
EI 1557-3265
J9 CLIN CANCER RES
JI Clin. Cancer Res.
PD JAN 15
PY 2022
VL 28
IS 2
BP 327
EP 337
DI 10.1158/1078-0432.CCR-21-2394
PG 11
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA YK9TA
UT WOS:000745545000001
PM 34615724
OA hybrid, Green Published, Green Submitted
DA 2025-01-04
ER

PT J
AU Yang, JA
   Kong, WH
   Sung, DK
   Kim, H
   Kim, TH
   Lee, KC
   Hahn, SK
AF Yang, Jeong-A
   Kong, Won Ho
   Sung, Dong Kyung
   Kim, Hyemin
   Kim, Tae Hyung
   Lee, Kang Choon
   Hahn, Sei Kwang
TI Hyaluronic acid-tumor necrosis factor-related apoptosis-inducing ligand
   conjugate for targeted treatment of liver fibrosis
SO ACTA BIOMATERIALIA
LA English
DT Article
DE Hyaluronic acid; TRAIL; Conjugate; Targeted delivery; Liver fibrosis
ID TRAIL-INDUCED APOPTOSIS; TUMORICIDAL ACTIVITY; STELLATE CELLS;
   HEPATITIS-C; RECEPTOR; CD44; CIRRHOSIS; THERAPY; DISEASE
AB Liver fibrosis is a chronic liver disease caused by viral infection and/or metabolic, genetic and cholestatic disorders. The inhibition of hepatic stellate cell (HSC) activation and the selective apoptosis of activated HSCs can be a good strategy to treat liver fibrosis. The activated HSCs are known to be more susceptible to tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) induced apoptosis than normal HSCs because death receptor 5 is overexpressed on the cell surface. In this work, a target-specific and long-acting hyaluronic acid (HA)-TRAIL conjugate was successfully developed for the treatment of liver fibrosis. The HA-TRAIL conjugate was synthesized by a coupling reaction between aldehyde-modified HA and the N-terminal amine group of TRAIL. The biological activity of the HA-TRAIL conjugate was confirmed by an in vitro anti-proliferation assay and caspase-3 expression in human colon cancer HCT116 cells. In vivo real-time bioimaging exhibited the target-specific delivery of near-infrared fluorescence dye-labeled HA-TRAIL conjugate to the liver in mice. According to pharmacokinetic analysis, the HA-TRAIL conjugate was detected for more than 4 days after single intravenous injection into Sprague-Dawley (SD) rats. Finally, we could confirm the antifibrotic effect of HA-TRAIL conjugate in an N-nitrosodimethylamine-induced liver fibrosis model SD rats. (C) 2014 Acta Materialia Inc. Published by Elsevier Ltd. All rights reserved.
C1 [Yang, Jeong-A; Kong, Won Ho; Kim, Hyemin; Hahn, Sei Kwang] Pohang Univ Sci & Technol, Dept Mat Sci & Engn, POSTECH, Pohang 790784, Kyungbuk, South Korea.
   [Sung, Dong Kyung] Sungkyunkwan Univ, Sch Med, Dept Pediat, Samsung Med Ctr, Seoul 135710, South Korea.
   [Kim, Tae Hyung; Lee, Kang Choon] Sungkyunkwan Univ, Coll Pharm, Suwon 440746, South Korea.
C3 Pohang University of Science & Technology (POSTECH); Sungkyunkwan
   University (SKKU); Samsung Medical Center; Sungkyunkwan University
   (SKKU)
RP Hahn, SK (corresponding author), Pohang Univ Sci & Technol, Dept Mat Sci & Engn, POSTECH, San 31, Pohang 790784, Kyungbuk, South Korea.
EM skhanb@postech.ac.kr
RI Kim, Hyemin/I-1547-2018; Lee, Kang/A-9556-2010; Hahn, Sei/L-6037-2019
OI Kim, Hyemin/0000-0001-8534-3886; Hahn, Sei Kwang/0000-0002-7718-6259
FU Converging Research Center Program through the National Research
   Foundation of Korea (NRF) - Ministry of Education, Science and
   Technology [2009-0081871]; Mid-career Researcher Program through NRF -
   MEST [2012R1A2 A2A06045773]
FX This research was supported by the Converging Research Center Program
   through the National Research Foundation of Korea (NRF) funded by the
   Ministry of Education, Science and Technology (2009-0081871). This study
   was also supported by Mid-career Researcher Program through NRF grant
   funded by the MEST (No. 2012R1A2 A2A06045773).
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NR 35
TC 44
Z9 48
U1 0
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PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 1742-7061
EI 1878-7568
J9 ACTA BIOMATER
JI Acta Biomater.
PD JAN 15
PY 2015
VL 12
BP 174
EP 182
DI 10.1016/j.actbio.2014.10.002
PG 9
WC Engineering, Biomedical; Materials Science, Biomaterials
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Engineering; Materials Science
GA CA1QF
UT WOS:000348686100019
PM 25305513
DA 2025-01-04
ER

PT J
AU Walter, D
   Schnitzbauer, AA
   Schulze, F
   Trojan, J
AF Walter, Dirk
   Schnitzbauer, Andreas A.
   Schulze, Falko
   Trojan, Joerg
TI The Diagnosis and Treatment of Ampullary Carcinoma
SO DEUTSCHES ARZTEBLATT INTERNATIONAL
LA English
DT Article
ID ADJUVANT THERAPY; PERIAMPULLARY ADENOCARCINOMA; SMALL-BOWEL; OPEN-LABEL;
   PHASE-II; CANCER; GEMCITABINE; SURVIVAL; PANCREATICOBILIARY;
   CHEMOTHERAPY
AB Background: Ampullary or papillary carcinoma is a malignant tumor arising from the mucosa in the region of the major duodenal papilla, also known as the ampulla of Vater. Uniform treatment recommendations are lacking both for the adjuvant situation and for palliative care.Methods: A selective literature search was carried out in PubMed in order to identify the most informative publications concerning the epidemiology, clinicopathological background, and surgical and medical treatment of this condition.Results: Ampullary carcinoma has an incidence of 0.5 to 0.9 per 100 000 persons and a poor prognosis, with a 5-year survival rate of 41% to 45% for locally confined and 4% to 7% for metastatic disease. Most such tumors are of an intestinal or a pan creaticobiliary immunohistochemical subtype; the latter has a worse prognosis (median survival, 72-80 vs. 33-41 months). Targeted treatment is not yet available for either subtype, nor is there enough scientific evidence available for the formulation of specific therapeutic recommendations in either the adjuvant or the palliative situation. The treatment of choice for ampullary carcinoma is radical oncological resection of the head of the pancreas with systematic lymphadenectomy. Five-year overall survival is between 10% and 75% depending on the stage. No definitive recommendation for adjuvant therapy can be given. Palliative therapy can be oriented to the published treatment strategies for cancer of the colon, pancreas, and bile duct.Conclusion: The current state of the evidence on the treatment of ampullary carcinoma is poor. Therapeutic decisions should be discussed in an interdisciplinary tumor board and should, in our opinion, take the histological subtype into account.
C1 [Walter, Dirk; Trojan, Joerg] JW Goethe Univ Hosp, Dept Internal Med, Frankfurt, Germany.
   [Schnitzbauer, Andreas A.] JW Goethe Univ Hosp, Dept Gen Visceral Transplant & Thorac Surg, Frankfurt, Germany.
   [Schulze, Falko] Goethe Univ Frankfurt Am Main, Univ Hosp Frankfurt, Dr Senckenberg Inst Pathol, Frankfurt, Germany.
   [Walter, Dirk] Univ Klinikum Frankfurt, Med Klin 1, Theodor Stern Kai 7, D-60590 Frankfurt, Germany.
C3 Goethe University Frankfurt; Goethe University Frankfurt Hospital;
   Goethe University Frankfurt; Goethe University Frankfurt Hospital;
   Goethe University Frankfurt; Goethe University Frankfurt Hospital;
   Goethe University Frankfurt; Goethe University Frankfurt Hospital
RP Walter, D (corresponding author), Univ Klinikum Frankfurt, Med Klin 1, Theodor Stern Kai 7, D-60590 Frankfurt, Germany.
EM dirk.walter@kgu.de
RI Trojan, Jörg/C-1616-2009
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NR 40
TC 2
Z9 2
U1 1
U2 2
PU DEUTSCHER AERZTE-VERLAG GMBH
PI COLOGNE
PA DIESELSTRABE 2, POSTFACH 400265, D-50859 COLOGNE, GERMANY
SN 1866-0452
J9 DTSCH ARZTEBL INT
JI Dtsch. Arztebl. Int.
PD OCT 27
PY 2023
VL 120
IS 43
BP 729
EP +
PG 11
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA Z9CX8
UT WOS:001114991000001
PM 37656482
OA Green Published
DA 2025-01-04
ER

PT J
AU Javan, MR
   Khosrojerdi, A
   Moazzeni, SM
AF Javan, Mohammad Reza
   Khosrojerdi, Arezou
   Moazzeni, Seyed Mohammad
TI New Insights Into Implementation of Mesenchymal Stem Cells in Cancer
   Therapy: Prospects for Anti-angiogenesis Treatment
SO FRONTIERS IN ONCOLOGY
LA English
DT Review
DE angiogenesis; mesenchymal stem cells; tumor microenvironment; cancer
   therapy; drug delivery
ID ENDOTHELIAL GROWTH-FACTOR; UMBILICAL-CORD BLOOD; TYROSINE KINASE
   INHIBITOR; HUMAN BONE-MARROW; STROMAL CELLS; BREAST-CANCER; IN-VITRO;
   TUMOR ANGIOGENESIS; ESTROGEN-RECEPTOR; INTERFERON-BETA
AB Tumor microenvironment interacts with tumor cells, establishing an atmosphere to contribute or suppress the tumor development. Among the cells which play a role in the tumor microenvironment, mesenchymal stem cells (MSCs) have been demonstrated to possess the ability to orchestrate the fate of tumor cells, drawing the attention to the field. MSCs have been considered as cells with double-bladed effects, implicating either tumorigenic or anti-tumor activity. On the other side, the promising potential of MSCs in treating human cancer cells has been observed from the clinical studies. Among the bene ficial characteristics of MSCs is the natural tumor-trophic migration ability, providing facility for drug delivery and, therefore, targeted treatment to detach tumor and metastatic cells. Moreover, these cells have been the target of engineering approaches, due to their easily implemented traits, in order to obtain the desired expression of anti-angiogenic, anti-proliferative, and pro-apoptotic properties, according to the tumor type. Tumor angiogenesis is the key characteristic of tumor progression and metastasis. Manipulation of angiogenesis has become an attractive approach for cancer therapy since the introduction of the first angiogenesis inhibitor, namely bevacizumab, for metastatic colorectal cancer therapy. This review tries to conclude the approaches, with focus on anti-angiogenesis approach, in implementing the MSCs to combat against tumor cell progression.
C1 [Javan, Mohammad Reza; Khosrojerdi, Arezou; Moazzeni, Seyed Mohammad] Tarbiat Modares Univ, Fac Med Sci, Dept Immunol, Tehran, Iran.
C3 Tarbiat Modares University
RP Moazzeni, SM (corresponding author), Tarbiat Modares Univ, Fac Med Sci, Dept Immunol, Tehran, Iran.
EM moazzeni@modares.ac.ir
RI javan, mohammad/C-4862-2016; Moazzeni, Seyed Mohammad/AFV-4912-2022
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NR 219
TC 49
Z9 50
U1 0
U2 11
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 2234-943X
J9 FRONT ONCOL
JI Front. Oncol.
PD AUG 28
PY 2019
VL 9
AR 840
DI 10.3389/fonc.2019.00840
PG 17
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA IT5LN
UT WOS:000482904400002
PM 31555593
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Yang, PP
   Li, CS
   Zhou, Q
   Zhang, XQ
   Kou, YY
   Feng, QS
   Wang, H
   Su, RJ
   Hasegawa, T
   Liu, HR
   Li, MQ
AF Yang, Panpan
   Li, Congshan
   Zhou, Qin
   Zhang, Xiaoqi
   Kou, Yuying
   Feng, Qiushi
   Wang, He
   Su, Rongjian
   Hasegawa, Tomoka
   Liu, Hongrui
   Li, Minqi
TI Notum leads to potential pro-survival of OSCC through crosstalk between
   Shh and Wnt/β-catenin signaling via p-GSK3β
SO INTERNATIONAL JOURNAL OF BIOCHEMISTRY & CELL BIOLOGY
LA English
DT Article
DE OSCC; Notum; Proliferation; Migration; P-GSK3?
ID NUCLEAR ANTIGEN PCNA; HEPATOCELLULAR-CARCINOMA; HEDGEHOG; WNT; PATHWAY;
   PROGRESSION; MECHANISMS; EXPRESSION; APOPTOSIS; HOMOLOG
AB Notum, which belongs to the alpha/beta hydrolase family, is a deacylated extracellular protein that regulates the Wnt signaling pathway. Studies have found that Notum participates in the progression of colorectal cancer and he-patocellular carcinoma, but its role in oral squamous cell carcinoma (OSCC) is currently unclear. This study aimed to explore the role of Notum in regulating OSCC and further reveal the underlying mechanisms. Various approaches including bioinformatics analysis, enzyme-linked immunosorbent assay and immunohistochemical staining were used to detect the expression of Notum in OSCC cells and tissues. Cell counting kit-8 assay, clone formation assay, wound healing assay, transwell assay and in-gel zymography assay were explored to evaluate the regulation of Notum in OSCC proliferation and migration. Hoechst 33342/PI assay, cell immunofluorescence, flow cytometry and in vivo tumorigenesis experiment were applied for OSCC apoptosis. Real-time quantitative polymerase chain reaction analysis was performed for mRNA level while western blotting was conducted to detect protein expression. The results showed that Notum was highly expressed in OSCC tissues and cells, and Notum promoted the proliferation and migration of OSCC cells while it inhibited their apoptosis. Furthermore, signaling pathway analysis showed that Notum led to potential pro-survival of OSCC through crosstalk between sonic hedgehog (Shh) and Wnt/beta-catenin signaling via phosphorylation of glycogen synthase kinase-3 beta. These results will help to elucidate the mechanism and also provide new ideas for targeted treatment of OSCC.
C1 [Yang, Panpan; Li, Congshan; Zhou, Qin; Kou, Yuying; Feng, Qiushi; Wang, He; Liu, Hongrui; Li, Minqi] Shandong Univ, Sch & Hosp Stomatol, Cheeloo Coll Med, Dept Bone Metab, Jinan 250012, Peoples R China.
   [Yang, Panpan; Li, Congshan; Zhou, Qin; Kou, Yuying; Feng, Qiushi; Wang, He; Liu, Hongrui; Li, Minqi] Shandong Key Lab Oral Tissue Regenerat, Jinan 250012, Peoples R China.
   [Yang, Panpan; Li, Congshan; Zhou, Qin; Kou, Yuying; Feng, Qiushi; Wang, He; Liu, Hongrui; Li, Minqi] Shandong Engn Lab Dent Mat & Oral Tissue Regenerat, Jinan 250012, Peoples R China.
   [Zhang, Xiaoqi] Sichuan Univ, West China Hosp Stomatol, Natl Clin Res Ctr Oral Dis, Dept Orthodont,State Key Lab Oral Dis, Chengdu 610041, Peoples R China.
   [Su, Rongjian] Jinzhou Med Univ, Coll Basic Med, Cell Biol & Genet Dept, Life Sci Inst,Key Lab Mol & Cellular Biol,Educ Dep, Jinzhou 121001, Peoples R China.
   [Hasegawa, Tomoka] Hokkaido Univ, Grad Sch Dent Med, Dept Dev Biol Hard Tissue, Sapporo 0608586, Japan.
   [Liu, Hongrui; Li, Minqi] Shandong Univ, Sch & Hosp Stomatol, Cheeloo Coll Med, Dept Bone Metab,Shandong Key Lab Oral Tissue Regen, Wenhua West Rd 44-1, Jinan 250012, Peoples R China.
   [Liu, Hongrui; Li, Minqi] Shandong Engn Lab Dent Mat & Oral Tissue Regenerat, Wenhua West Rd 44-1, Jinan 250012, Peoples R China.
C3 Shandong University; Sichuan University; Jinzhou Medical University;
   Hokkaido University; Shandong University
RP Liu, HR; Li, MQ (corresponding author), Shandong Univ, Sch & Hosp Stomatol, Cheeloo Coll Med, Dept Bone Metab, Jinan 250012, Peoples R China.; Liu, HR; Li, MQ (corresponding author), Shandong Univ, Sch & Hosp Stomatol, Cheeloo Coll Med, Dept Bone Metab,Shandong Key Lab Oral Tissue Regen, Wenhua West Rd 44-1, Jinan 250012, Peoples R China.; Liu, HR; Li, MQ (corresponding author), Shandong Engn Lab Dent Mat & Oral Tissue Regenerat, Wenhua West Rd 44-1, Jinan 250012, Peoples R China.
EM yf1blhr@126.com; liminqi@sdu.edu.cn
RI Lin, LiHan/KYQ-4405-2024; Liu, Hong-Rui/AAH-5073-2019; Zhang,
   Xiaoqi/P-9671-2019
OI Zhang, Xiaoqi/0000-0003-0707-0928
FU National Natural Science Foundation of China; Construction Engineering
   Special Fund of?Taishan Scholars?of Shan- dong Province;  [81800982]; 
   [tsqn202103177]
FX Funding This work was partially supported by the National Natural
   Science Foundation of China (Grant No. 81972072) to M Li, the National
   Natural Science Foundation of China (Grant No. 81800982) to HR Liu and
   the Construction Engineering Special Fund of?Taishan Scholars?of Shan-
   dong Province (No. tsqn202103177) to HR Liu.
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NR 57
TC 11
Z9 11
U1 4
U2 20
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 1357-2725
EI 1878-5875
J9 INT J BIOCHEM CELL B
JI Int. J. Biochem. Cell Biol.
PD DEC
PY 2022
VL 153
AR 106316
DI 10.1016/j.biocel.2022.106316
EA NOV 2022
PG 15
WC Biochemistry & Molecular Biology; Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Cell Biology
GA 6E0GS
UT WOS:000883064700002
PM 36280040
DA 2025-01-04
ER

PT J
AU Cho, SY
   Chae, J
   Na, D
   Kang, W
   Lee, A
   Min, S
   Kang, J
   Choi, B
   Lee, J
   Sung, CO
   Chuang, JH
   Lee, C
   Lee, WS
   Park, H
   Kim, JI
AF Cho, Sung-Yup
   Chae, Jeesoo
   Na, Deukchae
   Kang, Wonyoung
   Lee, Ahra
   Min, Seoyeon
   Kang, Jinjoo
   Choi, Boram
   Lee, Jieun
   Sung, Chang Ohk
   Chuang, Jeffrey H.
   Lee, Charles
   Lee, Won-Suk
   Park, Hansoo
   Kim, Jong-Il
TI Unstable Genome and Transcriptome Dynamics during Tumor Metastasis
   Contribute to Therapeutic Heterogeneity in Colorectal Cancers
SO CLINICAL CANCER RESEARCH
LA English
DT Article
ID INTRATUMOR HETEROGENEITY; HUMAN COLON; EVOLUTION; XENOGRAFTS; MUTATIONS;
   INSTABILITY; RESISTANCE; MODELS
AB Purpose: Genomic and transcriptomic alterations during metastasis are considered to affect clinical outcome of colorectal cancers, but detailed clinical implications of metastatic alterations are not fully uncovered. We aimed to investigate the effect of metastatic evolution on in vivo treatment outcome, and identify genomic and transcriptomic alterations associated with drug responsiveness.
   Experimental Design: We developed and analyzed patient-derived xenograft (PDX) models from 35 patients with colorectal cancer including 5 patients with multiple organ metastases (MOMs). We performed whole-exome, DNA methylation, and RNA sequencing for patient and PDX tumors. With samples from patients with MOMs, we conducted phylogenetic and subclonal analysis and in vivo drug efficacy test on the corresponding PDX models.
   Results: Phylogenetic analysis using mutation, expression, and DNA methylation data in patients with MOMs showed that mutational alterations were closely connected with transcriptomic and epigenomic changes during the tumor evolution. Subclonal analysis revealed that initial primary tumors with larger number of subclones exhibited more dynamic changes in subclonal architecture according to metastasis, and loco-regional and distant metastases occurred in a parallel or independent fashion. The PDX models from MOMs demonstrated therapeutic heterogeneity for targeted treatment, due to subclonal acquisition of additional mutations or transcriptomic activation of bypass signaling pathway during tumor evolution.
   Conclusions: This study demonstrated in vivo therapeutic heterogeneity of colorectal cancers using PDX models, and suggests that acquired subclonal alterations in mutations or gene expression profiles during tumor metastatic processes can be associated with the development of drug resistance and therapeutic heterogeneity of colorectal cancers.
C1 [Cho, Sung-Yup] Seoul Natl Univ, Dept Biochem & Mol Biol, Coll Med, Seoul, South Korea.
   [Cho, Sung-Yup; Chae, Jeesoo; Kim, Jong-Il] Seoul Natl Univ, Dept Biomed Sci, Coll Med, Seoul, South Korea.
   [Na, Deukchae] Ewha Womans Univ, Ewha Inst Convergence Med, Mokdong Hosp, Seoul, South Korea.
   [Kang, Wonyoung; Lee, Ahra; Min, Seoyeon; Kang, Jinjoo; Choi, Boram; Lee, Jieun; Lee, Charles] Ewha Womans Univ, Dept Life Sci, Seoul, South Korea.
   [Sung, Chang Ohk] Univ Ulsan, Asan Med Ctr, Dept Pathol, Coll Med, Seoul, South Korea.
   [Chuang, Jeffrey H.; Lee, Charles] Jackson Lab Genom Med, Farmington, CT USA.
   [Lee, Won-Suk] Gachon Univ, Gil Med Ctr, Dept Surg, Incheon, South Korea.
   [Park, Hansoo] GIST, Dept Biomed Sci & Engn, Gwangju, South Korea.
   [Kim, Jong-Il] Seoul Natl Univ, Canc Res Inst, Coll Med, Seoul, South Korea.
   [Kim, Jong-Il] Seoul Natl Univ, Med Res Ctr, GMI, Seoul, South Korea.
C3 Seoul National University (SNU); Seoul National University (SNU); Ewha
   Womans University; Ewha Womans University; University of Ulsan; Asan
   Medical Center; Jackson Laboratory; Gachon University; Gwangju Institute
   of Science & Technology (GIST); Seoul National University (SNU); Seoul
   National University (SNU)
RP Kim, JI (corresponding author), Seoul Natl Univ, Coll Med, 103 Daehak Ro, Seoul 03080, South Korea.; Lee, WS (corresponding author), Gachon Univ, Gil Med Ctr, 1198 Guwol Dong, Incheon 21565, South Korea.; Park, H (corresponding author), GIST, 123 Cheomdangwagi Ro, Gwangju 61005, South Korea.
EM lws@gilhospital.com; hspark27@gist.ac.kr; jongil@snu.ac.kr
RI KIM, JONG-IL/D-1019-2011; lee, wj/JNR-4926-2023; lee,
   charles/AAW-6627-2021; Lee, Yoon/ABA-8808-2020
OI Lee, Jieun/0000-0002-5808-912X; KIM, JONG-IL/0000-0002-7240-3744; Chae,
   Jeesoo/0000-0002-6869-2213; Sung, Chang Ohk/0000-0002-8567-456X; Chuang,
   Jeffrey/0000-0002-3298-2358; Lee, Charles/0000-0001-7317-6662
FU Gil Hospital Research Grant [GCU-2015-5092]; Korean Healthcare
   Technology R&D project through the Korean Health Industry Development
   Institute (KHIDI) - Ministry of Health & Welfare, Republic of Korea
   [HI13C2148]; International Research & Development Program of the
   National Research Foundation of Korea (NRF) - Ministry of Science, ICT &
   Future Planning [2015K1A4A3047851]; National Research Foundation of
   Korea (NRF) - Korea government (MSIP) [2016R1E1A1A01943469,
   2017R1C1B2002183]; Basic Science Research Program through the National
   Research Foundation of Korea (NRF) - Ministry of Education
   [2017R1D1A1B03035453]; National Cancer Institute of the NIH
   [P30CA034196]; Ewha Womans University
FX This work was supported by Gil Hospital Research Grant (Grant No.
   GCU-2015-5092); the Korean Healthcare Technology R&D project through the
   Korean Health Industry Development Institute (KHIDI) funded by the
   Ministry of Health & Welfare, Republic of Korea (Grant No. HI13C2148);
   the International Research & Development Program of the National
   Research Foundation of Korea (NRF) funded by the Ministry of Science,
   ICT & Future Planning (Grant No. 2015K1A4A3047851); the National
   Research Foundation of Korea (NRF) grant funded by the Korea government
   (MSIP; Grant No. 2016R1E1A1A01943469 and 2017R1C1B2002183); the Basic
   Science Research Program through the National Research Foundation of
   Korea (NRF) funded by the Ministry of Education (Grant No.
   2017R1D1A1B03035453); and the National Cancer Institute of the NIH
   (Grant No. P30CA034196). C. Lee is a distinguished Ewha Womans
   University Professor supported in part by the Ewha Womans University
   Research grant of 2018.
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NR 50
TC 10
Z9 11
U1 0
U2 4
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1078-0432
EI 1557-3265
J9 CLIN CANCER RES
JI Clin. Cancer Res.
PD MAY 1
PY 2019
VL 25
IS 9
BP 2821
EP 2834
DI 10.1158/1078-0432.CCR-18-3460
PG 14
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA HW5ZM
UT WOS:000466767900016
PM 30670495
OA Green Submitted, Green Accepted, Bronze
DA 2025-01-04
ER

PT J
AU Andersson, A
   Conde, ME
   Surova, O
   Vermeulen, P
   Wählby, C
   Nilsson, M
   Nyström, H
AF Andersson, Axel
   Escriva Conde, Maria
   Surova, Olga
   Vermeulen, Peter
   Wahlby, Carolina
   Nilsson, Mats
   Nystrom, Hanna
TI Spatial Transcriptome Mapping of the Desmoplastic Growth Pattern of
   Colorectal Liver Metastases by <i>In Situ</i> Sequencing Reveals a
   Biologically Relevant Zonation of the Desmoplastic Rim
SO CLINICAL CANCER RESEARCH
LA English
DT Article
ID CANCER; ANGIOGENESIS; EXPRESSION; KEY
AB Purpose: We describe the fibrotic rim formed in the desmoplastic histopathologic growth pattern (DHGP) of colorectal cancer liver metastasis (CLM) using in situ sequencing (ISS). The origin of the desmoplastic rim is still a matter of debate, and the detailed cellular organization has not yet been fully elucidated. Understanding the biology of the DHGP in CLM can lead to targeted treatment and improve survival. Experimental Design: We used ISS, targeting 150 genes, to characterize the desmoplastic rim by unsupervised clustering of gene coexpression patterns. The cohort comprised 10 chemo-na & iuml;ve liver metastasis resection samples with a DHGP. Results: Unsupervised clustering of spatially mapped genes revealed molecular and cellular diversity within the desmoplastic rim. We confirmed the presence of the ductular reaction and cancer-associated fibroblasts. Importantly, we discovered angiogenesis and outer and inner zonation in the rim, characterized by nerve growth factor receptor and periostin expression. Conclusions: ISS enabled the analysis of the cellular organization of the fibrous rim surrounding CLM with a DHGP and suggests a transition from the outer part of the rim, with nonspecific liver injury response, into the inner part, with gene expression indicating collagen synthesis and extracellular matrix remodeling influenced by the interaction with cancer cells, creating a cancer cell-supportive environment. Moreover, we found angiogenic processes in the rim. Our results provide a potential explanation of the origin of the rim in DHGP and lead to exploring novel targeted treatments for patients with CLM to improve survival.
C1 [Andersson, Axel; Wahlby, Carolina] Uppsala Univ, Dept Informat Technol, Sci Life Lab, Uppsala, Sweden.
   [Escriva Conde, Maria; Surova, Olga; Nilsson, Mats] Stockholm Univ, Dept Biochem & Biophys, Sci Life Lab, Solna, Sweden.
   [Vermeulen, Peter] GZA Hosp Sint Augustinus, Translat Canc Res Unit, Antwerp, Belgium.
   [Nystrom, Hanna] Umea Univ, Dept Surg & Perioperat Sci, Surg, Umea, Sweden.
   [Nystrom, Hanna] Umea Univ, Wallenberg Ctr Mol Med, Umea, Sweden.
C3 Uppsala University; Stockholm University; Umea University; Umea
   University
RP Nyström, H (corresponding author), Norrlands Univ Sjukhus, Kirurgcentrum, S-90185 Umea, Sweden.
EM hanna.nystrom@umu.se
OI Vermeulen, Peter/0000-0002-5676-3141; Wahlby,
   Carolina/0000-0002-4139-7003; Andersson, Axel/0000-0002-4714-3127;
   Nilsson, Mats/0000-0001-9985-0387
FU SciLifeLab; National Microscopy Infrastructure; Chan Zuckerberg
   Initiative; Science for Life Laboratory, Sweden; Swedish Cancer Society;
   Wallenberg Foundations/Knut and Alice Wallenbergs Stiftelse [2021/1726];
   Vaesterbotten County Council; Cancerforskningsfonden Norrland; Umea
   University; U-CAN Umea; U-CAN Uppsala; Swedish Research Council
   [2019-01238]; European Research Council via ERC Consolidator grant [CoG
   682810]; Technology Development Project from SciLifeLab; Swedish
   Research Council [2019-01238] Funding Source: Swedish Research Council
FX We thank Anette Berglund for skillful technical assistance; Christophe
   Avenel and Fredrik Nysjoe from the SciLifeLab Bioimage Informatics Unit
   (a unit of the National Bioinformatics Infrastructure Sweden, with
   funding from SciLifeLab, the National Microscopy Infrastructure, and the
   Chan Zuckerberg Initiative) for providing support on data handling and
   visualization in TissUUmaps; and Erik Wernersson from Karolinska
   Institutet for fruitful discussions about image restoration. We thank
   the in situ sequencing facility unit, part of the spatial biology
   platform, funded by Science for Life Laboratory, Sweden, for technical
   assistance with the ISS experiments. This research was funded by The
   Swedish Cancer Society (H. Nystroem and M. Nilsson), Wallenberg
   Foundations/Knut and Alice Wallenbergs Stiftelse (H. Nystroem and M.
   Nilsson: 2021/1726), Vaesterbotten County Council (H. Nystroem),
   Cancerforskningsfonden Norrland (H. Nystroem), Umea University (H.
   Nystroem), U-CAN Umea (H. Nystroem), U-CAN Uppsala (M. Nilsson), the
   Swedish Research Council (M. Nilsson: 2019-01238), the European Research
   Council via ERC Consolidator grant CoG 682810 (C. Waehlby), and a
   Technology Development Project from SciLifeLab (C. Waehlby).
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NR 60
TC 1
Z9 1
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1078-0432
EI 1557-3265
J9 CLIN CANCER RES
JI Clin. Cancer Res.
PD OCT 1
PY 2024
VL 30
IS 19
BP 4517
EP 4529
DI 10.1158/1078-0432.CCR-23-3461
PG 13
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA H8K5V
UT WOS:001325875500025
PM 39052239
OA Green Published, hybrid
DA 2025-01-04
ER

PT J
AU Cannarile, MA
   Weisser, M
   Jacob, W
   Jegg, AM
   Ries, CH
   Rüttinger, D
AF Cannarile, Michael A.
   Weisser, Martin
   Jacob, Wolfgang
   Jegg, Anna-Maria
   Ries, Carola H.
   Ruettinger, Dominik
TI Colony-stimulating factor 1 receptor (CSF1R) inhibitors in cancer
   therapy
SO JOURNAL FOR IMMUNOTHERAPY OF CANCER
LA English
DT Review
DE CSF1; CSF1R; Tumor-associated macrophage; Clinical trial; Cancer
   therapy; PVNS; Dt-GCT
ID TUMOR-ASSOCIATED MACROPHAGES; RHEUMATOID-ARTHRITIS; COLORECTAL-CANCER;
   CSF-1R INHIBITOR; FETAL MONOCYTES; CELL; BLOCKADE; NIVOLUMAB; ANTIBODY;
   GROWTH
AB fueled interest in therapeutically targeting these cells. In this context, the colony-stimulating factor 1 ( CSF1)/ colony-stimulating factor 1 receptor (CSF1R) axis has gained the most attention, and various approaches targeting either the ligands or the receptor are currently in clinical development. Emerging data on the tolerability of CSF1/ CSF1R-targeting agents suggest a favorable safety profile, making them attractive combination partners for both standard treatment modalities and immunotherapeutic agents. The specificity of these agents and their potent blocking activity has been substantiated by impressive response rates in diffuse-type tenosynovial giant cell tumors, a benign connective tissue disorder driven by CSF1 in an autocrine fashion. In the malignant disease setting, data on the clinical activity of immunotherapy combinations with CSF1/ CSF1R-targeting agents are pending. As our knowledge of macrophage biology expands, it becomes apparent that the complex phenotypic and functional properties of macrophages are heavily influenced by a continuum of survival, differentiation, recruitment, and polarization signals within their specific tissue environment. Thus, the role of macrophages in regulating tumorigenesis and the impact of depleting and/or reprogramming TAM as therapeutic approaches for cancer patients may vary greatly depending on organ-specific characteristics of these cells. We review the currently available clinical safety and efficacy data with CSF1/CSF1R-targeting agents and provide a comprehensive overview of ongoing clinical studies. Furthermore, we discuss the local tissue macrophage and tumor-type specificities and their potential impact on CSF1/CSF1R-targeting treatment strategies for the future.
C1 [Cannarile, Michael A.; Weisser, Martin; Jacob, Wolfgang; Jegg, Anna-Maria; Ries, Carola H.; Ruettinger, Dominik] Roche Innovat Ctr Munich, Roche Pharmaceut Res & Early Dev, Nonnenwald 2, D-82377 Penzberg, Germany.
RP Cannarile, MA (corresponding author), Roche Innovat Ctr Munich, Roche Pharmaceut Res & Early Dev, Nonnenwald 2, D-82377 Penzberg, Germany.
EM Michael.cannarile@roche.com
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TC 715
Z9 800
U1 9
U2 114
PU BMJ PUBLISHING GROUP
PI LONDON
PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND
EI 2051-1426
J9 J IMMUNOTHER CANCER
JI J. Immunother. Cancer
PD JUL 18
PY 2017
VL 5
AR 53
DI 10.1186/s40425-017-0257-y
PG 13
WC Oncology; Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Immunology
GA FB1HB
UT WOS:000405893200001
PM 28716061
OA gold, Green Published
HC Y
HP N
DA 2025-01-04
ER

PT J
AU Miyamoto, S
   Hirohashi, Y
   Morita, R
   Miyazaki, A
   Ogi, K
   Kanaseki, T
   Ide, K
   Shirakawa, J
   Tsukahara, T
   Murai, A
   Sasaya, T
   Koike, K
   Kina, S
   Kawano, T
   Goto, T
   Ntege, EH
   Shimizu, Y
   Torigoe, T
AF Miyamoto, Sho
   Hirohashi, Yoshihiko
   Morita, Rena
   Miyazaki, Akihiro
   Ogi, Kazuhiro
   Kanaseki, Takayuki
   Ide, Kentaro
   Shirakawa, Jumpei
   Tsukahara, Tomohide
   Murai, Aiko
   Sasaya, Takashi
   Koike, Kazushige
   Kina, Shinichiro
   Kawano, Toshihiro
   Goto, Takahiro
   Ntege, Edward Hosea
   Shimizu, Yusuke
   Torigoe, Toshihiko
TI Exploring olfactory receptor family 7 subfamily C member 1 as a novel
   oral cancer stem cell target for immunotherapy
SO CANCER SCIENCE
LA English
DT Article
DE cancer immunotherapy; cancer stem cell; OR7C1; oral cancer; peptide
   vaccine
ID LOCALLY ADVANCED HEAD; INITIATING CELLS; ACQUIRED-RESISTANCE;
   LUNG-CANCER; IDENTIFICATION; RADIOTHERAPY; CARCINOMA; CETUXIMAB; GROWTH;
   CISPLATIN
AB The mortality rate of oral cancer has not improved over the past three decades despite remarkable advances in cancer therapies. Oral cancers contain a subpopulation of cancer stem cells (CSCs) that share characteristics associated with normal stem cells, including self-renewal and multi-differentiation potential. CSCs are tumorigenic, play a critical role in cancer infiltration, recurrence, and distant metastasis, and significantly contribute to drug resistance to current therapeutic strategies, including immunotherapy. Cytotoxic CD8+ T lymphocytes (CTLs) are key immune cells that effectively recognize peptide antigens presented by the major histocompatibility complex class I molecules. Increasing evidence suggests that cancer antigen-specific targeting by CTLs effectively regulates CSCs that drive cancer progression. In this study, we utilized data from public domains and performed various bioassays on human oral squamous cell carcinoma clinical samples and cell lines, including HSC-2 and HSC-3, to investigate the potential role of olfactory receptor family 7 subfamily C member 1 (OR7C1), a seven transmembrane G-protein-coupled olfactory receptor that is also expressed in nonolfactory tissues and was previously reported as a novel marker and target of colon cancer initiating cell-targeted immunotherapy, in CSC-targeted treatment against oral cancer. We found that the OR7C1 gene was expressed only in oral CSCs, and that CTLs reacted with human leukocyte antigen-A24-restricted OR7C1 oral CSC-specific peptides. Taken together, our findings suggest that OR7C1 represents a novel target for potent CSC-targeted immunotherapy in oral cancer.
C1 [Miyamoto, Sho; Miyazaki, Akihiro; Ogi, Kazuhiro; Sasaya, Takashi; Koike, Kazushige] Sapporo Med Univ, Dept Oral Surg, Sch Med, Sapporo, Japan.
   [Hirohashi, Yoshihiko; Kanaseki, Takayuki; Tsukahara, Tomohide; Murai, Aiko; Sasaya, Takashi; Torigoe, Toshihiko] Sapporo Med Univ, Dept Pathol, Sch Med, Sapporo, Japan.
   [Morita, Rena] Hlth Sci Univ Hokkaido, Sch Nursing & Social Serv, Div Fundamental Hlth Sci, Tobetsu, Japan.
   [Ide, Kentaro; Shirakawa, Jumpei; Kawano, Toshihiro; Goto, Takahiro; Ntege, Edward Hosea] Univ Ryukyus, Grad Sch Med, Dept Oral & Maxillofacial Funct Rehabil, Nishihara, Japan.
   [Kina, Shinichiro] Gunma Univ, Ctr Med Educ, Grad Sch Med, Maebashi, Japan.
   [Ntege, Edward Hosea; Shimizu, Yusuke] Univ Ryukyus, Grad Sch Med, Dept Plast & Reconstruct Surg, Nishihara, Japan.
   [Miyamoto, Sho] Sapporo Med Univ, Dept Oral Surg, Sch Med, South 1 West 16,Chuo Ku, Sapporo 0608543, Japan.
C3 Sapporo Medical University; Sapporo Medical University; Health Sciences
   University of Hokkaido; University of the Ryukyus; Gunma University;
   University of the Ryukyus
RP Miyamoto, S (corresponding author), Sapporo Med Univ, Dept Oral Surg, Sch Med, South 1 West 16,Chuo Ku, Sapporo 0608543, Japan.
EM miyamoto.sho@sapmed.ac.jp
RI Shimizu, Yusuke/AHD-8342-2022; Kanaseki, Takayuki/LKK-0993-2024; Ntege,
   Edward/AAT-1107-2020; Hirohashi, Yoshihiko/AFQ-4227-2022
OI Ntege, Edward H./0000-0003-2388-4542; Kanaseki,
   Takayuki/0000-0001-7294-6880; Miyamoto, Sho/0000-0001-9573-1161;
   SHIMIZU, YUSUKE/0000-0002-2528-2003
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NR 51
TC 1
Z9 1
U1 3
U2 6
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1347-9032
EI 1349-7006
J9 CANCER SCI
JI Cancer Sci.
PD SEP
PY 2023
VL 114
IS 9
BP 3496
EP 3508
DI 10.1111/cas.15873
EA JUN 2023
PG 13
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA S2XO1
UT WOS:001019130500001
PM 37344992
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Obaid, G
   Chambrier, I
   Cook, MJ
   Russell, DA
AF Obaid, Girgis
   Chambrier, Isabelle
   Cook, Michael J.
   Russell, David A.
TI Cancer targeting with biomolecules: a comparative study of photodynamic
   therapy efficacy using antibody or lectin conjugated phthalocyanine-PEG
   gold nanoparticles
SO PHOTOCHEMICAL & PHOTOBIOLOGICAL SCIENCES
LA English
DT Article
ID BREAST-CANCER; SINGLET OXYGEN; MONOCLONAL-ANTIBODY; DRUG-DELIVERY;
   RECEPTOR; COLON; HEMATOPORPHYRIN; LOCALIZATION; PATHWAY; LIGAND
AB The functionalisation of therapeutic nanoparticle constructs with cancer-specific biomolecules can enable selective tumour accumulation and targeted treatment. Water soluble gold nanoparticles (ca. 4 nm) stabilised by a mixed monolayer of a hydrophobic zinc phthalocyanine photosensitiser (C11Pc) and hydrophilic polyethylene glycol (PEG) have been prepared. The C11Pc-PEG gold nanoparticle constructs were further functionalised with jacalin, a lectin specific for the cancer-associated Thomsen-Friedenreich (T) carbohydrate antigen, or with monoclonal antibodies specific for the human epidermal growth factor receptor-2 (HER-2). The two biofunctionalised nanoparticle conjugates produced similar levels of singlet oxygen upon irradiation at 633 nm. Importantly, both nanoparticle conjugates demonstrated extensive, yet comparable, phototoxicity in HT-29 colorectal adenocarcinoma cells (80-90%) and in SK-BR-3 breast adenocarcinoma cells (>99%). Non-conjugated C11Pc-PEG gold nanoparticles were only minimally phototoxic. Lysosomal colocalisation studies performed with the HT-29 colon cancer cells and the SK-BR-3 breast cancer cells revealed that both nanoparticle conjugates were partially localised within acidic organelles, which is typical of receptor-mediated endocytosis. The similarity of the targeted PDT efficacy of the two biofunctionalised C11Pc-PEG gold nanoparticles is discussed with respect to targeting ligand binding affinity and cell surface antigen density as key determinants of targeting efficiency. This study highlights how targeting small cell-surface molecules, such as the T antigen, can mediate a selective photodynamic treatment response which is similar to that achieved when targeting overexpressed protein receptors, such as HER-2. The high prevalence of the T antigen present on the cellular surface of primary tumours emphasises the broad potential applications for lectin-targeted therapies.
C1 [Obaid, Girgis; Chambrier, Isabelle; Cook, Michael J.; Russell, David A.] Univ E Anglia, Sch Chem, Norwich NR4 7TJ, Norfolk, England.
C3 University of East Anglia
RP Russell, DA (corresponding author), Univ E Anglia, Sch Chem, Norwich Res Pk, Norwich NR4 7TJ, Norfolk, England.
EM d.russell@uea.ac.uk
OI Obaid, Girgis/0000-0002-9452-4467
FU EPSRC
FX The authors are grateful to the EPSRC for a post-graduate studentship
   for G.O. and to Dr Paul Thomas for assistance with the confocal
   microscopy.
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NR 46
TC 111
Z9 116
U1 0
U2 97
PU SPRINGERNATURE
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON, N1 9XW, ENGLAND
SN 1474-905X
EI 1474-9092
J9 PHOTOCH PHOTOBIO SCI
JI Photochem. Photobiol. Sci.
PY 2015
VL 14
IS 4
BP 737
EP 747
DI 10.1039/c4pp00312h
PG 11
WC Biochemistry & Molecular Biology; Biophysics; Chemistry, Physical
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Biophysics; Chemistry
GA CF1DF
UT WOS:000352283100010
PM 25604735
DA 2025-01-04
ER

PT J
AU Zhu, LQ
   Yu, QF
   Li, YH
   Zhang, M
   Peng, ZW
   Wang, S
   Quan, ZY
   Gao, D
AF Zhu, Lingqin
   Yu, Qiongfang
   Li, Yuanheng
   Zhang, Meng
   Peng, Zhiwei
   Wang, Song
   Quan, Ziyi
   Gao, Dian
TI SKAP1 Is a Novel Biomarker and Therapeutic Target for Gastric Cancer:
   Evidence from Expression, Functional, and Bioinformatic Analyses
SO INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
LA English
DT Article
DE gastric cancer; SKAP1; JAK; PI3K; AKT axis; proliferation; invasion;
   migration; immunity
ID POOR-PROGNOSIS; PROTEIN; INNATE; IMMUNITY; BINDING
AB Gastric cancer (GC) is the third leading cause of cancer-related death worldwide. Due to the lack of early symptoms, GC is often diagnosed at an advanced stage when treatment options are limited. There is an urgent need to identify biomarkers for early detection, prognosis evaluation, and targeted treatment of GC. Studies have shown that Src kinase-associated phosphoprotein 1 (SKAP1) promotes cell proliferation and invasion and is associated with poor prognosis in colorectal cancer, malignant fibrous histiocytoma, and breast cancer. However, the role and mechanism of SKAP1 in GC are unclear. Here, analyses of multiple databases and experiments revealed that SKAP1 expression was higher in GC than in adjacent normal tissues. The Cancer Genome Atlas data showed that high SKAP1 expression was associated with poor GC prognosis. SKAP1 expression was higher in GC than in normal gastric epithelial cells. SKAP1 silencing reduced the proliferation, migration and invasion of the GC cell lines MKN45 and HGC27. Rescue experiments suggest that SKAP1 may promote GC progression by activating JAK1/PI3K/AKT signaling and regulating GC cell proliferation, invasion, migration, and other functions. Bioinformatics analysis revealed that SKAP1 was associated with immune cell infiltration and checkpoint expression in GC. High SKAP1 expression was associated with poorer immunotherapy outcomes, suggesting its potential as a predictive biomarker of GC immunotherapy efficacy. In summary, SKAP1 is overexpressed in GC, where it promotes cell proliferation, invasion and migration and is associated with poor prognosis and poor immunotherapy outcomes. SKAP1 may represent a biomarker and therapeutic target in GC and regulates cellular functions through JAK1/PI3K/AKT signaling.
C1 [Zhu, Lingqin; Yu, Qiongfang; Wang, Song] Nanchang Univ, Affiliated Hosp 2, Dept Gastroenterol & Hepatol, Nanchang 330006, Peoples R China.
   [Li, Yuanheng] Nanchang Univ, Queen Mary Sch, Nanchang 330031, Peoples R China.
   [Zhang, Meng; Peng, Zhiwei; Quan, Ziyi; Gao, Dian] Nanchang Univ, Dept Pathogen Biol & Immunol, Med Coll, Nanchang 330006, Peoples R China.
C3 Nanchang University; Nanchang University; Nanchang University
RP Gao, D (corresponding author), Nanchang Univ, Dept Pathogen Biol & Immunol, Med Coll, Nanchang 330006, Peoples R China.
EM lqzhu@email.ncu.edu.cn; qiongfangyu@yeah.net;
   217121235@email.ncu.edu.cn; zhangmeng@ncu.edu.cn;
   zhiweipengjc@ncu.edu.cn; ws2773719169@163.com; 18070132515@163.com;
   gaodian@ncu.edu.cn
RI Li, Yuanheng/V-1073-2019; GAO, DIAN/E-4494-2014
OI Gao, Dian/0000-0002-9391-1756
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NR 42
TC 3
Z9 3
U1 4
U2 11
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
SN 1661-6596
EI 1422-0067
J9 INT J MOL SCI
JI Int. J. Mol. Sci.
PD JUL
PY 2023
VL 24
IS 14
AR 11870
DI 10.3390/ijms241411870
PG 20
WC Biochemistry & Molecular Biology; Chemistry, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Chemistry
GA N3FJ0
UT WOS:001035908800001
PM 37511629
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Schneider, MA
   Eden, J
   Pache, B
   Laminger, F
   Lopez-Lopez, V
   Steffen, T
   Hübner, M
   Kober, F
   Roka, S
   Campos, PC
   Roth, L
   Gupta, A
   Siebenhüner, A
   Kepenekian, V
   Passot, G
   Gertsch, P
   Glehen, O
   Lehmann, K
AF Schneider, Marcel Andre
   Eden, Janina
   Pache, Basile
   Laminger, Felix
   Lopez-Lopez, Victor
   Steffen, Thomas
   Hubner, Martin
   Kober, Friedrich
   Roka, Sebastian
   Campos, Pedro Cascales
   Roth, Lilian
   Gupta, Anurag
   Siebenhuner, Alexander
   Kepenekian, Vahan
   Passot, Guillaume
   Gertsch, Philippe
   Glehen, Olivier
   Lehmann, Kuno
TI Mutations of <i>RAS</i>/<i>RAF</i> Proto-oncogenes Impair Survival After
   Cytoreductive Surgery and HIPEC for Peritoneal Metastasis of Colorectal
   Origin
SO ANNALS OF SURGERY
LA English
DT Article
DE colorectal carcinoma; cytoreductive surgery (CRS); hyperthermic
   intraperitoneal chemotherapy (HIPEC); KRAS/NRAS/BRAF; peritoneal
   metastasis
ID INTRAPERITONEAL CHEMOTHERAPY; POSTOPERATIVE COMPLICATIONS; PROGNOSTIC
   NOMOGRAM; PREDICTION MODEL; LIVER RESECTION; KRAS STATUS; STAGE-II;
   CANCER; BRAF; CARCINOMATOSIS
AB Background: Adequate selection of patients with peritoneal metastasis (PM) for cytoreductive surgery (CRS) and hyperthermic intraperitoneal chemotherapy (HIPEC) remains critical for successful long-term outcomes. Factors reflecting tumor biology are currently poorly represented in the selection process. The prognostic relevance of RAS/RAF mutations in patients with PM remains unclear.
   Methods: Survival data of patients with colorectal PM operated in 6 European tertiary centers were retrospectively collected and predictive factors for survival identified by Cox regression analyses. A simple point-based risk score was developed to allow patient selection and outcome prediction.
   Results: Data of 524 patients with a median age of 59 years and a median peritoneal cancer index of 7 (interquartile range: 3-12) were collected. A complete resection was possible in 505 patients; overall morbidity and 90-day mortality were 50.9% and 2.1%, respectively. PCI [hazard ratio (HR): 1.08], N1 stage (HR: 2.15), N2 stage (HR: 2.57), G3 stage (HR: 1.80) as well as KRAS (HR: 1.46) and BRAF (HR: 3.97) mutations were found to significantly impair survival after CRS/HIPEC on multivariate analyses. Mutations of RAS/RAF impaired survival independently of targeted treatment against EGFR. Consequently, a simple point-based risk score termed BIOSCOPE (BIOlogical Score of COlorectal PEritoneal metastasis) based on PCI, N-, G-, and RAS/RAF status was developed, which showed good discrimination [development area under the curve (AUC) = 0.72, validation AUC = 0.70], calibration (P = 0.401) and allowed categorization of patients into 4 groups with strongly divergent survival outcomes.
   Conclusion: RAS/RAF mutations impair survival after CRS/HIPEC. The novel BIOSCOPE score reflects tumor biology, adequately stratifies longterm outcomes, and improves patient assessment and selection.
C1 [Schneider, Marcel Andre; Roth, Lilian; Gupta, Anurag; Gertsch, Philippe; Lehmann, Kuno] Univ Hosp Zurich, Dept Surg & Transplantat, Raemistr 100, CH-8091 Zurich, Switzerland.
   [Eden, Janina; Steffen, Thomas] Cantonal Hosp St Gallen, Dept Surg, St Gallen, Switzerland.
   [Pache, Basile; Hubner, Martin] Lausanne Univ Hosp CHUV, Dept Surg, Lausanne, Switzerland.
   [Laminger, Felix; Kober, Friedrich; Roka, Sebastian] Hanusch Hosp, Ctr Peritoneal Carcinomatosis, Dept Surg, Vienna, Austria.
   [Lopez-Lopez, Victor; Campos, Pedro Cascales] Hosp Clin Univ Virgen Arrixaca, Dept Surg, Murcia, Spain.
   [Siebenhuner, Alexander] Univ Hosp Zurich, Dept Med Oncol, Zurich, Switzerland.
   [Kepenekian, Vahan; Passot, Guillaume; Glehen, Olivier] Univ Hosp Lyon, Dept Digest Surg & Surg Oncol, Lyon, France.
C3 University of Zurich; University Zurich Hospital; Kantonsspital St.
   Gallen; University of Lausanne; Centre Hospitalier Universitaire Vaudois
   (CHUV); WGKK - Hanusch Hospital; Hospital Clinico Universitario Virgen
   de la Arrixaca; University of Zurich; University Zurich Hospital; CHU
   Lyon
RP Lehmann, K (corresponding author), Univ Hosp Zurich, Dept Surg & Transplantat, Raemistr 100, CH-8091 Zurich, Switzerland.
EM Kuno.Lehmann@usz.ch
RI Passot, Guillaume/K-6271-2012; Steffen, Thomas/HKW-6395-2023; Lehmann,
   Kuno/M-8504-2016; Kepenekian, Vahan/AFF-8361-2022; Schneider, Marcel
   Andre/AAW-9712-2020; hubner, martin/J-6715-2017
OI Glehen, Olivier/0000-0002-2802-4974; Roka,
   Sebastian/0000-0002-9888-5892; Laminger, Felix/0000-0003-2349-4050;
   Gupta, Anurag/0000-0001-6850-3489; Lehmann, Kuno/0000-0002-6177-9543;
   Kepenekian, Vahan/0000-0001-9885-8600; Schneider, Marcel
   Andre/0000-0002-6723-8879; Pache, Basile/0000-0003-0969-7345; Steffen,
   Thomas/0000-0001-9374-5703; hubner, martin/0000-0002-4521-8279
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NR 40
TC 85
Z9 88
U1 0
U2 6
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 0003-4932
EI 1528-1140
J9 ANN SURG
JI Ann. Surg.
PD NOV
PY 2018
VL 268
IS 5
BP 845
EP 853
DI 10.1097/SLA.0000000000002899
PG 9
WC Surgery
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Surgery
GA HD6PL
UT WOS:000452663900019
PM 30303876
OA Green Published
DA 2025-01-04
ER

PT J
AU Montaño-Samaniego, M
   Bravo-Estupiñan, DM
   Méndez-Guerrero, O
   Alarcón-Hernández, E
   Ibáñez-Hernández, M
AF Montano-Samaniego, Mariela
   Bravo-Estupinan, Diana M.
   Mendez-Guerrero, Oscar
   Alarcon-Hernandez, Ernesto
   Ibanez-Hernandez, Miguel
TI Strategies for Targeting Gene Therapy in Cancer Cells With
   Tumor-Specific Promoters
SO FRONTIERS IN ONCOLOGY
LA English
DT Review
DE cancer; gene therapy; targeted treatment; specific promoters; non-viral
   vectors
ID COLORECTAL-CANCER; SUICIDE GENE; HEPATOCELLULAR-CARCINOMA; EXPRESSION;
   DELIVERY; COMBINATION; BIOMARKERS; GROWTH; SIRNA; THERAPEUTICS
AB Cancer is the second cause of death worldwide, surpassed only by cardiovascular diseases, due to the lack of early diagnosis, and high relapse rate after conventional therapies. Chemotherapy inhibits the rapid growth of cancer cells, but it also affects normal cells with fast proliferation rate. Therefore, it is imperative to develop other safe and more effective treatment strategies, such as gene therapy, in order to significantly improve the survival rate and life expectancy of patients with cancer. The aim of gene therapy is to transfect a therapeutic gene into the host cells to express itself and cause a beneficial biological effect. However, the efficacy of the proposed strategies has been insufficient for delivering the full potential of gene therapy in the clinic. The type of delivery vehicle (viral or non viral) chosen depends on the desired specificity of the gene therapy. The first gene therapy trials were performed with therapeutic genes driven by viral promoters such as the CMV promoter, which induces non-specific toxicity in normal cells and tissues, in addition to cancer cells. The use of tumor-specific promoters over-expressed in the tumor, induces specific expression of therapeutic genes in a given tumor, increasing their localized activity. Several cancer- and/or tumor-specific promoters systems have been developed to target cancer cells. This review aims to provide up-to-date information concerning targeting gene therapy with cancer- and/or tumor-specific promoters including cancer suppressor genes, suicide genes, anti-tumor angiogenesis, gene silencing, and gene-editing technology, as well as the type of delivery vehicle employed. Gene therapy can be used to complement traditional therapies to provide more effective treatments.
C1 [Montano-Samaniego, Mariela; Bravo-Estupinan, Diana M.; Mendez-Guerrero, Oscar; Ibanez-Hernandez, Miguel] Inst Politecn Nacl, Escuela Nacl Ciencias Biol, Dept Bioquim, Lab Terapia Genica, Mexico City, DF, Mexico.
   [Alarcon-Hernandez, Ernesto] Inst Politecn Nacl, Escuela Nacl Ciencias Biol, Dept Bioquim, Lab Genet Mol, Mexico City, DF, Mexico.
C3 Instituto Politecnico Nacional - Mexico; Instituto Politecnico Nacional
   - Mexico
RP Ibáñez-Hernández, M (corresponding author), Inst Politecn Nacl, Escuela Nacl Ciencias Biol, Dept Bioquim, Lab Terapia Genica, Mexico City, DF, Mexico.
EM mibanez@ipn.mx
OI Bravo Estupinan, Diana Marcela/0009-0000-0416-9290; Ibanez Hernandez,
   Miguel Angel Antonio/0000-0003-4013-6888
FU COFAA-IPN [20200448]
FX Funding obtained from COFAA-IPN, linked to SIP project #20200448:
   Evaluacio ' n de la transfeccio ' n con liposomas que contienen un nuevo
   li ' pido catio ' nico y determinacion de la direccionalidad de la
   expresio ' n gene ' tica.
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NR 207
TC 74
Z9 79
U1 4
U2 49
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 2234-943X
J9 FRONT ONCOL
JI Front. Oncol.
PD DEC 14
PY 2020
VL 10
AR 605380
DI 10.3389/fonc.2020.605380
PG 18
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA PK6SY
UT WOS:000602573300001
PM 33381459
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Thapa, R
   Afzal, O
   Gupta, G
   Bhat, AA
   Almalki, WH
   Alzarea, SI
   Kazmi, I
   Altamimi, ASA
   Subramaniyan, V
   Thangavelu, L
   Singh, SK
   Dua, K
AF Thapa, Riya
   Afzal, Obaid
   Gupta, Gaurav
   Bhat, Asif Ahmad
   Almalki, Waleed Hassan
   Alzarea, Sami I.
   Kazmi, Imran
   Altamimi, Abdulmalik Saleh Alfawaz
   Subramaniyan, Vetriselvan
   Thangavelu, Lakshmi
   Singh, Sachin Kumar
   Dua, Kamal
TI Unveiling the connection: Long-chain non-coding RNAs and critical
   signaling pathways in breast cancer
SO PATHOLOGY RESEARCH AND PRACTICE
LA English
DT Review
DE LncRNA; Breast cancer; NF-kappa B; TGF-beta; Wnt/beta-catenin; Notch
ID EPITHELIAL-MESENCHYMAL TRANSITION; SQUAMOUS-CELL CARCINOMA; PROMOTES
   PROLIFERATION; COLORECTAL-CANCER; DOWN-REGULATION;
   HEPATOCELLULAR-CARCINOMA; INHIBITS PROLIFERATION; PI3K/AKT/MTOR PATHWAY;
   CCAT2 PROMOTES; LNCRNA HOTAIR
AB Breast cancer is a complex and diverse condition that disrupts multiple signaling pathways essential for cell proliferation, survival, and differentiation. Recently, the significant involvement of long-chain non-coding RNAs (lncRNAs) in controlling key signaling pathways associated with breast cancer development has been discovered. This review aims to explore the interaction between lncRNAs and various pathways, including the AKT/PI3K/ mTOR, Wnt/beta-catenin, Notch, DNA damage response, TGF-beta, Hedgehog, and NF-kappa B signaling pathways, to gain a comprehensive understanding of their roles in breast cancer. The AKT/PI3K/mTOR pathway regulates cell growth, survival, and metabolic function. Recent data suggests that specific lncRNAs can influence the functioning of this pathway, acting as either oncogenes or tumor suppressors. Dysregulation of this pathway is commonly observed in breast cancer cases. Moreover, breast cancer development has been associated with other pathways such as Wnt/beta-catenin, Notch, TGF-beta, Hedgehog, and NF-kappa B. Emerging studies have identified lncRNAs that modulate breast cancer's growth, progression, and metastasis by interacting with these pathways. To advance the development of innovative diagnostic tools and targeted treatment options, it is crucial to comprehend the intricate relationship between lncRNAs and vital signaling pathways in breast cancer. By fully harnessing the therapeutic potential of lncRNAs, there is a possibility of developing more effective and personalized therapy choices for breast cancer patients. Further investigation is necessary to comprehensively understand the role of lncRNAs within breast cancer signaling pathways and fully exploit their therapeutic potential.
C1 [Thapa, Riya; Gupta, Gaurav; Bhat, Asif Ahmad] Suresh Gyan Vihar Univ, Sch Pharm, Mahal Rd, Jaipur, India.
   [Afzal, Obaid; Altamimi, Abdulmalik Saleh Alfawaz] Prince Sattam Bin Abdulaziz Univ, Coll Pharm, Dept Pharmaceut Chem, Al Kharj 11942, Saudi Arabia.
   [Gupta, Gaurav] Uttaranchal Univ, Uttaranchal Inst Pharmaceut Sci, Dehra Dun, India.
   [Almalki, Waleed Hassan] Umm Al Qura Univ, Coll Pharm, Dept Pharmacol, Mecca, Saudi Arabia.
   [Alzarea, Sami I.] Jouf Univ, Coll Pharm, Dept Pharmacol, Sakaka, Al Jouf, Saudi Arabia.
   [Kazmi, Imran] King Abdulaziz Univ, Fac Sci, Dept Biochem, Jeddah, Saudi Arabia.
   [Subramaniyan, Vetriselvan] MONASH Univ, Jeffrey Cheah Sch Med & Hlth Sci, Dept Pharmacol, Clayton, Malaysia.
   [Thangavelu, Lakshmi] Saveetha Univ, Saveetha Inst Med & Tech Sci, Saveetha Med Coll, Ctr Global Hlth Res, Chennai, India.
   [Singh, Sachin Kumar] Lovely Profess Univ, Sch Pharmaceut Sci, Phagwara 144411, India.
   [Singh, Sachin Kumar; Dua, Kamal] Univ Technol, Fac Hlth, Australian Res Ctr Complementary & Integrat Med, Ultimo, NSW 2007, Australia.
   [Dua, Kamal] Univ Technol, Discipline Pharm, Grad Sch Hlth, Ultimo, NSW 2007, Australia.
   [Gupta, Gaurav] Graph Era Hill Univ, Sch Pharm, Dehra Dun 248007, India.
C3 Prince Sattam Bin Abdulaziz University; Uttaranchal University; Umm Al
   Qura University; Al Jouf University; King Abdulaziz University; Saveetha
   Institute of Medical & Technical Science; Saveetha Medical College &
   Hospital; Lovely Professional University; University of Technology
   Sydney; University of Technology Sydney
RP Thangavelu, L (corresponding author), Saveetha Univ, Saveetha Inst Med & Tech Sci, Saveetha Med Coll, Ctr Global Hlth Res, Chennai, India.
EM drlakshmi.thangavelu25@gmail.com
RI Thangavelu, Lakshmi/AAL-4695-2020; Gupta, Gaurav/AAX-4935-2020; Kazmi,
   Imran/GRJ-9647-2022; subramaniyan, vetriselvan/AAC-5548-2020; Hussain,
   Afzal/AAF-6644-2019; Alzarea, Sami/GQH-7031-2022; Afzal,
   Obaid/AAW-8710-2020
OI Vetriselvan, Subramaniayan/0000-0002-9629-9494; Alzarea,
   Sami/0000-0003-4007-4023; Afzal, Obaid/0000-0002-4188-5592; Almalki,
   Prof.Dr.Waleed/0000-0001-5890-6030; BHAT, ASIF
   AHMAD/0000-0003-4346-8319; Kazmi, Imran/0000-0003-1881-5219; Thapa,
   Riya/0000-0001-9271-5756; Gupta, Gaurav/0000-0001-7941-0229
FU Deanship for Research & Innovation, Ministry of Education in Saudi
   Arabia [IFP22UQU4310387DSR186]
FX The authors extend their appreciation to the Deanship for Research &
   Innovation, Ministry of Education in Saudi Arabia for <B>Funding</B>
   this research work through the project number: IFP22UQU4310387DSR186.
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NR 225
TC 61
Z9 63
U1 11
U2 24
PU ELSEVIER GMBH
PI MUNICH
PA HACKERBRUCKE 6, 80335 MUNICH, GERMANY
SN 0344-0338
EI 1618-0631
J9 PATHOL RES PRACT
JI Pathol. Res. Pract.
PD SEP
PY 2023
VL 249
AR 154736
DI 10.1016/j.prp.2023.154736
EA AUG 2023
PG 18
WC Pathology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pathology
GA T2ZW6
UT WOS:001076727900001
PM 37579591
HC Y
HP N
DA 2025-01-04
ER

PT J
AU Wang, JL
   Hua, SN
   Bao, HJ
   Yuan, J
   Zhao, Y
   Chen, S
AF Wang, Jie-Lin
   Hua, Sheng-Ni
   Bao, Hai-Juan
   Yuan, Jing
   Zhao, Yang
   Chen, Shuo
TI Pyroptosis and inflammasomes in cancer and inflammation
SO MEDCOMM
LA English
DT Review
DE cancer; inflammasome; inflammation; pyroptosis; targeted treatment
ID CELL LUNG-CANCER; NF-KAPPA-B; NLRP3 INFLAMMASOME; COLORECTAL-CANCER;
   OVARIAN-CANCER; GASDERMIN D; INDUCE PYROPTOSIS; SUPPRESSOR-CELLS; PYRIN
   DOMAIN; ACTIVATION
AB Nonprogrammed cell death (NPCD) and programmed cell death (PCD) are two types of cell death. Cell death is significantly linked to tumor development, medication resistance, cancer recurrence, and metastatic dissemination. Therefore, a comprehensive understanding of cell death is essential for the treatment of cancer. Pyroptosis is a kind of PCD distinct from autophagy and apoptosis in terms of the structure and function of cells. The defining features of pyroptosis include the release of an inflammatory cascade reaction and the expulsion of lysosomes, inflammatory mediators, and other cellular substances from within the cell. Additionally, it displays variations in osmotic pressure both within and outside the cell. Pyroptosis, as evidenced by a growing body of research, is critical for controlling the development of inflammatory diseases and cancer. In this paper, we reviewed the current level of knowledge on the mechanism of pyroptosis and inflammasomes and their connection to cancer and inflammatory diseases. This article presents a theoretical framework for investigating the potential of therapeutic targets in cancer and inflammatory diseases, overcoming medication resistance, establishing nanomedicines associated with pyroptosis, and developing risk prediction models in refractory cancer. Given the link between pyroptosis and the emergence of cancer and inflammatory diseases, pyroptosis-targeted treatments may be a cutting-edge treatment strategy.
   Pyroptosis is characterized by cell swelling as well as the release of inflammatory mediators, which has been identified that it was induced by four distinct signaling pathways. Pyroptosis is crucial for controlling the development of cancer and inflammation diseases. It can be pro- or anti-cancer. Given the link between pyroptosis and the emergence of cancer and inflammatory diseases, pyroptosis-targeted treatments may be a cutting-edge treatment strategy.#image
C1 [Wang, Jie-Lin; Bao, Hai-Juan; Yuan, Jing; Zhao, Yang; Chen, Shuo] Guangzhou Med Univ, Dept Obstet & Gynecol, Guangzhou Key Lab Targeted Therapy Gynecol Oncol, Guangdong Prov Key Lab Major Obstet Dis,Affiliated, Guangzhou, Peoples R China.
   [Wang, Jie-Lin; Bao, Hai-Juan; Yuan, Jing; Zhao, Yang; Chen, Shuo] Guangzhou Med Univ, Dept Gynecol Oncol, Guangzhou Key Lab Targeted Therapy Gynecol Oncol, Guangdong Prov Key Lab Major Obstet Dis,Affiliated, Guangzhou, Peoples R China.
   [Hua, Sheng-Ni] Jinan Univ, Zhuhai Peoples Hosp, Zhuhai Hosp, Dept Radiat Oncol, Zhuhai, Peoples R China.
C3 Guangzhou Medical University; Guangzhou Medical University; Jinan
   University
RP Zhao, Y; Chen, S (corresponding author), Guangzhou Med Univ, Dept Obstet & Gynecol, Guangzhou Key Lab Targeted Therapy Gynecol Oncol, Guangdong Prov Key Lab Major Obstet Dis,Affiliated, Guangzhou, Peoples R China.
EM yida.zhaoyang@163.com; chenshuo077003@163.com
RI Liu, Xiaoling/HGD-3566-2022; Chen, Shuo/ADR-6229-2022; hua,
   shengni/HDN-5084-2022
OI hua, shengni/0000-0002-6014-1476
FU I would like to acknowledge my teammates for their wonderful
   collaboration. Many thanks to the FIGDRAW website for their help during
   the production process of Figure.
FX I would like to acknowledge my teammates for their wonderful
   collaboration. Many thanks to the FIGDRAW website for their help during
   the production process of Figure.
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NR 247
TC 10
Z9 11
U1 4
U2 16
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
EI 2688-2663
J9 MEDCOMM
JI MedComm
PD OCT
PY 2023
VL 4
IS 5
AR e374
DI 10.1002/mco2.374
PG 27
WC Medicine, Research & Experimental
WE Emerging Sources Citation Index (ESCI)
SC Research & Experimental Medicine
GA S1RX6
UT WOS:001069024700001
PM 37752941
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Fassan, M
   Milione, M
   Maddalena, G
   Cremolini, C
   Schirripa, M
   Pietrantonio, F
   Pella, N
   Dell'Aquila, E
   Sperti, E
   Zichi, C
   Bergamo, F
   Volante, M
   Boccaccino, A
   Morano, F
   Cortiula, F
   De Maglio, G
   Rimassa, L
   Smiroldo, V
   Calvetti, L
   Aprile, G
   Salvatore, L
   Santini, D
   Salmaso, R
   Centonze, G
   Biason, P
   Borga, C
   Lonardi, S
   Zagonel, V
   Dei Tos, AP
   Di Maio, M
   Loupakis, F
AF Fassan, Matteo
   Milione, Massimo
   Maddalena, Giulia
   Cremolini, Chiara
   Schirripa, Marta
   Pietrantonio, Filippo
   Pella, Nicoletta
   Dell'Aquila, Emanuela
   Sperti, Elisa
   Zichi, Clizia
   Bergamo, Francesca
   Volante, Marco
   Boccaccino, Alessandra
   Morano, Federica
   Cortiula, Francesco
   De Maglio, Giovanna
   Rimassa, Lorenza
   Smiroldo, Valeria
   Calvetti, Lorenzo
   Aprile, Giuseppe
   Salvatore, Lisa
   Santini, Daniele
   Salmaso, Roberta
   Centonze, Giovanni
   Biason, Paola
   Borga, Chiara
   Lonardi, Sara
   Zagonel, Vittorina
   Dei Tos, Angelo P.
   Di Maio, Massimo
   Loupakis, Fotios
TI Synaptophysin expression in <SUP><i>V600EBRAF</i>-</SUP>mutated advanced
   colorectal cancers identifies a new subgroup of tumours with worse
   prognosis
SO EUROPEAN JOURNAL OF CANCER
LA English
DT Article
DE Colorectal cancer; Synaptophysin; (V600E)BRAF; Immunohistochemistry;
   Neuroendocrine; Prognostic markers
ID NEUROENDOCRINE DIFFERENTIATION; BRAF MUTATIONS; CARCINOMA;
   ADENOCARCINOMAS; PHENOTYPE; SUBTYPES; CELLS; COLON; POOR
AB Background: Neuroendocrine differentiation has been extensively associated with worse prognosis and to mechanisms of therapy resistance in several epithelial cancers. A high prevalence of neuroendocrine differentiation was recently described in (V600EBRAF-)mutated ( BRAFmt) metastatic colorectal cancers (mCRCs) but no data are available about its prognostic impact in this setting.
   Methods: We assessed synaptophysin immunohistochemical expression in a multi-institutional series of 159 BRAFmt mCRCs with matched clinical and pathological information. Tumours were dichotomized as synaptophysin high and low. Overall survival (OS) and progression-free survival (PFS) were evaluated by Kaplan-Meier and log-rank tests.
   Results: Thirty-five tumours (22.0%) showed any level of positivity for synaptophysin, and 18 (11.3%) were characterized by positivity in at least 20% of tumour cells. Four cases resulted 100% synaptophysin positive. The histotype of synaptophysin-positive tumours (i.e. >= 20%) was not otherwise specified in 11 cases (61.1%) and mucinous adenocarcinoma in 4 cases (22.2%). Four cases were DNA mismatch repair deficient (22.2%) and 7 (38.9%) were characterized by a high number of tumour-infiltrating lymphocytes. At multivariate analysis, high synaptophysin expression was a negative independent prognostic factor for both PFS (HR = 2.00, 95% confidence interval [CI] 1.21-3.33, p = 0.006) and OS (HR = 2.27, 95% CI 1.35-3.85, p = 0.001).
   Conclusions: Among BRAFmt mCRCs, synaptophysin-positive tumours are characterized by worse PFS and OS. Further studies should investigate the molecular mechanisms involved in the acquisition of the neuroendocrine phenotype to identify novel-targeted treatment strategies. (C) 2021 Elsevier Ltd. All rights reserved.
C1 [Fassan, Matteo; Salmaso, Roberta; Borga, Chiara; Dei Tos, Angelo P.] Univ Padua, Dept Med DIMED, Surg Pathol Unit, Padua, Italy.
   [Milione, Massimo; Centonze, Giovanni] Fdn IRCCS Ist Nazl Tumori, Dept Pathol & Lab Med, Pathol Div 1, Milan, Italy.
   [Maddalena, Giulia; Schirripa, Marta; Bergamo, Francesca; Biason, Paola; Lonardi, Sara; Zagonel, Vittorina; Loupakis, Fotios] Veneto Inst Oncol IOV IRCCS, Dept Oncol, Unit Oncol 1, Padua, Italy.
   [Cremolini, Chiara; Boccaccino, Alessandra] Univ Pisa, Dept Translat Res & New Technol Med & Surg, Pisa, Italy.
   [Pietrantonio, Filippo; Morano, Federica] Fdn IRCCS Ist Nazl Tumori, Dept Med Oncol, Milan, Italy.
   [Pietrantonio, Filippo] Univ Milan, Dept Oncol & Hematooncol, Milan, Italy.
   [Pella, Nicoletta; Cortiula, Francesco] Univ & Gen Hosp, Dept Oncol, Udine, Italy.
   [Dell'Aquila, Emanuela; Santini, Daniele] Campus Biomed Univ Rome, Dept Med Oncol, Rome, Italy.
   [Sperti, Elisa; Zichi, Clizia; Di Maio, Massimo] Univ Turin Umberto I Ordine Mauriziano Hosp, Dept Oncol, Turin, Italy.
   [Volante, Marco] Univ Turin, Dept Oncol, San Luigi Hosp, Orbassano, TO, Italy.
   [Cortiula, Francesco] Univ Udine, Dept Med DAME, Udine, Italy.
   [De Maglio, Giovanna] Univ Hosp Udine, Dept Pathol, Udine, Italy.
   [Rimassa, Lorenza; Smiroldo, Valeria] IRCCS Humanitas Res Hosp, Humanitas Canc Ctr, Med Oncol & Hematol Unit, Milan, Italy.
   [Calvetti, Lorenzo; Aprile, Giuseppe] San Bortolo Gen Hosp, Dept Oncol, AULSS8 Ber, Vicenza, Italy.
   [Salvatore, Lisa] Fdn Policlin Univ Agostino Gemelli IRCCS, UOC Oncol, Rome, Italy.
   [Rimassa, Lorenza] Humanitas Univ, Dept Biomed Sci, Milan, Italy.
C3 University of Padua; Fondazione IRCCS Istituto Nazionale Tumori Milan;
   IRCCS Istituto Oncologico Veneto (IOV); University of Pisa; Fondazione
   IRCCS Istituto Nazionale Tumori Milan; University of Milan; University
   of Udine; University Hospital of Udine; University Campus Bio-Medico -
   Rome Italy; University of Turin; University of Udine; University of
   Udine; University Hospital of Udine; ULSS 8 Berica; Ospedale San Bortolo
   di Vicenza; Catholic University of the Sacred Heart; IRCCS Policlinico
   Gemelli; Humanitas University
RP Fassan, M (corresponding author), Univ Padua, Dept Med DIMED, Via Gabelli 61, Padua, Italy.; Loupakis, F (corresponding author), IRCCS, Veneto Inst Oncol IOV, Via Gattamelata 64, Padua, Italy.
EM matteo.fassan@unipd.it; fotios.loupakis@iov.veneto.it
RI DI MAIO, Massimo/AAB-6074-2019; Morano, Federica/B-7910-2018; Cortiula,
   Francesco/ABD-6581-2020; Bergamo, Francesca/AAB-9010-2019; Schirripa,
   Marta/F-3688-2017; Dell'Aquila, Emanuela/HZI-5685-2023; Zichi,
   Clizia/AAB-7700-2022; Cremolini, Chiara/AAC-1889-2019; Centonze,
   Giovanni/H-5896-2018; Loupakis, Fotios/I-7243-2012; zagonel,
   vittorina/F-4226-2014; Fassan, Matteo/F-5152-2012; Pietrantonio,
   Filippo/C-2180-2017; DI MAIO, Massimo/K-9990-2016; Rimassa,
   Lorenza/N-4884-2016; Lonardi, Sara/F-4228-2014; Salvatore,
   Lisa/L-7746-2019; Biason, Paola/N-6528-2013
OI Fassan, Matteo/0000-0001-6515-5482; Cortiula,
   Francesco/0000-0002-2719-3653; Pietrantonio,
   Filippo/0000-0002-8530-8420; DI MAIO, Massimo/0000-0001-8906-3785;
   Zichi, Clizia/0000-0001-8981-4155; Dell'Aquila,
   Emanuela/0000-0002-7258-1364; Rimassa, Lorenza/0000-0001-9957-3615;
   CREMOLINI, CHIARA/0000-0002-0520-4841; Lonardi,
   Sara/0000-0002-7593-8138; Salvatore, Lisa/0000-0003-3864-0719; DEI TOS,
   ANGELO/0000-0002-1228-8940; Biason, Paola/0000-0002-2298-101X
FU Italian Health Ministry's Research program [NET2016-02363853]; Regione
   Veneto [RP-2014-00000395]
FX This work was partly supported by a grant of the Italian Health
   Ministry's Research program (ID: NET2016-02363853) and Regione Veneto
   (RP-2014-00000395). The funding agencies had no role in the design and
   performance of the study.
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NR 41
TC 10
Z9 10
U1 1
U2 3
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 0959-8049
EI 1879-0852
J9 EUR J CANCER
JI Eur. J. Cancer
PD MAR
PY 2021
VL 146
BP 145
EP 154
DI 10.1016/j.ejca.2021.01.016
EA FEB 2021
PG 10
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA QS4KF
UT WOS:000625869300015
PM 33607478
DA 2025-01-04
ER

PT J
AU Yin, LN
   Gao, Y
   Zhang, XX
   Wang, J
   Ding, DF
   Zhang, YP
   Zhang, JX
   Chen, HH
AF Yin, Lina
   Gao, Yun
   Zhang, Xuxia
   Wang, Jing
   Ding, Defang
   Zhang, Yaping
   Zhang, Junxiang
   Chen, Honghong
TI Niclosamide sensitizes triple-negative breast cancer cells to ionizing
   radiation in association with the inhibition of Wnt/β-catenin signaling
SO ONCOTARGET
LA English
DT Article
DE niclosamide; radiosensitization; Wnt/beta-catenin signaling;
   triple-negative breast cancer
ID DEPENDENT PROTEIN-KINASE; BETA-CATENIN; RADIORESISTANCE FACTOR;
   COLORECTAL-CANCER; THERAPEUTIC TARGET; GLIOBLASTOMA CELLS; INDUCED
   APOPTOSIS; PROGENITOR CELLS; WNT PATHWAY; SURVIVIN
AB Triple-negative breast cancer (TNBC) is one of the most difficult breast cancers to treat because there is no targeted treatment, and conventional cytotoxic chemotherapy followed by adjuvant radiation therapy is the standard of care for patients with TNBC. We herein reported that ionizing radiation (IR) induced Wnt3a, LRP6 and beta-catenin expression and consequently activated Wnt/beta-catenin signaling in TNBC MDA-MB-231, MDA-MB-468 and Hs578T cells. Moreover, depletion of beta-catenin by shRNA sensitized TNBC cells to IR, whereas treatment of Wnt3a protein or overexpression of beta-catenin resulted in radioresistance of TNBC cells. Niclosamide, a potent inhibitor of Wnt/beta-catenin signaling, not only inhibited constitutive Wnt/beta-catenin signaling, but also blocked IR-induced Wnt/beta-catenin signaling in TNBC cells. In addition, niclosamide sensitized TNBC cells to IR, prevented Wnt3a-induced radioresistance, and overcame beta-catenin-induced radioresistance in TNBC cells. Importantly, animals treated with the combination of niclosamide and eta-ray local tumor irradiation had significant inhibition of MDA-MB-231 tumor growth compared with treated with local tumor irradiation alone. These findings indicate that Wnt/beta-catenin signaling pathway plays an important role in the development of radioresistance of TNBC cells, and that niclosamide had significant radiosensitizing effects by inhibiting Wnt/beta-catenin signaling in TNBC cells. Our study also provides rationale for further preclinical and clinical evaluation of niclosamide in TNBC management.
C1 [Yin, Lina; Gao, Yun; Zhang, Xuxia; Wang, Jing; Ding, Defang; Zhang, Yaping; Zhang, Junxiang; Chen, Honghong] Fudan Univ, Inst Radiat Med, Dept Radiat Biol, Shanghai, Peoples R China.
C3 Fudan University
RP Chen, HH (corresponding author), Fudan Univ, Inst Radiat Med, Dept Radiat Biol, Shanghai, Peoples R China.
EM hhchen@shmu.edu.cn
RI Zhang, YP/AAK-3011-2020; Lou, Xiaoding/JOZ-2300-2023; Zhang,
   Junxiang/HIZ-6904-2022; Chen, zhuo/JWO-5404-2024
FU National Nature Science Foundation of China [31370839]
FX This work was supported by the National Nature Science Foundation of
   China (31370839).
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Z9 49
U1 0
U2 14
PU IMPACT JOURNALS LLC
PI ORCHARD PARK
PA 6666 E QUAKER ST, STE 1, ORCHARD PARK, NY 14127 USA
EI 1949-2553
J9 ONCOTARGET
JI Oncotarget
PD JUL 5
PY 2016
VL 7
IS 27
BP 42126
EP 42138
DI 10.18632/oncotarget.9704
PG 13
WC Oncology; Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Cell Biology
GA DS7DI
UT WOS:000380942600091
PM 27363012
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Chibuk, J
   Flory, A
   Kruglyak, KM
   Leibman, N
   Nahama, A
   Dharajiya, N
   van den Boom, D
   Jensen, TJ
   Friedman, JS
   Shen, MR
   Clemente-Vicario, F
   Chorny, I
   Tynan, JA
   Lytle, KM
   Holtvoigt, LE
   Murtaza, M
   Diaz, LA
   Tsui, DWY
   Grosu, DS
AF Chibuk, Jason
   Flory, Andi
   Kruglyak, Kristina M.
   Leibman, Nicole
   Nahama, Alexis
   Dharajiya, Nilesh
   van den Boom, Dirk
   Jensen, Taylor J.
   Friedman, Jeffrey S.
   Shen, M. Richard
   Clemente-Vicario, Francisco
   Chorny, Ilya
   Tynan, John A.
   Lytle, Katherine M.
   Holtvoigt, Lauren E.
   Murtaza, Muhammed
   Diaz, Luis A.
   Tsui, Dana W. Y.
   Grosu, Daniel S.
TI Horizons in Veterinary Precision Oncology: Fundamentals of Cancer
   Genomics and Applications of Liquid Biopsy for the Detection,
   Characterization, and Management of Cancer in Dogs
SO FRONTIERS IN VETERINARY SCIENCE
LA English
DT Review
DE dog; cfDNA; cell-free DNA; circulating tumor DNA; cancer; genomic;
   liquid biopsy; one health
ID CELL-FREE DNA; CIRCULATING TUMOR DNA; TYROSINE KINASE INHIBITOR;
   C-REACTIVE PROTEIN; PLASMA DNA; COLORECTAL-CANCER; MICROSATELLITE
   ALTERATIONS; ADJUVANT CHEMOTHERAPY; MUTATIONAL PROCESSES; INCIDENTAL
   DETECTION
AB Cancer is the leading cause of death in dogs, in part because many cases are identified at an advanced stage when clinical signs have developed, and prognosis is poor. Increased understanding of cancer as a disease of the genome has led to the introduction of liquid biopsy testing, allowing for detection of genomic alterations in cell-free DNA fragments in blood to facilitate earlier detection, characterization, and management of cancer through non-invasive means. Recent discoveries in the areas of genomics and oncology have provided a deeper understanding of the molecular origins and evolution of cancer, and of the "one health" similarities between humans and dogs that underlie the field of comparative oncology. These discoveries, combined with technological advances in DNA profiling, are shifting the paradigm for cancer diagnosis toward earlier detection with the goal of improving outcomes. Liquid biopsy testing has already revolutionized the way cancer is managed in human medicine - and it is poised to make a similar impact in veterinary medicine. Multiple clinical use cases for liquid biopsy are emerging, including screening, aid in diagnosis, targeted treatment selection, treatment response monitoring, minimal residual disease detection, and recurrence monitoring. This review article highlights key scientific advances in genomics and their relevance for veterinary oncology, with the goal of providing a foundational introduction to this important topic for veterinarians. As these technologies migrate from human medicine into veterinary medicine, improved awareness and understanding will facilitate their rapid adoption, for the benefit of veterinary patients.
C1 [Chibuk, Jason; Flory, Andi; Kruglyak, Kristina M.; Chorny, Ilya; Tynan, John A.; Lytle, Katherine M.; Holtvoigt, Lauren E.; Tsui, Dana W. Y.; Grosu, Daniel S.] PetDx, La Jolla, CA 92037 USA.
   [Leibman, Nicole] Anim Med Ctr, Canc Inst, New York, NY USA.
   [Nahama, Alexis] ARK Anim Hlth, San Diego, CA USA.
   [Dharajiya, Nilesh] Healthbitai Inc, San Diego, CA USA.
   [van den Boom, Dirk] PetDx, San Diego, CA USA.
   [Jensen, Taylor J.] Lab Corp Amer, Durham, NC USA.
   [Friedman, Jeffrey S.] Friedman Bioventure Inc, San Diego, CA USA.
   [Shen, M. Richard] RS Technol Ventures LLC, Rancho Santa Fe, CA USA.
   [Clemente-Vicario, Francisco] La Merced Vet Oncol, Calpe, Spain.
   [Murtaza, Muhammed] Univ Wisconsin, Dept Surg, Madison, WI USA.
   [Murtaza, Muhammed] Univ Wisconsin, Ctr Human Genom & Precis Med, Madison, WI USA.
   [Diaz, Luis A.] Mem Sloan Kettering Canc Ctr, Div Solid Tumor Oncol, New York, NY 10021 USA.
C3 University of Wisconsin System; University of Wisconsin Madison;
   University of Wisconsin System; University of Wisconsin Madison;
   Memorial Sloan Kettering Cancer Center
RP Chibuk, J; Flory, A; Tsui, DWY (corresponding author), PetDx, La Jolla, CA 92037 USA.
EM jchibuk@petdx.com; aflory@petdx.com; dtsui@petdx.com
RI Diaz, Luis/ABD-5602-2021
OI Lytle, Katherine/0000-0002-7826-0107; Chibuk, Jason/0000-0003-1903-8829
FU PetDx
FX This article funded by PetDx.
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NR 273
TC 23
Z9 23
U1 0
U2 11
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
EI 2297-1769
J9 FRONT VET SCI
JI Front. Vet. Sci.
PD MAR 23
PY 2021
VL 8
AR 664718
DI 10.3389/fvets.2021.664718
PG 23
WC Veterinary Sciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Veterinary Sciences
GA RI6EX
UT WOS:000637000300001
PM 33834049
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Gulei, D
   Mehterov, N
   Ling, H
   Stanta, G
   Braicu, C
   Berindan-Neagoe, I
AF Gulei, Diana
   Mehterov, Nikolay
   Ling, Hui
   Stanta, Giorgio
   Braicu, Cornelia
   Berindan-Neagoe, Ioana
TI The "good-cop bad-cop" TGF-beta role in breast cancer modulated by
   non-coding RNAs
SO BIOCHIMICA ET BIOPHYSICA ACTA-GENERAL SUBJECTS
LA English
DT Review
DE Breast cancer; EMT; TGF-beta; miRNA; lncRNA
ID EPITHELIAL-MESENCHYMAL TRANSITION; GROWTH-FACTOR-BETA; SQUAMOUS-CELL
   CARCINOMA; NEGATIVE FEEDBACK LOOP; POOR-PROGNOSIS; DRUG-RESISTANCE;
   DOWN-REGULATION; MICRORNA-200 FAMILY; COLORECTAL-CANCER;
   TUMOR-SUPPRESSOR
AB Background: Lack of early diagnosis methods and the development of drug resistance are among the main reasons for increased mortality rates within breast cancer patients. These two aspects are governed by specific pro-carcinogenic modifications, where TGB beta-induced EMT is one of the leading actors. Endowment of the epithelial cells with mesenchymal characteristics allows them to migrate and invade secondary tissues in order to form malignant sites and also confers chemoresistance. TGE beta which role switches from the tumor suppressor cytokine to the oncogenic one favoring the tumor microenvironment regulates this process.
   Scope of review: This review aims to comprehensively present the updated TGF beta-induced EMT in breast cancer, including the regulatory role of the non-coding RNAs with focus on the miR-200 family and newly discovered lncRNAs such as HOTAIRM1. Additionally, a new phenotype, P-EMT, also modulated by miR-200 and miR-34 families that form complex feedback loops with TGF beta, SNAIL and ZEB1/2 is presented under an updated form.
   Major conclusions: The hallmarks of EMT are becoming increasingly associated with aggressive forms of breast cancer and low survival rates among patients. Considering that this phenotypical switch can trigger drug resistance, invasion and metastasis, inhibition of EMT could represent an important milestone in mammary cancer treatment.
   General significance: The present review assembles the most recent data regarding TGF beta induced EMT, including the input of non-coding RNAs, contributing to the possible development of new targeted treatment strategies for cancer patients.
C1 [Gulei, Diana; Berindan-Neagoe, Ioana] Univ Med & Farm Iuliu Hatieganu, MEDFUTURE Res Ctr Adv Med, Marinescu 23 St, Cluj Napoca, Romania.
   [Berindan-Neagoe, Ioana] Oncol Inst Prof Dr Ion Chiricuta, Dept Funct Genom & Expt Pathol, Republicii 34-36 St, Cluj Napoca, Romania.
   [Mehterov, Nikolay] Med Univ Plovdiv, Dept Med Biol, Vasil Aprilov 15-A St, Plovdiv, Bulgaria.
   [Mehterov, Nikolay] Technol Ctr Emergency Med, Vasil Aprilov 15-A St, Plovdiv, Bulgaria.
   [Ling, Hui] Univ Texas MD Anderson Canc Ctr, Dept Expt Therapeut, Houston, TX 77054 USA.
   [Stanta, Giorgio] Univ Trieste, Dept Med Sci, Fiume 447 St, Trieste, Italy.
   [Braicu, Cornelia; Berindan-Neagoe, Ioana] Iuliu Hatieganu Univ Med & Pharm, Res Ctr Funct Genom Biomed & Translat Med, Marinescu 23 St,23, Cluj Napoca 400337, Romania.
C3 Iuliu Hatieganu University of Medicine & Pharmacy; Oncology Institute
   Prof. Dr. Ion Chiricuta; Medical University Plovdiv; University of Texas
   System; UTMD Anderson Cancer Center; University of Trieste; Iuliu
   Hatieganu University of Medicine & Pharmacy
RP Braicu, C; Berindan-Neagoe, I (corresponding author), Iuliu Hatieganu Univ Med & Pharm, Res Ctr Funct Genom Biomed & Translat Med, Marinescu 23 St,23, Cluj Napoca 400337, Romania.
EM diana.gulei@umfcluj.ro; cornelia.braicu@umfcluj.ro;
   ioana.neagoe@umfcluj.ro
RI Gulei, Diana/U-2864-2017; Berindan-Neagoe, Ioana/AAH-9854-2019
OI Gulei, Diana/0000-0002-3030-8626
FU Medical University of Plovdiv [PN-II-RU-TE-2014-4-1464, 307, POSCCE 709,
   HO-18/2014]
FX This work was supported in part by Project PN-II-RU-TE-2014-4-1464; 307
   from 01/10/2015 - Targeting the TGF beta pathway: an alternative for
   breast cancer therapy; POSCCE 709 Breast Impact and Project HO-18/2014,
   funded by Medical University of Plovdiv.
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NR 155
TC 37
Z9 37
U1 0
U2 10
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0304-4165
EI 1872-8006
J9 BBA-GEN SUBJECTS
JI Biochim. Biophys. Acta-Gen. Subj.
PD JUL
PY 2017
VL 1861
IS 7
BP 1661
EP 1675
DI 10.1016/j.bbagen.2017.04.007
PG 15
WC Biochemistry & Molecular Biology; Biophysics
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Biophysics
GA FA0WV
UT WOS:000405158300001
PM 28411077
DA 2025-01-04
ER

PT J
AU Liu, GX
   Xu, XH
   Jiang, LQ
   Ji, HH
   Zhu, F
   Jin, BN
   Han, JJ
   Dong, XL
   Yang, FH
   Li, B
AF Liu, Guoxiang
   Xu, Xiaohui
   Jiang, Liangqian
   Ji, Huanhuan
   Zhu, Feng
   Jin, Bingnan
   Han, Jingjing
   Dong, Xiaolei
   Yang, Fanghao
   Li, Bing
TI Targeted Antitumor Mechanism of C-PC/CMC-CD55sp Nanospheres in HeLa
   Cervical Cancer Cells
SO FRONTIERS IN PHARMACOLOGY
LA English
DT Article
DE C-phycocyanin; carboxymethyl chitosan; CD55 ligand peptide; targeting
   nanospheres; HeLa cells
ID L-SELECTIN ADHESION; IN-VITRO; C-PHYCOCYANIN; TGF-BETA; CHITOSAN
   NANOPARTICLES; ELECTRON-MICROSCOPY; DENDRITIC CELLS; COLON-CANCER;
   APOPTOSIS; DELIVERY
AB In vitrostudies had shown that C-Phycocyanin (C-PC) inhibited cervical cancer HeLa cells growth. We constructed C-PC/CMC-CD55sp nanospheres using C-PC, Carboxymethyl Chitosan (CMC), and CD55 ligand peptide (CD55sp) to allow for targeted antitumor effects against HeLa cellsin vitroandin vivo. The characteristics of the nanospheres were determined using FTIR, electron microscopy, and laser particle size analysis. Flow cytometry, laser confocal microscopy and small animal imaging system showed the targeting of C-PC/CMC-CD55sp nanospheres on HeLa cells. Subsequently, the proliferation and apoptosis were analyzed by Cell Counting Kit-8 (CCK-8), flow cytometry, TUNEL assay and electron microscopy. The expression of the apoptosis-related protein was determined using western blot. The stainings of Hematoxylin and Eosin (HE) were employed to evaluate the cell condition of tumor tissue sections. The cytokines in the blood in tumor-bearing nude mice was determined using ELISA. These results showed that C-PC/CMC-CD55sp nanospheres were successfully constructed and targeted HeLa cells. The constructed nanospheres were more effective than C-PC alone in inhibiting the proliferation and inducing apoptosis in HeLa cells. We also found that C-PC/CMC-CD55sp nanospheres had a significant inhibitory effect on the expression of antiapoptotic protein Bcl-2 and a promotion on the transformation of caspase 3 to cleaved caspase 3. C-PC/CMC-CD55sp nanospheres played an important role in tumor suppression, reduced the expression TGF-beta, and increased IL-6 and TNF-alpha. This study demonstrates that the constructed new C-PC/CMC-CD55sp nanospheres exerted targeted antitumor effectsin vivoandin vitrowhich provided a novel idea for application of C-PC, and provided experimental basis for comprehensive targeted treatment of tumors.
C1 [Liu, Guoxiang; Xu, Xiaohui; Ji, Huanhuan; Zhu, Feng; Jin, Bingnan; Han, Jingjing; Dong, Xiaolei; Yang, Fanghao; Li, Bing] Qingdao Univ, Basic Med Coll, Dept Genet & Cell Biol, Qingdao, Peoples R China.
   [Jiang, Liangqian] Linyi Peoples Hosp, Dept Med Genet, Linyi, Shandong, Peoples R China.
   [Li, Bing] Qingdao Univ, Dept Hematol, Affiliated Hosp, Qingdao, Peoples R China.
C3 Qingdao University; Qingdao University
RP Li, B (corresponding author), Qingdao Univ, Basic Med Coll, Dept Genet & Cell Biol, Qingdao, Peoples R China.; Li, B (corresponding author), Qingdao Univ, Dept Hematol, Affiliated Hosp, Qingdao, Peoples R China.
EM libing_516@qdu.edu.cn
RI liu, guoxiang/I-8174-2013
OI Zhu, Feng/0009-0008-0475-2687
FU National Natural Science Foundation of China [81871231, 81471546,
   81001346]; Youth Innovation and Technology Plan of Shandong Colleges
   [2019KJK016]; Science and Technology Project of Qingdao [18-6-1-91-nsh]
FX This work was supported by grants from the National Natural Science
   Foundation of China (Nos. 81871231, 81471546, and 81001346), Youth
   Innovation and Technology Plan of Shandong Colleges (2019KJK016), and
   Science and Technology Project of Qingdao (No. 18-6-1-91-nsh).
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NR 90
TC 13
Z9 12
U1 0
U2 17
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
EI 1663-9812
J9 FRONT PHARMACOL
JI Front. Pharmacol.
PD JUN 18
PY 2020
VL 11
AR 906
DI 10.3389/fphar.2020.00906
PG 13
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA MJ8YP
UT WOS:000548373800001
PM 32636744
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Wang, XM
   Xu, JL
   Chen, J
   Jin, SD
   Yao, JQ
   Yu, TF
   Wang, W
   Guo, RH
AF Wang, Xiaomeng
   Xu, Jiali
   Chen, Jin
   Jin, Shidai
   Yao, Jiaqi
   Yu, Tongfu
   Wang, Wei
   Guo, Renhua
TI IL-22 Confers EGFR-TKI Resistance in NSCLC via the AKT and ERK Signaling
   Pathways
SO FRONTIERS IN ONCOLOGY
LA English
DT Article
DE IL-22; non-small cell lung cancer; EGFR; gefitinib; EGFR-TKI resistance
ID CELL LUNG-CANCER; TUMOR-ASSOCIATED MACROPHAGES; T-CELLS; UP-REGULATION;
   COLON-CANCER; INTERLEUKIN-22; MUTATION; MICROENVIRONMENT; PROLIFERATION;
   PROGRESSION
AB Background: The efficacy of an EGFR-targeted treatment strategy for non-small cell lung cancer (NSCLC) is reduced by drug resistance. IL-22 enhances tumor growth and induces chemotherapy resistance in human lung cancer cells. The present study elucidated the IL-22-induced mechanism underlying EGFR-tyrosine kinase inhibitor (TKI) resistance in NSCLC. Methods: The plasma and tissues of patients who received EGFR-TKIs were utilized to determine the association between IL-22 expression and gefitinib efficacy. The IL-22 effect on the EGFR/ERK/AKT pathways in NSCLC HCC827 and PC-9 cells was determined using the CCK-8 assay, western blot, and flow cytometric analysis. A PC-9 xenograft model of IL-22 exposure was established. Gefitinib was administered to mice in combination with IL-22 or vehicle. Results: We showed that IL-22 expression was higher in the EGFR-TKI-resistant group compared to EGFR-TKI-sensitive group. IL-22 expression was associated with EGFR-TKI efficacy in plasma. Additional treatment of IL-22 induced gefitinib resistance and reduced apoptosis in PC-9 and HCC827 cell lines. Furthermore, we showed that the effects of IL-22 attributed to p-ERK, p-EGFR, and p-AKT up-regulation. IL-22 neutralizing antibody completely abrogated the effects of IL-22 on apoptosis and AKT/EGFR/ERK signaling. Finally, we showed that IL-22 enhanced tumor growth and induced gefitinib resistance in the PC-9 xenograft model. Moreover, compared with gefitinib alone, the combination of IL-22 and gefitinib led to an increase in Ki67-positive staining and a reduction in TUNEL staining. Conclusions: Our findings indicate that IL-22 plays a role in tumor progression and EGFR-TKI resistance in NSCLC. Thus, IL-22 might serve as a novel biomarker to overcome resistance of EGFR-TKI.
C1 [Wang, Xiaomeng; Xu, Jiali; Jin, Shidai; Guo, Renhua] Nanjing Med Univ, Dept Oncol, Affiliated Hosp 1, Nanjing, Jiangsu, Peoples R China.
   [Wang, Xiaomeng] First Peoples Hosp Shangqiu, Dept Radiotherapy 2, Shangqiu, Peoples R China.
   [Chen, Jin] Nanjing Med Univ, Clin Med Coll 4, Nanjing, Jiangsu, Peoples R China.
   [Yao, Jiaqi] Nanjing Med Univ, Clin Med Coll 1, Nanjing, Jiangsu, Peoples R China.
   [Yu, Tongfu] Nanjing Med Univ, Affiliated Hosp 1, Dept Radiol, Nanjing, Jiangsu, Peoples R China.
   [Wang, Wei] Nanjing Med Univ, Affiliated Hosp 1, Dept Cardiothorac Surg, Nanjing, Jiangsu, Peoples R China.
C3 Nanjing Medical University; Nanjing Medical University; Nanjing Medical
   University; Nanjing Medical University; Nanjing Medical University
RP Guo, RH (corresponding author), Nanjing Med Univ, Dept Oncol, Affiliated Hosp 1, Nanjing, Jiangsu, Peoples R China.; Wang, W (corresponding author), Nanjing Med Univ, Affiliated Hosp 1, Dept Cardiothorac Surg, Nanjing, Jiangsu, Peoples R China.
EM Weiwang_surgery@163.com; Rhguo_oncology@sina.com
RI Xu, jiali/GRS-1598-2022; Wang, Wei/JAO-0499-2023
OI Wang, Wei/0000-0002-1614-0759; Guo, Renhua/0000-0003-4475-8617
FU National Natural Science Foundation of China [81972118]; Jiangsu
   Province Natural Science Foundation [BK20161593]; Medical Important
   Talent Foundation of Jiangsu Province [ZDRCA2016024]; Wu Jie-ping
   Foundation [320.6799.15032]; Nanjing Medical University High Level
   Innovation Team [JX102GSP201727]; Provincial key projects
   [201810312017Z]
FX This study was financed by the National Natural Science Foundation of
   China (Grant No. 81972118), the Jiangsu Province Natural Science
   Foundation (Grant No. BK20161593), the Medical Important Talent
   Foundation of Jiangsu Province (Grant No. ZDRCA2016024), the Wu Jie-ping
   Foundation (Grant No. 320.6799.15032), the Nanjing Medical University
   High Level Innovation Team (Grant No. JX102GSP201727), and the
   Provincial key projects (Grand No. 201810312017Z).
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NR 46
TC 15
Z9 17
U1 2
U2 12
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 2234-943X
J9 FRONT ONCOL
JI Front. Oncol.
PD NOV 5
PY 2019
VL 9
AR 1167
DI 10.3389/fonc.2019.01167
PG 10
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA JP8UO
UT WOS:000498534400001
PM 31750252
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Zhang, YL
   Ma, Y
   Zeng, YQ
   Liu, Y
   He, EP
   Liu, YT
   Qiao, FL
   Yu, R
   Wang, YS
   Wu, XY
   Leng, P
AF Zhang, Yan-Ling
   Ma, Yan
   Zeng, You-Qin
   Liu, Yan
   He, En-Ping
   Liu, Yi-Tong
   Qiao, Feng-Ling
   Yu, Rong
   Wang, Ying-Shuang
   Wu, Xin-Yu
   Leng, Ping
TI A narrative review of research progress on FoxM1 in breast cancer
   carcinogenesis and therapeutics
SO ANNALS OF TRANSLATIONAL MEDICINE
LA English
DT Review
DE Breast cancer; drug resistance; forkhead box transcription factor M1
   (FoxM1); therapeutics; tumorigenesis
ID FORKHEAD BOX M1; EPITHELIAL-MESENCHYMAL TRANSITION; POSITIVE FEEDBACK
   LOOP; INHIBITS CELL-GROWTH; TRANSCRIPTION FACTOR; COLORECTAL-CANCER;
   DOWN-REGULATION; POOR-PROGNOSIS; NONCODING RNAS; GASTRIC-CANCER
AB Objective: The purpose of this review is to clarify the potential roles of forkhead box transcription factor M1 (FoxM1) in the occurrence and progression of breast cancer, as well as the predictive value of FoxM1 as a prognostic biomarker and potential therapeutic target for breast cancer. Background: Breast cancer, well-known as a molecularly heterogeneous cancer, is still one of the most frequently diagnosed malignant tumors among females worldwide. Tumor recurrence and metastasis are the central causes of high mortality in breast cancer patients. Many factors contribute to the occurrence and progression of breast cancer, including FoxM1. FoxM1, widely regarded as a classic proliferation-related transcription factor, plays pivotal roles in the occurrence, proliferation, invasion, migration, drug resistance, and epithelial-mesenchymal transition (EMT) processes of multiple human tumors including breast cancer. Methods: The PubMed database was searched for articles published in English from February 2008 to May 2021 using related keywords such as "forkhead box transcription factor M1", "human breast cancer", "FoxM1", and "human tumor". About 90 research papers and reports written in English were identified, most of which were published after 2015. These papers mainly concentrated on the functions of FoxM1 in the occurrence, development, drug resistance, and treatment of human breast cancer. Conclusions: Considering that the abnormal expression of FoxM1 plays a significant role in the proliferation, invasion, metastasis, and chemotherapy drug resistance of breast cancer, and its overexpression is closely correlated with the unfavorable clinicopathological characteristics of breast tumor patients, it is considerably important to comprehend the regulatory mechanism of FoxM1 in breast cancer. This will provide strong evidence for FoxM1 as a potential biomarker for the targeted treatment and prognostic evaluation of breast cancer patients.
C1 [Zhang, Yan-Ling; Zeng, You-Qin; Liu, Yan; Liu, Yi-Tong; Qiao, Feng-Ling; Yu, Rong; Wang, Ying-Shuang; Wu, Xin-Yu; Leng, Ping] Chengdu Univ Tradit Chinese Med, Coll Med Technol, Chongqing Key Lab Sichuan Chongqing Coconstruct D, Chengdu 611137, Sichuan, Peoples R China.
   [Ma, Yan] Sichuan Univ, West China Sch Nursing, Emergency Dept, West China Hosp, Chengdu, Peoples R China.
   [Ma, Yan] Sichuan Univ, Inst Disaster Med, Chengdu, Peoples R China.
   [He, En-Ping] Nucl Ind 416 Hosp, Dept Clin Lab, Affiliated Hosp 2, Chengdu Med Coll, Chengdu, Peoples R China.
C3 Chengdu University of Traditional Chinese Medicine; Sichuan University;
   Sichuan University; Chengdu Medical College
RP Wu, XY; Leng, P (corresponding author), Chengdu Univ Tradit Chinese Med, Coll Med Technol, Chongqing Key Lab Sichuan Chongqing Coconstruct D, Chengdu 611137, Sichuan, Peoples R China.
EM 601587352@qq.com; 596353806@qq.com
RI WU, XINYU/KZL-3407-2024; zhang, yanling/GRJ-9862-2022
FU Xinglin Scholar Research Premotion Project of Chengdu University of
   Traditional Chinese Medicine [ZRYY2023]; Sichuan Collaborative
   Innovation Center of Elderly Care and Health [19Z15]
FX This work was supported by the Xinglin Scholar Research Premotion
   Project of Chengdu University of Traditional Chinese Medicine (grant No.
   ZRYY2023) , and the Sichuan Collaborative Innovation Center of Elderly
   Care and Health (grant No. 19Z15) .
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NR 167
TC 13
Z9 14
U1 1
U2 29
PU AME PUBLISHING COMPANY
PI SHATIN
PA FLAT-RM C 16F, KINGS WING PLAZA 1, NO 3 KWAN ST, SHATIN, HONG KONG
   00000, PEOPLES R CHINA
SN 2305-5839
EI 2305-5847
J9 ANN TRANSL MED
JI ANN. TRANSL. MED.
PD NOV
PY 2021
VL 9
IS 22
DI 10.21037/atm-21-5271
EA OCT 2021
PG 18
WC Oncology; Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Research & Experimental Medicine
GA XM9CS
UT WOS:000718192900001
PM 34988213
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Calvo, E
   Soria, JC
   Ma, WW
   Wang, T
   Bahleda, R
   Tolcher, AW
   Gernhardt, D
   O'Connell, J
   Millham, R
   Giri, N
   Wick, MJ
   Adjei, AA
   Hidalgo, M
AF Calvo, Emiliano
   Soria, Jean-Charles
   Ma, Wen Wee
   Wang, Tao
   Bahleda, Rastilav
   Tolcher, Anthony W.
   Gernhardt, Diana
   O'Connell, Joseph
   Millham, Robert
   Giri, Nagdeep
   Wick, Michael J.
   Adjei, Alex A.
   Hidalgo, Manuel
TI A Phase I Clinical Trial and Independent Patient-Derived Xenograft Study
   of Combined Targeted Treatment with Dacomitinib and Figitumumab in
   Advanced Solid Tumors
SO CLINICAL CANCER RESEARCH
LA English
DT Article
ID GROWTH-FACTOR RECEPTOR; CELL LUNG-CANCER; MONOCLONAL-ANTIBODY
   CP-751,871; TYROSINE KINASE INHIBITOR; ADENOID CYSTIC CARCINOMA;
   EXPRESSION; ERLOTINIB; RESISTANCE; GEFITINIB; IGF-1R
AB Purpose: This phase I, open-label, single-arm trial assessed the safety and tolerability of dacomitinib-figitumumab combination therapy in patients with advanced solid tumors.
   Experimental Design: A standard 3 + 3 dose escalation/deescalation design was utilized. Starting doses were figitumumab 20 mg/kg administered intravenously once every 3 weeks and dacomitinib 30 mg administered orally once daily. We also performed an independent study of the combination in patient-derived xenograft (avatar mouse) models of adenoid cystic carcinoma.
   Results: Of the 74 patients enrolled, the most common malignancies were non-small cell lung cancer (24.3%) and colorectal cancer (14.9%). The most common treatment-related adverse events in the 71 patients who received treatment across five dose levels were diarrhea (59.2%), mucosal inflammation (47.9%), and fatigue and acneiform dermatitis (45.1% each). The most common dose-limiting toxicity was mucosal inflammation. Dosing schedules of dacomitinib 10 or 15 mg daily plus figitumumab 20 mg/kg every 3 weeks after a figitumumab loading dose were tolerated by patients over multiple cycles and considered recommended doses for further evaluation. Objective responses were seen in patients with adenoid cystic carcinoma, ovarian carcinoma, and salivary gland cancer. Pharmacokinetic analysis did not show any significant drug - drug interaction. In the adenoid cystic carcinoma xenograft model, figitumumab exerted significant antitumor activity, whereas dacomitinib did not. Figitumumab-sensitive tumors showed downregulation of genes in the insulin-like growth factor receptor 1 pathway.
   Conclusions: Dacomitinib - figitumumab combination therapy was tolerable with significant dose reductions of both agents to less than the recommended single-agent phase II dose of each drug. Preliminary clinical activity was demonstrated in the potential target tumor adenoid cystic carcinoma. (C)2016 AACR.
C1 [Calvo, Emiliano; Hidalgo, Manuel] START Madrid, Ctr Integral Oncol Clara Campal, Madrid, Spain.
   [Soria, Jean-Charles; Bahleda, Rastilav] Inst Gustave Roussy, Paris, France.
   [Ma, Wen Wee; Adjei, Alex A.] Roswell Pk Canc Inst, Buffalo, NY 14263 USA.
   [Wang, Tao; Gernhardt, Diana; Millham, Robert] Pfizer Inc, Groton, CT 06340 USA.
   [Tolcher, Anthony W.; Wick, Michael J.] START, San Antonio, TX USA.
   [O'Connell, Joseph] Pfizer Inc, New York, NY USA.
   [Giri, Nagdeep] Pfizer Inc, La Jolla, CA USA.
C3 UNICANCER; Gustave Roussy; Roswell Park Comprehensive Cancer Center;
   Pfizer; Pfizer; Pfizer
RP Calvo, E (corresponding author), START Madrid HM CIOCC, Ctr Integral Oncol Clara Campal, Calle Ona 10, Madrid 28050, Spain.
EM emiliano.calvo@start.stoh.com
RI Soria, Jean-Charles/F-3619-2014; Wang, Tao/AAT-3028-2020
OI Calvo, Emiliano/0000-0003-4921-829X
FU Pfizer Inc.; ACCRF
FX This study was sponsored by Pfizer Inc. Funding for the adenoid cystic
   carcinoma preclinical model studies was provided by the ACCRF
   (www.accrf.org). Editorial assistance was funded by Pfizer Inc.
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NR 31
TC 27
Z9 29
U1 0
U2 4
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1078-0432
EI 1557-3265
J9 CLIN CANCER RES
JI Clin. Cancer Res.
PD MAR 1
PY 2017
VL 23
IS 5
BP 1177
EP 1185
DI 10.1158/1078-0432.CCR-15-2301
PG 9
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA EN4ZO
UT WOS:000396015600008
PM 27733479
OA Green Submitted, Bronze
DA 2025-01-04
ER

PT J
AU Su, HB
   Xie, SP
   Wang, SS
   Huang, LY
   Lyu, J
   Pan, YL
AF Su, Hongbo
   Xie, Shuping
   Wang, Shanshan
   Huang, Liying
   Lyu, Jun
   Pan, Yunlong
TI New findings in prognostic factor assessment for adenocarcinoma of
   transverse colon: a comparison study between competing-risk and COX
   regression analysis
SO FRONTIERS IN MEDICINE
LA English
DT Article
DE adenocarcinoma of transverse colon; competing-risk analysis; SEER; Cox
   regression; subdistribution hazard function
ID FOLLOW-UP; CANCER; RESECTION; SURGERY; SURVIVAL; MODELS
AB Purpose Competing-risk analysis was used to accurately assess prognostic factors for cancer-specific death in patients with adenocarcinoma of transverse colon (ATC), and the results were compared with those from a conventional Cox regression analysis.Materials and Methods Patients diagnosed with ATC between 2000 and 2019 were selected from the Surveillance, Epidemiology, and End Results database. The crude mortality rates of patients with ATC were calculated and their differences were tested using the Gray's test, respectively. In performing multivariate analysis, the Cox regression model and the subdistribution hazard function (SD) in competing risk analysis were utilized, respectively.Results This study included 21,477 eligible patients. The SD model indicated that age, etc. are actual independent prognostic factors. In contrast to previous recognition, the results of the Cox regression showed false-positives for sex and Carcinoembryonic antigen, and underestimated point-estimates in the stage and American Joint Committee on Cancer stage due to competing events. A detailed comparison of treatment revealed that the larger surgical scopes were prognostic risk factors compared with the smaller scope of local tumor excision, partial colectomy, or segmental resection. Patients treated with external proton beam radiotherapy had an increased risk compared with those with no radiotherapy and internal radiotherapy.Conclusions After comparing the results of the two methods and mitigating the significant bias introduced by Cox regression, we found independent factors that really affect the prognosis of ATC. On the other hand, in terms of ATC, a larger surgical scope and external proton beam radiotherapy may not improve the long-term survival of patients. Therefore, when faced with ATC patients, these differences should be noted and treated differently from common colorectal cancer patients. Thus, clinicians are able to give more targeted treatment plans and prognostic assessments.
C1 [Su, Hongbo; Pan, Yunlong] Jinan Univ, Dept Gen Surg, Affiliated Hosp 1, Guangzhou, Guangdong, Peoples R China.
   [Xie, Shuping] Shanxi Med Univ, Sch Publ Hlth, Dept Hlth Stat, Taiyuan, Peoples R China.
   [Wang, Shanshan] Shanxi Med Univ, Dept Special Med, Sect Occupat Med, Taiyuan, Shanxi, Peoples R China.
   [Huang, Liying; Lyu, Jun] Jinan Univ, Dept Clin Res, Affiliated Hosp 1, Guangzhou, Guangdong, Peoples R China.
   [Lyu, Jun] Guangdong Acad Med Sci, Guangzhou, Guangdong, Peoples R China.
C3 Jinan University; Shanxi Medical University; Shanxi Medical University;
   Jinan University; Guangdong Academy of Medical Sciences & Guangdong
   General Hospital
RP Pan, YL (corresponding author), Jinan Univ, Dept Gen Surg, Affiliated Hosp 1, Guangzhou, Guangdong, Peoples R China.; Lyu, J (corresponding author), Jinan Univ, Dept Clin Res, Affiliated Hosp 1, Guangzhou, Guangdong, Peoples R China.; Lyu, J (corresponding author), Guangdong Acad Med Sci, Guangzhou, Guangdong, Peoples R China.
EM lyujun2020@jnu.edu.cn; tpanyl@jnu.edu.cn
RI Huang, Liying/HLP-8304-2023; Lyu, Jun/AAS-1229-2021
OI Lyu, Jun/0000-0002-2237-8771
FU Guangzhou Science and Technology Plan City-School Joint Funding Project
   [202201020084, 202201020065]; Clinical Frontier Technology Program of
   the First Affiliated Hospital of Jinan University, China
   [JNU1AF-CFTP-2022a01223]; Guangdong Provincial Key Laboratory of
   Traditional Chinese Medicine Informatization [2021B1212040007]
FX The author(s) declare financial support was received for the research,
   authorship, and/or publication of this article. This work was supported
   by the Guangzhou Science and Technology Plan City-School Joint Funding
   Project (202201020084 and 202201020065), the Clinical Frontier
   Technology Program of the First Affiliated Hospital of Jinan University,
   China (No. JNU1AF-CFTP-2022a01223), and the Guangdong Provincial Key
   Laboratory of Traditional Chinese Medicine Informatization
   (2021B1212040007).
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NR 42
TC 0
Z9 0
U1 2
U2 4
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
EI 2296-858X
J9 FRONT MED-LAUSANNE
JI Front. Med.
PD JAN 31
PY 2024
VL 11
AR 1301487
DI 10.3389/fmed.2024.1301487
PG 12
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA HO1X6
UT WOS:001160365100001
PM 38357650
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Collienne, M
   Neven, A
   Caballero, C
   Kataoka, K
   Carrion-Alvarez, L
   Nilsson, H
   Désolneux, G
   Rivoire, M
   Ruers, T
   Gruenberger, T
   Protic, M
   Troisi, RI
   Primavesi, F
   Staettner, S
   Rahbari, N
   Schnitzbauer, A
   Malik, H
   Swijnenburg, RJ
   Mauer, M
   Ducreux, M
   Evrard, S
AF Collienne, Maike
   Neven, Anouk
   Caballero, Carmela
   Kataoka, Kozo
   Carrion-Alvarez, Lucia
   Nilsson, Henrik
   Desolneux, Gregoire
   Rivoire, Michel
   Ruers, Theo
   Gruenberger, Thomas
   Protic, Mladjan
   Troisi, Roberto Ivan
   Primavesi, Florian
   Staettner, Stefan
   Rahbari, Nuh
   Schnitzbauer, Andreas
   Malik, Hassan
   Swijnenburg, Rutger-Jan
   Mauer, Murielle
   Ducreux, Michel
   Evrard, Serge
TI EORTC 1409 GITCG/ESSO 01-A prospective colorectal liver metastasis
   database for borderline or initially unresectable diseases (CLIMB):
   Lessons learnt from real life. From paradigm to unmet need
SO EJSO
LA English
DT Article
DE Colorectal cancer; Colorectal liver metastasis; Parenchyma sparing
   surgery; Major hepatectomy; 2-Stage hepatectomies; ALPPS; Postoperative
   complications; Quality control; Prospective non-randomized study
ID SURGICAL COMPLICATIONS; SURGERY; CLASSIFICATION; CHEMOTHERAPY
AB Aim: Multidisciplinary management of metastatic colorectal liver metastases (CRLM) is still challenging. To assess postoperative complications in initially unresectable or borderline resectable CRLM, the prospective EORTC-1409 ESSO 01-CLIMB trial capturing 'real-life data' of European centres specialized in liver surgery was initiated.
   Material and methods: A total of 219 patients were registered between May 2015 and January 2019 from 15 centres in nine countries. Eligible patients had borderline or initially unresectable CRLM assessed by pre-operative multidisciplinary team discussion (MDT). Primary endpoints were postoperative complications, 30-day and 90-days mortality post-surgery, and quality indicators. We report the final results of the 151 eligible patients that underwent at least one liver surgery.
   Results: Perioperative chemotherapy with or without targeted treatment were administered in 100 patients (69.4%). One stage resection (OSR) was performed in 119 patients (78.8%). Two stage resections (TSR, incl. Associating Liver Partition and Portal Vein Ligation for Staged hepatectomy (ALPPS)) were completed in 24 out of 32 patients (75%). Postoperative complications were reported in 55.5% (95% CI: 46.1-64.6%), 64.0% (95% CI: 42.5-82%), and 100% (95% CI: 59-100%) of the patients in OSR, TSR and ALPPS, respectively. Post-hepatectomy liver failure occurred in 6.7%, 20.0%, and 28.6% in OSR, TSR, and ALPPS, respectively. In total, four patients (2.6%) died after surgery.
   Conclusion: Across nine countries, OSR was more often performed than TSR and tended to result in less post-operative complications. Despite many efforts to register patients across Europe, it is still challenging to set up a prospective CRLM database.
C1 [Collienne, Maike; Neven, Anouk; Mauer, Murielle] European Org Res & Treatment Canc EORTC Headquart, Ave E Mounier 83-11, B-1200 Brussels, Belgium.
   [Neven, Anouk] Luxembourg Inst Hlth, Competence Ctr Methodol & Stat, Strassen, Luxembourg.
   [Caballero, Carmela] Breast Int Grp BIG Aisbl, Brussels, Belgium.
   [Kataoka, Kozo] Hyogo Med Univ, Sch Med, Div Lower GI, Dept Surg Gastroenterol, Nishinomiya, Hyogo, Japan.
   [Carrion-Alvarez, Lucia] Hosp Univ Fuenlabrada, Madrid, Spain.
   [Nilsson, Henrik] Karolinska Inst, Dept Clin Sci Danderyd, Stockholm, Sweden.
   [Desolneux, Gregoire] Inst Bergonie, Surg Oncol, Bordeaux, France.
   [Rivoire, Michel] Ctr Leon Berard, Lyon, France.
   [Ruers, Theo] Antoni van Leeuwenhoek Hosp, Netherlands Canc Inst, Amsterdam, Netherlands.
   [Gruenberger, Thomas] Hlth Network Vienna, HPB Ctr, Clin Favoriten, Vienna, Austria.
   [Gruenberger, Thomas] Sigmund Freud Univ, Vienna, Austria.
   [Protic, Mladjan] Univ Novi Sad, Fac Med, Novi Sad, Serbia.
   [Protic, Mladjan] Oncol Inst Vojvodina, Sremska Kamenica, Serbia.
   [Troisi, Roberto Ivan] Univ Ghent, Dept Human Struct & Repair, Ghent, Belgium.
   [Primavesi, Florian; Staettner, Stefan] Med Univ Innsbruck, Dept Visceral Transplantat & Thorac Surg, Innsbruck, Austria.
   [Primavesi, Florian; Staettner, Stefan] Salzkammergutklinikum, Dept Gen Visceral & Vasc Surg, Bad Ischl, Austria.
   [Rahbari, Nuh] Univ Med Mannheim, Dept Surg, Mannheim, Germany.
   [Schnitzbauer, Andreas] Goethe Univ Frankfurt Main, Univ Klinikum Frankfurt, Klin Allgemein & Viszeralchirurg, Frankfurt, Germany.
   [Malik, Hassan] Aintree Univ Hosp NHS Fdn Trust, Liverpool, Merseyside, England.
   [Swijnenburg, Rutger-Jan] Leiden Univ Med Ctr, Leiden, Netherlands.
   [Swijnenburg, Rutger-Jan] Vrije Univ Amsterdam, Amsterdam UMC, Canc Ctr Amsterdam, Dept Surg, Amsterdam, Netherlands.
   [Ducreux, Michel] Univ Paris Saclay, Gustave Roussy, INSERM, U1279, Paris, France.
   [Evrard, Serge] Univ Bordeaux, INSERM, Inst Bergonie, U1312, Bordeaux, France.
   [Troisi, Roberto Ivan] Federico II Univ Hosp Naples, Dept Clin Med & Surg, Renal Transplantat Serv, Div HPB Minimally Invas & Robot Surg, Naples, Italy.
C3 Luxembourg Institute of Health; Breast International Group; Hyogo
   Medical University; Hospital Universitario Fuenlabrada; Karolinska
   Institutet; UNICANCER; Institut Bergonie; UNICANCER; Centre Leon Berard;
   Netherlands Cancer Institute; University of Novi Sad; Ghent University;
   Medical University of Innsbruck; Ruprecht Karls University Heidelberg;
   Goethe University Frankfurt; Goethe University Frankfurt Hospital;
   Aintree University Hospitals NHS Foundation Trust; Leiden University;
   Leiden University Medical Center (LUMC); Vrije Universiteit Amsterdam;
   University of Amsterdam; Institut National de la Sante et de la
   Recherche Medicale (Inserm); Universite Paris Saclay; UNICANCER; Gustave
   Roussy; UNICANCER; Institut Bergonie; Institut National de la Sante et
   de la Recherche Medicale (Inserm); Universite de Bordeaux
RP Collienne, M (corresponding author), European Org Res & Treatment Canc EORTC Headquart, Ave E Mounier 83-11, B-1200 Brussels, Belgium.
EM maike.collienne@eortc.org; s.evrard@bordeaux.unicancer.fr
RI Primavesi, Florian/JJC-7715-2023; Gruenberger, Thomas/ABA-1661-2020;
   Collienne, Maike/ABB-8192-2020; Nilsson, Henrik/AAB-6041-2020
OI Carrion-Alvarez, Lucia/0000-0003-2301-2795; Nilsson,
   Henrik/0000-0002-8503-4984; Caballero, Carmela
   Isabel/0000-0002-3586-6598; Neven, Anouk/0000-0003-2253-0427;
   Gruenberger, Thomas/0000-0002-2671-0540; Kataoka,
   Kozo/0000-0003-2043-8184
FU Bruckner Foundation; European Society of Surgical Oncology (ESSO);
   European Organisation for Research and Treatment of Cancer (EORTC);
   EORTC Cancer Research Fund (ECRF)
FX This publication was supported by a donation from the Bruckner
   Foundation, from the European Society of Surgical Oncology (ESSO) and
   from the European Organisation for Research and Treatment of Cancer
   (EORTC). Maike Collienne's work as Fellow at EORTC Headquarters was
   supported by a grant from the EORTC Cancer Research Fund (ECRF).
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NR 25
TC 2
Z9 3
U1 1
U2 3
PU ELSEVIER SCI LTD
PI London
PA 125 London Wall, London, ENGLAND
SN 0748-7983
EI 1532-2157
J9 EJSO-EUR J SURG ONC
JI EJSO
PD NOV
PY 2023
VL 49
IS 11
AR 107081
DI 10.1016/j.ejso.2023.107081
EA OCT 2023
PG 8
WC Oncology; Surgery
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Surgery
GA JL7J3
UT WOS:001173385800001
PM 37793303
DA 2025-01-04
ER

PT J
AU Zhang, XS
   Li, QR
   Zhao, H
   Ma, LP
   Meng, T
   Qian, JC
   Jin, R
   Shen, JK
   Yu, K
AF Zhang, Xuesai
   Li, Qingrou
   Zhao, Hui
   Ma, Lanping
   Meng, Tao
   Qian, Jianchang
   Jin, Rui
   Shen, Jingkang
   Yu, Ker
TI Pathological expression of tissue factor confers promising antitumor
   response to a novel therapeutic antibody SC1 in triple negative breast
   cancer and pancreatic adenocarcinoma
SO ONCOTARGET
LA English
DT Article
DE tissue factor; triple negative breast cancer; pancreatic adenocarcinoma;
   metastasis; antibody-drug conjugate
ID EPITHELIAL-MESENCHYMAL TRANSITION; FACTOR CYTOPLASMIC DOMAIN;
   GROWTH-FACTOR RECEPTOR; TUMOR-GROWTH; DUCTAL ADENOCARCINOMA; COAGULATION
   CASCADE; VENOUS THROMBOSIS; COLORECTAL-CANCER; DRUG CONJUGATE; SOLID
   TUMORS
AB The pathological presence of tissue factor (TF) in cancer cells promotes tumor-initiated thrombosis and cancer metastasis. We found that TF is aberrantly present in large percentage of aggressive triple negative breast cancer (TNBC) and pancreatic adenocarcinoma (PaC), two most lethal forms of malignancy that urgently need effective treatment. TF expression in TNBC clustered with higher levels of vimentin, basal-type keratins KRT5/14 and caveolin-1 but lower levels of luminaltype biomarkers. We developed a novel and specific anti-TF therapeutic antibody SC1, which displayed an exceedingly high potency against TF extracellular domain (EC50: 0.019 nM), TF-positive TNBC-or PaC cells (EC50: 2.5 nM), intracellular protease activated receptor 2 (PAR2) signaling (IC50: 2-3 nM) and tumor-initiated coagulation (IC50: < 10 nM). Depletion of TF or SC1-treatment in TNBC or PaC cells inhibited TF-induced cell migration, lung metastasis and tumor growth in vivo, accompanied by diminished levels of tumor angiogenesis and stromal fibrosis. We further propose TF as a promising target for antibody-drug conjugate (ADC) development based on its rapid and efficient internalization of SC1-drug conjugate. Both SC1-DM1 and SC1-MMAE elicited exquisite cytotoxicity in TF-positive TNBC and PaC cells (IC50: 0.02-0.1 nM) but not in TF-negative cells (> 100 nM) achieving > 5000 fold target selectivity. Following a weekly intravenous administration, SC1-MMAE and its humanized hSC1-MMAE inhibited TNBC-and PaC tumor growth achieving MED of 0.3-1 mg/kg and were both well tolerated. Thus, the prevalent TF expression in TNBC and PaC renders these challenging tumors highly susceptible to TF-targeted treatment and may offer new opportunity in cancer patients.
C1 [Zhang, Xuesai; Li, Qingrou; Zhao, Hui; Qian, Jianchang; Jin, Rui; Yu, Ker] Fudan Univ, Sch Pharm, Dept Pharmacol, Shanghai, Peoples R China.
   [Ma, Lanping; Meng, Tao; Shen, Jingkang] Chinese Acad Sci, Shanghai Inst Mat Med, State Key Lab Drug Res, Dept Med Chem, Shanghai, Peoples R China.
C3 Fudan University; Chinese Academy of Sciences; Shanghai Institute of
   Materia Medica, CAS
RP Yu, K (corresponding author), Fudan Univ, Sch Pharm, Dept Pharmacol, Shanghai, Peoples R China.
EM keryu@fudan.edu.cn
RI jin, rui/KHW-6854-2024
FU Fudan University [EZF301002]; National Natural Science Foundation of
   China [81273367]; National Basic Research 973 Program of China
   [2013CB932500]
FX This work was supported by a startup grant from Fudan University
   (EZF301002), National Natural Science Foundation of China (81273367) and
   National Basic Research 973 Program of China (2013CB932500). We thank
   Dr. Qing Lin, Dr. Liyuan Zhu, Dr. Qun He and Mengjun Shu for technical
   assistance.
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NR 53
TC 37
Z9 45
U1 0
U2 13
PU IMPACT JOURNALS LLC
PI ORCHARD PARK
PA 6666 E QUAKER ST, STE 1, ORCHARD PARK, NY 14127 USA
EI 1949-2553
J9 ONCOTARGET
JI Oncotarget
PD AUG 29
PY 2017
VL 8
IS 35
BP 59086
EP 59102
DI 10.18632/oncotarget.19175
PG 17
WC Oncology; Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Cell Biology
GA FF4RD
UT WOS:000408941900095
PM 28938620
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Zeng, MY
   Feng, Q
   Lu, M
   Zhou, J
   Yang, ZY
   Tang, JL
AF Zeng, Minyan
   Feng, Qi
   Lu, Ming
   Zhou, Jun
   Yang, Zuyao
   Tang, Jinling
TI Predictive role of skin rash in advanced pancreatic cancer patients
   treated with gemcitabine plus erlotinib: a systematic review and
   meta-analysis
SO ONCOTARGETS AND THERAPY
LA English
DT Review
DE pancreatic neoplasms; targeted treatment; acne; prognosis
ID TYROSINE KINASE INHIBITOR; PHASE-III TRIAL; CUTANEOUS TOXICITIES;
   COLORECTAL-CANCER; FUNNEL-PLOT; OPEN-LABEL; RECEPTOR; SURVIVAL;
   COMBINATION; EFFICACY
AB Purpose: The survival benefit from gemcitabine plus erlotinib was on average marginal for advanced pancreatic cancer (APC) patients. Skin rash developed shortly after starting treatment seemed to be associated with better efficacy and might be used to assist clinical decision-making, but the results across studies were inconsistent. Thus, we conducted a systematic review and meta-analysis. M
   Methods: PubMed, Embase, Cochrane Central Register of Controlled Trials, three Chinese databases, and the abstracts of important conferences were searched for eligible studies. The primary outcome was overall survival (OS), and the secondary outcomes were progression-free survival (PFS) and objective response. The random-effects model was used to pool results across studies if heterogeneity was substantial. Otherwise, the fixed-effect model was used.
   Results: A total of 16 studies with 1,776 patients were included. Patients who developed skin rash during treatment had longer OS (8.9 vs 4.9 months, HR=0.57, 95% CI 0.50-0.64) and longer PFS (4.5 vs 2.4 months, HR=0.53, 95% CI 0.40-0.68) than those who did not. A dose-response relationship was also observed for both OS (HR=0.64 for grade-1 rash vs no rash and HR=0.46 for >= grade-2 rash vs no rash) and PFS (HR=0.72 for grade-1 rash vs no rash and HR=0.43 for >= grade-2 rash vs no rash).
   Conclusion: Skin rash was associated with better OS and PFS in APC patients treated with gemcitabine plus erlotinib. It might be used as a marker for efficacy to guide clinical decision-making toward a more precise and personalized treatment.
C1 [Zeng, Minyan; Feng, Qi; Yang, Zuyao; Tang, Jinling] Chinese Univ Hong Kong, JC Sch Publ Hlth & Primary Care, Div Epidemiol, 30-32 Ngan Shing St, Hong Kong, Hong Kong, Peoples R China.
   [Lu, Ming; Zhou, Jun] Peking Univ, Dept GI Med Oncol, Key Lab Carcinogenesis & Translat Res, Minist Educ,Canc Hosp & Inst, Beijing, Peoples R China.
   [Yang, Zuyao; Tang, Jinling] Chinese Univ Hong Kong, JC Sch Publ Hlth & Primary Care, Cochrane Hong Kong, Hong Kong, Hong Kong, Peoples R China.
C3 Chinese University of Hong Kong; Peking University; Chinese University
   of Hong Kong
RP Yang, ZY (corresponding author), Chinese Univ Hong Kong, JC Sch Publ Hlth & Primary Care, Div Epidemiol, 30-32 Ngan Shing St, Hong Kong, Hong Kong, Peoples R China.
EM zyang@cuhk.edu.hk
RI Ma, Mingyang/JDW-6179-2023; An, Mingyang/ABA-2541-2021
OI Yang, Zuyao/0000-0003-2386-2431; FENG, QI/0000-0001-9323-9421
FU Food and Health Bureau, Hong Kong [14152141]
FX This study was funded by Health and Medical Research Fund (Ref No
   14152141), Food and Health Bureau, Hong Kong.
CR [Anonymous], CHIN J CLIN RATIONAL
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NR 52
TC 2
Z9 2
U1 0
U2 4
PU DOVE MEDICAL PRESS LTD
PI ALBANY
PA PO BOX 300-008, ALBANY, AUCKLAND 0752, NEW ZEALAND
SN 1178-6930
J9 ONCOTARGETS THER
JI OncoTargets Ther.
PY 2018
VL 11
BP 6633
EP 6646
DI 10.2147/OTT.S168418
PG 14
WC Biotechnology & Applied Microbiology; Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biotechnology & Applied Microbiology; Oncology
GA GW2UV
UT WOS:000446743400005
PM 30349297
OA Green Published, gold, Green Submitted
DA 2025-01-04
ER

PT J
AU Xiao, YJ
   Xiao, XF
   Zhang, X
   Yi, DX
   Li, T
   Hao, QQ
   Zhang, F
   Li, X
   Wang, NN
AF Xiao, Yuji
   Xiao, Xuefei
   Zhang, Xue
   Yi, Dongxin
   Li, Tao
   Hao, Qiangqiang
   Zhang, Feng
   Li, Xu
   Wang, Ningning
TI Mediterranean diet in the targeted prevention and personalized treatment
   of chronic diseases: evidence, potential mechanisms, and prospects
SO EPMA JOURNAL
LA English
DT Review
DE Mediterranean diet; Well-being; Optimal dietary treatment;
   Individualized patient profile; MedDiet; Chronic disease prevention;
   Cardiovascular disease; Hypertension; Type 2 diabetes mellitus; Obesity;
   Metabolic syndrome; Osteoporosis; Cancer; Predictive preventive
   personalized medicine; Personalized dietary customization; Healthcare
   economy; PPPM / 3PM; Mitochondria; Anti-inflammatory and antioxidant
   effects; Improved individual outcomes; Primary and secondary care
ID OLIVE OIL CONSUMPTION; IMPROVES ENDOTHELIAL FUNCTION; COLORECTAL-CANCER
   RISK; METABOLIC SYNDROME; CARDIOVASCULAR-DISEASE; BLOOD-PRESSURE;
   BREAST-CANCER; WEIGHT CHANGE; ADHERENCE; PATTERNS
AB The prevalence of chronic diseases is currently a major public health issue worldwide and is exploding with the population growth and aging. Dietary patterns are well known to play a important role in our overall health and well-being, and therefore, poor diet and malnutrition are among the most critical risk factors for chronic disease. Thus, dietary recommendation and nutritional supplementation have significant clinical implications for the targeted treatment of some of these diseases. Multiple dietary patterns have been proposed to prevent chronic disease incidence, like Dietary Approaches to Stop Hypertension (DASH) and Diabetes Risk Reduction Diet (DRRD). Among them, the MedDiet, which is one of the most well-known and studied dietary patterns in the world, has been related to a wide extent of health benefits. Substantial evidence has supported an important reverse association between higher compliance to MedDiet and the risk of chronic disease. Innovative strategies within the healthcare framework of predictive, preventive, and personalized medicine (PPPM/3PM) view personalized dietary customization as a predictive medical approach, cost-effective preventive measures, and the optimal dietary treatment tailored to the characteristics of patients with chronic diseases in primary and secondary care. Through a comprehensive collection and review of available evidence, this review summarizes health benefits of MedDiet in the context of PPPM/3PM for chronic diseases, including cardiovascular disease, hypertension, type 2 diabetes, obesity, metabolic syndrome, osteoporosis, and cancer, thereby a working hypothesis that MedDiet can personalize the prevention and treatment of chronic diseases was derived.
C1 [Xiao, Yuji; Zhang, Xue; Yi, Dongxin; Hao, Qiangqiang; Zhang, Feng] Dalian Med Univ, Sch Publ Hlth, Dalian, Liaoning, Peoples R China.
   [Xiao, Yuji; Xiao, Xuefei] Chongqing Med Univ, Bishan Hosp, Chongqing, Peoples R China.
   [Zhang, Xue] Second Peoples Hosp Dalian, Dalian, Liaoning, Peoples R China.
   [Li, Tao] Dalian Med Univ, Dept Cardiol, Affiliated Hosp 1, Dalian, Liaoning, Peoples R China.
   [Li, Xu] Dalian Med Univ, Dept Clin Nutr, Affiliated Hosp 2, Dalian, Liaoning, Peoples R China.
   [Wang, Ningning] Dalian Med Univ, Global Hlth Res Ctr, Sch Publ Hlth, Dept Nutr & Food Hyg, Dalian, Liaoning, Peoples R China.
   [Wang, Ningning] Dalian Med Univ, Global Hlth Res Ctr, Dalian, Liaoning, Peoples R China.
C3 Dalian Medical University; Chongqing Medical University; Dalian Medical
   University; Dalian Medical University; Dalian Medical University; Dalian
   Medical University
RP Li, X (corresponding author), Dalian Med Univ, Dept Clin Nutr, Affiliated Hosp 2, Dalian, Liaoning, Peoples R China.; Wang, NN (corresponding author), Dalian Med Univ, Global Hlth Res Ctr, Sch Publ Hlth, Dept Nutr & Food Hyg, Dalian, Liaoning, Peoples R China.; Wang, NN (corresponding author), Dalian Med Univ, Global Hlth Res Ctr, Dalian, Liaoning, Peoples R China.
EM lixu-29@163.com; zkxwnn@dmu.edu.cn
FU National Natural Science Foundation of China
FX No Statement Available
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NR 120
TC 10
Z9 10
U1 9
U2 9
PU SPRINGER INT PUBL AG
PI CHAM
PA GEWERBESTRASSE 11, CHAM, CH-6330, SWITZERLAND
SN 1878-5077
EI 1878-5085
J9 EPMA J
JI EPMA J.
PD JUN
PY 2024
VL 15
IS 2
BP 207
EP 220
DI 10.1007/s13167-024-00360-w
PG 14
WC Medicine, General & Internal; Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine; Research & Experimental Medicine
GA SX9R9
UT WOS:001237872500001
PM 38841625
DA 2025-01-04
ER

PT J
AU Li, DS
   Yang, J
   Xu, ZY
   Li, YB
   Sun, YG
   Wang, YC
   Zou, HY
   Wang, K
   Yang, LL
   Wu, LA
   Sun, XL
AF Li, Daoshuang
   Yang, Jie
   Xu, Zuoyu
   Li, Yingbo
   Sun, Yige
   Wang, Yuchen
   Zou, Hongyan
   Wang, Kai
   Yang, Lili
   Wu, Lina
   Sun, Xilin
TI c-Met-Targeting 19F MRI Nanoparticles with Ultralong Tumor Retention for
   Precisely Detecting Small or Ill-Defined Colorectal Liver Metastases
SO INTERNATIONAL JOURNAL OF NANOMEDICINE
LA English
DT Article
DE c-Met-targeted; perfluorocarbon; 19 F MRI; colorectal liver metastases;
   precise detection
ID MAGNETIC-RESONANCE; CONTRAST AGENT; DRUG-DELIVERY; SIZE
AB Purpose: Precisely detecting colorectal liver metastases (CLMs), the leading cause of colorectal cancer-associated mortality, is extremely important. 1H MRI with high soft tissue resolution plays a key role in the diagnosing liver lesions; however, precise detecting CLMs by 1H MRI is a great challenge due to the limited sensitivity. Even though contrast agents may improve the sensitivity, due to their short half-life, repeated injections are required to monitor the changes of CLMs. Herein, we synthesized c-Met-targeting peptide-functionalized perfluoro-15-crown-5-ether nanoparticles (AH111972-PFCE NPs), for highly sensitive and early diagnosis ofMethods: The size, morphology and optimal properties of the AH111972-PFCE NPs were characterized. c-Met specificity of the AH111972-PFCE NPs was validated by in vitro experiment and in vivo 19F MRI study in the subcutaneous tumor murine model. The molecular imaging practicability and long tumor retention of the AH111972-PFCE NPs were evaluated in the liver metastases mouse model. The biocompatibility of the AH111972-PFCE NPs was assessed by toxicity study.Results: AH111972-PFCE NPs with regular shape have particle size of 89.3 +/- 17.8 nm. The AH111972-PFCE NPs exhibit high specificity, strong c-Met-targeting ability, and precise detection capability of CLMs, especially small or ill-defined fused metastases in 1H MRI. Moreover, AH111972-PFCE NPs could be ultralong retained in metastatic liver tumors for at least 7 days, which is conductive to the implementation of continuous therapeutic efficacy monitoring. The NPs with minimal side effects and good biocompatibility are cleared mainly via the spleen and liver.Conclusion: The c-Met targeting and ultralong tumor retention of AH111972-PFCE NPs will contribute to increasing therapeutic agent accumulation in metastatic sites, laying a foundation for CLMs diagnosis and further c-Met targeted treatment integration. This work provides a promising nanoplatform for the future clinical application to patients with CLMs.
C1 [Li, Daoshuang; Yang, Jie; Xu, Zuoyu; Li, Yingbo; Sun, Yige; Wang, Yuchen; Zou, Hongyan; Wang, Kai; Yang, Lili; Wu, Lina; Sun, Xilin] Harbin Med Univ, Hosp 4, Dept Nucl Med, Harbin, Heilongjiang, Peoples R China.
   [Li, Daoshuang; Yang, Jie; Xu, Zuoyu; Li, Yingbo; Sun, Yige; Wang, Yuchen; Zou, Hongyan; Wang, Kai; Yang, Lili; Wu, Lina; Sun, Xilin] Harbin Med Univ, NHC Key Lab Mol Probe & Targeted Diag & Therapy, Mol Imaging Res Ctr MIRC, Harbin, Heilongjiang, Peoples R China.
   [Wu, Lina; Sun, Xilin] Harbin Med Univ, Hosp 4, Dept Nucl Med, 766 Xiangan N St, Harbin 150028, Heilongjiang, Peoples R China.
C3 Harbin Medical University; Harbin Medical University; Harbin Medical
   University
RP Wu, LA; Sun, XL (corresponding author), Harbin Med Univ, Hosp 4, Dept Nucl Med, 766 Xiangan N St, Harbin 150028, Heilongjiang, Peoples R China.
EM LinaWu@hrbmu.edu.cn; sunxl@ems.hrbmu.edu.cn
RI Sun, Xilin/GXH-0270-2022; Li, Yingbo/KLC-3013-2024; ZOU,
   HONGYAN/O-2301-2014; Li, Daoshuang/KQV-4412-2024; Wu, Lina/JXO-0074-2024
FU National Natural Science Foundation of China [81627901, 82102101];
   Natural Science Foundation of Heilongjiang Province [JQ2020H002]; HMU
   Marshal Initiative Funding [HMUMIF-21003]; Tou-Yan Innovation Team
   Program of the Heilongjiang Province [2019-15]; Heilongjiang Provincial
   Key Laboratory of Molecular Imaging foundation
FX Daoshuang Li and Jie Yang contributed equally to this work. This work
   was supported by the National Natural Science Foundation of China
   (81627901 and 82102101) , Natural Science Foundation of Heilongjiang
   Province (Grant No. JQ2020H002) , HMU Marshal Initiative Funding
   (HMUMIF-21003) , the Tou-Yan Innovation Team Program of the Heilongjiang
   Province (2019-15) , and Heilongjiang Provincial Key Laboratory of
   Molecular Imaging foundation.
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NR 40
TC 5
Z9 5
U1 2
U2 10
PU DOVE MEDICAL PRESS LTD
PI ALBANY
PA PO BOX 300-008, ALBANY, AUCKLAND 0752, NEW ZEALAND
SN 1178-2013
J9 INT J NANOMED
JI Int. J. Nanomed.
PY 2023
VL 18
BP 2181
EP 2196
DI 10.2147/IJN.S403190
PG 16
WC Nanoscience & Nanotechnology; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Science & Technology - Other Topics; Pharmacology & Pharmacy
GA F3NA9
UT WOS:000981433200001
PM 37131548
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Szupryczynski, K
   Czelen, P
   Jelinski, T
   Szefler, B
AF Szupryczynski, Kamil
   Czelen, Przemyslaw
   Jelinski, Tomasz
   Szefler, Beata
TI What is the Reason That the Pharmacological Future of Chemotherapeutics
   in the Treatment of Lung Cancer Could Be Most Closely Related to
   Nanostructures? Platinum Drugs in Therapy of Non-Small and Small Cell
   Lung Cancer and Their Possible Interactions. The Review
SO INTERNATIONAL JOURNAL OF NANOMEDICINE
LA English
DT Review
DE fullerenes; nanotube; nanoparticles; drug delivery; personalized
   medicine; platinum-based drugs; cisplatin; carboplatin; oxaliplatin;
   nedaplatin
ID CISPLATIN-INDUCED OTOTOXICITY; IRON-OXIDE NANOPARTICLES;
   QUANTUM-MECHANICAL CALCULATIONS; METASTATIC COLORECTAL-CANCER;
   RANDOMIZED PHASE-III; MOLECULAR-MECHANISMS; CARBON NANOTUBES; IN-VITRO;
   LIPOSOMAL CISPLATIN; MAGNETIC NANOPARTICLES
AB Over the course of several decades, anticancer treatment with chemotherapy drugs for lung cancer has not changed significantly. Unfortunately, this treatment prolongs the patient's life only by a few months, causing many side effects in the human body. It has also been proven that drugs such as Cisplatin, Carboplatin, Oxaliplatin and others can react with other substances containing an aromatic ring in which the nitrogen atom has a free electron group in its structure. Thus, such structures may have a competitive effect on the nucleobases of DNA. Therefore, scientists are looking not only for new drugs, but also for new alternative ways of delivering the drug to the cancer site. Nanotechnology seems to be a great hope in this matter. Creating a new nanomedicine would reduce the dose of the drug to an absolute minimum, and thus limit the toxic effect of the drug; it would allow for the exclusion of interactions with competitive compounds with a structure similar to nucleobases; it would also permit using the so-called targeted treatment and bypassing healthy cells; it would allow for the introduction of other treatment options, such as radiotherapy directly to the cancer site; and it would provide diagnostic possibilities. This article is a review that aims to systematize the knowledge regarding the anticancer treatment of lung cancer, but not only. It shows the clear possibility of interactions of chemotherapeutics with compounds competitive to the nitrogenous bases of DNA. It also shows the possibilities of using nanostructures as potential Platinum drug carriers, and proves that nanomedicine can easily become a new medicinal product in personalized medicine.
C1 [Szupryczynski, Kamil] Nicolaus Copernicus Univ, Doctoral Sch Med & Hlth Sci, Fac Pharm, Coll Med, Bydgoszcz, Poland.
   [Czelen, Przemyslaw; Jelinski, Tomasz; Szefler, Beata] Nicolaus Copernicus Univ, Coll Med, Fac Pharm, Dept Phys Chem, Bydgoszcz, Poland.
C3 Nicolaus Copernicus University; Nicolaus Copernicus University
RP Szefler, B (corresponding author), Nicolaus Copernicus Univ, Coll Med, Fac Pharm, Dept Phys Chem, Bydgoszcz, Poland.
EM beatas@cm.umk.pl
RI Jeliński, Tomasz/F-9657-2014; Szefler, Beata/F-9695-2014
FU Doctoral School of Medical and Faculty of Pharmacy, Collegium Medicum,
   Nicolaus Copernicus University, Jagiellonska, Bydgoszcz, Poland
FX Funding Publication of this article (Article Processing Charge) was
   financially supported by the Doctoral School of Medical and Faculty of
   Pharmacy, Collegium Medicum, Nicolaus Copernicus University,
   Jagiellonska 13, 85-067 Bydgoszcz, Poland.
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NR 484
TC 0
Z9 0
U1 14
U2 14
PU DOVE MEDICAL PRESS LTD
PI ALBANY
PA PO BOX 300-008, ALBANY, AUCKLAND 0752, NEW ZEALAND
SN 1178-2013
J9 INT J NANOMED
JI Int. J. Nanomed.
PY 2024
VL 19
BP 9503
EP 9547
DI 10.2147/IJN.S469217
PG 45
WC Nanoscience & Nanotechnology; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Science & Technology - Other Topics; Pharmacology & Pharmacy
GA G2I1R
UT WOS:001314917700001
PM 39296940
OA gold
DA 2025-01-04
ER

PT J
AU Golubnitschaja, O
   Polivka, J
   Yeghiazaryan, K
   Berliner, L
AF Golubnitschaja, Olga
   Polivka, Jiri, Jr.
   Yeghiazaryan, Kristina
   Berliner, Leonard
TI Liquid biopsy and multiparametric analysis in management of liver
   malignancies: new concepts of the patient stratification and prognostic
   approach
SO EPMA JOURNAL
LA English
DT Article
DE Hepatocellular carcinoma; Colorectal cancer; Breast cancer; Metastatic
   disease; Selective internal radiation therapy (SIRT); Transarterial
   chemoembolisation (TACE); Survival; Predictive preventive personalised
   medicine; Multi-omics; Biomarker pattern; Individual outcome
ID BREAST-CANCER; HEPATOCELLULAR-CARCINOMA; OXIDATIVE STRESS; S100A8;
   EXPRESSION; PREDICTION; DISEASE; PROFILES; MARKERS; PROTEIN
AB Background The annually recorded incidence of primary hepatic carcinomas has significantly increased over the past two decades accounting for over 800 thousand of annual deaths caused by hepatocellular carcinoma (HCC) alone globally. Further, secondary liver malignancies are much more widespread compared to primary hepatic carcinomas: almost all solid malignancies are able to metastasise into the liver. The primary tumours most frequently metastasising to the liver are breast followed by colorectal carcinomas. Given the increased incidence of both primary and metastatic liver cancers, a new, revised approach is needed to advance medical care based on predictive diagnostics, innovative screening programmes, targeted preventive measures, and patient stratification for treatment algorithms tailored to individualised patient profile.
   Advantages of the approach taken The current pilot study took advantage of systemic alterations characteristic for liver malignancies. utilising liquid biopsy (blood samples) and specific biomarker patterns detected. Key molecular pathways relevant for pathomechanisms of liver cancels have been considered opening a perspective for both-individualised diagnostics and targeted treatment. Systemic alterations have been analysed prior to the therapy application avoiding molecular biological effects potentially diminishing predictive power of the biomarker-panel proposed. Multi-omics at DNA and protein (both expression and activity) levels has been applied. An established biomarker panel is considered as a powerful tool for individualised patient profiling and improved multi-level diagnostics-both predictive and prognostic ones.
   Results and conclusions Biomarker panels have been created for the patient stratification, prediction of a more optimal therapy and prognosis of survival based on the individualised patient profiling. Although there are some limitations of the pilot study performed, the results are encouraging, as it may be possible, through further research along these lines, to find a clinically and cost-effective means of stratifying liver cancer patients for personalised care and therapy. The benefits to the patient and society of accurate treatment stratification cannot be overemphasised.
C1 [Golubnitschaja, Olga; Yeghiazaryan, Kristina] Rhein Friedrich Wilhelms Univ Bonn, Dept Radiol, Sigmund Freud Str 25, D-53105 Bonn, Germany.
   [Golubnitschaja, Olga; Yeghiazaryan, Kristina] Rhein Friedrich Wilhelms Univ Bonn, Breast Canc Res Ctr, Bonn, Germany.
   [Golubnitschaja, Olga; Yeghiazaryan, Kristina] Rhein Friedrich Wilhelms Univ Bonn, Ctr Integrated Oncol, Bonn, Germany.
   [Polivka, Jiri, Jr.] Charles Univ Prague, Fac Med Pilsen, Dept Histol & Embryol, Prague, Czech Republic.
   [Polivka, Jiri, Jr.] Charles Univ Prague, Fac Med Pilsen, Biomed Ctr, Prague, Czech Republic.
   [Polivka, Jiri, Jr.] Univ Hosp Plzen, Dept Neurol, Plzen, Czech Republic.
   [Berliner, Leonard] New York Presbyterian Brooklyn Methodist Hosp, Dept Radiol, Intervent Radiol, Brooklyn, NY USA.
C3 University of Bonn; University of Bonn; University of Bonn; Charles
   University Prague; Charles University Prague; University Hospital Plzen;
   NewYork-Presbyterian Hospital; NewYork-Presbyterian Brooklyn Methodist
   Hospital
RP Golubnitschaja, O (corresponding author), Rhein Friedrich Wilhelms Univ Bonn, Dept Radiol, Sigmund Freud Str 25, D-53105 Bonn, Germany.; Golubnitschaja, O (corresponding author), Rhein Friedrich Wilhelms Univ Bonn, Breast Canc Res Ctr, Bonn, Germany.; Golubnitschaja, O (corresponding author), Rhein Friedrich Wilhelms Univ Bonn, Ctr Integrated Oncol, Bonn, Germany.
EM Olga.Golubnitschaja@ukbonn.de
RI Berliner, Leonard/KFR-7642-2024
OI Golubnitschaja, Prof. Dr., Olga/0000-0001-5427-2018
FU European Association for Predictive, Preventive and Personalised
   Medicine (EPMA, Brussels, Belgium)
FX The study funding has been performed by the Department of Radiology,
   University of Bonn, Germany. Kristina Yeghiazaryan has been awarded a
   research fellowship with the European Association for Predictive,
   Preventive and Personalised Medicine (EPMA, Brussels, Belgium).
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NR 43
TC 31
Z9 31
U1 0
U2 9
PU SPRINGER INTERNATIONAL PUBLISHING AG
PI CHAM
PA GEWERBESTRASSE 11, CHAM, CH-6330, SWITZERLAND
EI 1878-5085
J9 EPMA J
JI EPMA J.
PD SEP
PY 2018
VL 9
IS 3
BP 271
EP 285
DI 10.1007/s13167-018-0146-6
PG 15
WC Medicine, General & Internal; Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine; Research & Experimental Medicine
GA GR5CO
UT WOS:000442644000005
PM 30174763
OA Green Published
DA 2025-01-04
ER

PT J
AU Domingo-Sabugo, C
   Willis-Owen, SAG
   Mandal, A
   Nastase, A
   Dwyer, S
   Brambilla, C
   Gálvez, JH
   Zhuang, QW
   Popat, S
   Eveleigh, R
   Munter, M
   Lim, E
   Nicholson, AG
   Lathrop, GM
   Cookson, WOC
   Moffatt, MF
AF Domingo-Sabugo, Clara
   Willis-Owen, Saffron A. G.
   Mandal, Amit
   Nastase, Anca
   Dwyer, Sarah
   Brambilla, Cecilia
   Galvez, Jose Hector
   Zhuang, Qinwei
   Popat, Sanjay
   Eveleigh, Robert
   Munter, Markus
   Lim, Eric
   Nicholson, Andrew G.
   Lathrop, G. Mark
   Cookson, William O. C.
   Moffatt, Miriam F.
TI Genomic analysis defines distinct pancreatic and neuronal subtypes of
   lung carcinoid
SO JOURNAL OF PATHOLOGY
LA English
DT Article
DE molecular subtypes; lung carcinoid; neuroendocrine tumours; multiomics;
   mutational signatures; DNA methylation; functional enrichment; biomarker
   identification; clusters
ID NEUROENDOCRINE TUMORS; MUTATIONAL PROCESSES; AFLATOXIN B-1;
   CANCER-CELLS; COLON-CANCER; HOX GENES; SIGNATURES; TM4SF5; EXPRESSION;
   FAM3B
AB Lung carcinoids (L-CDs) are rare, poorly characterised neuroendocrine tumours (NETs). L-CDs are more common in women and are not the consequence of cigarette smoking. They are classified histologically as typical carcinoids (TCs) or atypical carcinoids (ACs). ACs confer a worse survival. Histological classification is imperfect, and there is increasing interest in molecular markers. We therefore investigated global transcriptomic and epigenomic profiles of 15 L-CDs resected with curative intent at Royal Brompton Hospital. We identified underlying mutations and structural abnormalities through whole-exome sequencing (WES) and single nucleotide polymorphism (SNP) genotyping. Transcriptomic clustering algorithms identified two distinct L-CD subtypes. These showed similarities either to pancreatic or neuroendocrine tumours at other sites and so were named respectively L-CD-PanC and L-CD-NeU. L-CD-PanC tumours featured upregulation of pancreatic and metabolic pathway genes matched by promoter hypomethylation of genes for beta cells and insulin secretion (p < 1 x 10(-6)). These tumours were centrally located and showed mutational signatures of activation-induced deaminase/apolipoprotein B editing complex activity, together with genome-wide DNA methylation loss enriched in repetitive elements (p = 2.2 x 10(-16)). By contrast, the L-CD-NeU group exhibited upregulation of neuronal markers (adjusted p < 0.01) and was characterised by focal spindle cell morphology (p = 0.04), peripheral location (p = 0.01), high mutational load (p = 2.17 x 10(-4)), recurrent copy number alterations, and enrichment for ACs. Mutations affected chromatin remodelling and SWI/SNF complex pathways. L-CD-NeU tumours carried a mutational signature attributable to aflatoxin and aristolochic acid (p = 0.05), suggesting a possible environmental exposure in their pathogenesis. Immunologically, myeloid and T-cell markers were enriched in L-CD-PanC and B-cell markers in L-CD-NeU tumours. The substantial epigenetic and non-coding differences between L-CD-PanC and L-CD-NeU open new possibilities for biomarker selection and targeted treatment of L-CD. (c) 2024 The Author(s). The Journal of Pathology published by John Wiley & Sons Ltd on behalf of The Pathological Society of Great Britain and Ireland.
C1 [Domingo-Sabugo, Clara; Willis-Owen, Saffron A. G.; Mandal, Amit; Nastase, Anca; Dwyer, Sarah; Brambilla, Cecilia; Nicholson, Andrew G.; Cookson, William O. C.; Moffatt, Miriam F.] Imperial Coll London, Natl Heart & Lung Inst, London SW3 6LY, England.
   [Brambilla, Cecilia; Nicholson, Andrew G.] Guys & St Thomas NHS Fdn Trust, Royal Brompton & Harefield Hosp, Dept Histopathol, London, England.
   [Galvez, Jose Hector; Zhuang, Qinwei; Eveleigh, Robert; Munter, Markus; Lathrop, G. Mark] McGill Univ, Victor Phillip Dahdaleh Inst Genom Med, Montreal, PQ, Canada.
   [Popat, Sanjay] Royal Marsden NHS Fdn Trust, London, England.
   [Popat, Sanjay] Royal Marsden Hosp NHS Fdn Trust, Surrey, England.
   [Popat, Sanjay] Inst Canc Res, London, England.
   [Lim, Eric] Royal Brompton Hosp, Dept Thorac Surg, London, England.
C3 Imperial College London; Royal Brompton Hospital; Guy's & St Thomas' NHS
   Foundation Trust; Royal Brompton & Harefield NHS Foundation Trust;
   Harefield Hospital; McGill University; Royal Marsden NHS Foundation
   Trust; Royal Marsden NHS Foundation Trust; Royal Marsden NHS Foundation
   Trust; University of London; Institute of Cancer Research - UK; Royal
   Brompton Hospital
RP Cookson, WOC; Moffatt, MF (corresponding author), Imperial Coll London, Natl Heart & Lung Inst, London SW3 6LY, England.
EM w.cookson@imperial.ac.uk; m.moffatt@imperial.ac.uk
FU UK Department of Health; Asmarley Trust [WT096964MA, WT097117MA];
   Wellcome; National Institute of Health Research (NIHR) Respiratory
   Disease Biomedical Research Unit at the Royal Brompton and Harefield NHS
   Foundation Trust
FX We thank the patients for participating to our study. We also thank Dr
   Alain Pacis and Paul Stretenowich for their help with the analysis of
   the WGBS data. This study was supported by the Asmarley Trust and by
   Wellcome (WT096964MA and WT097117MA). Sample collection for this study
   was supported by the National Institute of Health Research (NIHR)
   Respiratory Disease Biomedical Research Unit at the Royal Brompton and
   Harefield NHS Foundation Trust. The funding sources had no role in study
   design, collection, analysis, and interpretation of the data or in the
   writing of the manuscript.
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NR 61
TC 0
Z9 0
U1 3
U2 3
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0022-3417
EI 1096-9896
J9 J PATHOL
JI J. Pathol.
PD NOV
PY 2024
VL 264
IS 3
BP 332
EP 343
DI 10.1002/path.6352
EA SEP 2024
PG 12
WC Oncology; Pathology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Pathology
GA J4R3D
UT WOS:001321330900001
PM 39329437
OA hybrid
DA 2025-01-04
ER

PT J
AU Christensen, AG
   Ehmsen, S
   Terp, MG
   Batra, R
   Alcaraz, N
   Baumbach, J
   Noer, JB
   Moreira, J
   Leth-Larsen, R
   Larsen, MR
   Ditzel, HJ
AF Christensen, Anne G.
   Ehmsen, Sidse
   Terp, Mikkel G.
   Batra, Richa
   Alcaraz, Nicolas
   Baumbach, Jan
   Noer, Julie B.
   Moreira, Jose
   Leth-Larsen, Rikke
   Larsen, Martin R.
   Ditzel, Henrik J.
TI Elucidation of Altered Pathways in Tumor-Initiating Cells of
   Triple-Negative Breast Cancer: A Useful Cell Model System for Drug
   Screening
SO STEM CELLS
LA English
DT Article
DE Cancer stem cells; Triple-negative breast cancer; Apoptosis; NF-kappa B;
   Mammospheres; Targeted treatment
ID NF-KAPPA-B; EPITHELIAL-MESENCHYMAL TRANSITION; GROWTH-FACTOR-BETA;
   CONTAINING SUPEROXIDE-DISMUTASE; HUMAN COLORECTAL-CANCER; STEM-CELLS;
   TGF-BETA; ALDEHYDE DEHYDROGENASE; MAMMARY TUMORIGENESIS;
   NUCLEAR-LOCALIZATION
AB A limited number of cancer cells within a tumor are thought to have self-renewing and tumor-initiating capabilities that produce the remaining cancer cells in a heterogeneous tumor mass. Elucidation of central pathways preferentially used by tumor-initiating cells/cancer stem cells (CSCs) may allow their exploitation as potential cancer therapy targets. We used single cell cloning to isolate and characterize four isogenic cell clones from a triple-negative breast cancer cell line; two exhibited mesenchymal-like and two epithelial-like characteristics. Within these pairs, one, but not the other, resulted in tumors in immunodeficient NOD/Shi-scid/IL-2 R gamma null mice and efficiently formed mammospheres. Quantitative proteomics and phosphoproteomics were used to map signaling pathways associated with the tumor-initiating ability. Signaling associated with apoptosis was suppressed in tumor-initiating versus nontumorigenic counterparts with pro-apoptotic proteins, such as Bcl2-associated agonist of cell death (BAD), FAS-associated death domain protein (FADD), and myeloid differentiation primary response protein (MYD88), downregulated in tumor-initiating epithelial-like cells. Functional studies confirmed significantly lower apoptosis in tumor-initiating versus nontumorigenic cells. Moreover, central pathways, including beta-catenin and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-kappa B)-related signaling, exhibited increased activation in the tumor-initiating cells. To evaluate the CSC model as a tool for drug screening, we assessed the effect of separately blocking NF-kappa B and Wnt/beta-catenin signaling and found markedly reduced mammosphere formation, particularly for tumor-initiating cells. Similar reduction was also observed using patient-derived primary cancer cells. Furthermore, blocking NF-kappa B signaling in mice transplanted with tumor-initiating cells significantly reduced tumor outgrowth. Our study demonstrates that suppressed apoptosis, activation of pathways associated with cell viability, and CSCs are the major differences between tumor-initiating and nontumorigenic cells independent of their epithelial-like/mesenchymal-like phenotype. These altered pathways may provide targets for future drug development to eliminate CSCs, and the cell model may be a useful tool in such drug screenings.
C1 [Christensen, Anne G.; Ehmsen, Sidse; Terp, Mikkel G.; Leth-Larsen, Rikke; Ditzel, Henrik J.] Univ Southern Denmark, Inst Mol Med, Dept Canc & Inflammat Res, JB Winslowsvej 25, DK-5000 Odense C, Denmark.
   [Batra, Richa; Alcaraz, Nicolas; Baumbach, Jan] Univ Southern Denmark, Fac Sci, Dept Math & Comp Sci, Odense, Denmark.
   [Larsen, Martin R.] Univ Southern Denmark, Dept Biochem & Mol Biol, Odense, Denmark.
   [Noer, Julie B.; Moreira, Jose] Univ Copenhagen, Sect Mol Dis Biol, Dept Vet Dis Biol, Sect Mol Dis Biol, Frederiksberg C, Denmark.
   [Larsen, Martin R.] Odense Univ Hosp, Dept Clin Biochem & Pharmacol, Ctr Clin Prote, Odense, Denmark.
   [Ditzel, Henrik J.] Odense Univ Hosp, Dept Oncol, Odense, Denmark.
C3 University of Southern Denmark; University of Southern Denmark;
   University of Southern Denmark; University of Copenhagen; University of
   Southern Denmark; Odense University Hospital; University of Southern
   Denmark; Odense University Hospital
RP Ditzel, HJ (corresponding author), Univ Southern Denmark, Inst Mol Med, Dept Canc & Inflammat Res, JB Winslowsvej 25, DK-5000 Odense C, Denmark.
EM hditzel@health.sdu.dk
RI Baumbach, Jörg/E-3725-2014; Alcaraz, Nicolas/K-2758-2019; Moreira,
   Jose/KMX-4138-2024; Batra, Richa/ABF-1240-2021; Larsen, Martin
   Rossel/F-1411-2015
OI Ditzel, Henrik J./0000-0003-3927-5135; Batra, Richa/0000-0003-3708-0086;
   Noer, Julie/0000-0002-8184-7494; Alcaraz, Nicolas/0000-0003-0839-8423;
   Moreira, Jose/0000-0002-9944-1214; Larsen, Martin
   Rossel/0000-0001-6203-0123; Ehmsen, Sidse/0000-0002-4807-6325;
   Leth-Larsen, Rikke/0000-0002-1612-4089; Baumbach,
   Jan/0000-0002-0282-0462; Terp, Mikkel/0000-0002-4468-6900
FU Danish Cancer Society; Danish Cancer Research Foundation; Race Against
   Breast Cancer; Sino-Danish Breast Cancer Research Centre; NanoCAN
   Lundbeck Center of Excellence; Region of Southern Denmark; Danish
   Research Council; Academy of Geriatric Cancer Research (AgeCare); Danish
   Center for Translational Breast Cancer research (DCTB); Lundbeck
   Foundation (Junior Group Leader Fellowship)
FX We thank Lisbet Mortensen, Ole Nielsen, Anette Rasmussen, and Lene
   Egedal Johansen for excellent technical assistance and M. K. Occhipinti
   for editorial assistance. This work was supported in part by the Danish
   Cancer Society, Danish Research Council, the Danish Cancer Research
   Foundation, A Race Against Breast Cancer, Sino-Danish Breast Cancer
   Research Centre, NanoCAN Lundbeck Center of Excellence, Region of
   Southern Denmark, Danish Research Council, Academy of Geriatric Cancer
   Research (AgeCare), and Danish Center for Translational Breast Cancer
   research (DCTB). M. R. L. was supported by the Lundbeck Foundation
   (Junior Group Leader Fellowship).
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NR 79
TC 12
Z9 13
U1 0
U2 9
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1066-5099
EI 1549-4918
J9 STEM CELLS
JI Stem Cells
PD AUG
PY 2017
VL 35
IS 8
BP 1898
EP 1912
DI 10.1002/stem.2654
PG 15
WC Cell & Tissue Engineering; Biotechnology & Applied Microbiology;
   Oncology; Cell Biology; Hematology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology; Biotechnology & Applied Microbiology; Oncology; Hematology
GA FB8WG
UT WOS:000406419600003
PM 28600813
OA Bronze
DA 2025-01-04
ER

PT J
AU Jehn, CF
   Küpferling, S
   Oskay-Özcelik, G
   Lüftner, D
AF Jehn, C. F.
   Kuepferling, S.
   Oskay-Oezcelik, G.
   Lueftner, D.
TI A survey of treatment approaches of malignant ascites in Germany and
   Austria
SO SUPPORTIVE CARE IN CANCER
LA English
DT Article
DE Malignant ascites; Advanced cancer; Paracentesis; Catumaxomab
ID PERITONEOVENOUS SHUNTS; PARACENTESIS; MANAGEMENT; PALLIATION;
   CATUMAXOMAB
AB Malignant ascites (MA) is a common manifestation of advanced cancer. Currently, there are no evidence-based guidelines for the management of MA. We conducted a survey with physicians throughout Germany and Austria, to get an overview of current approaches and opinions in the treatment of MA.
   One hundred and twenty-eight medical oncologists (MO), gastroenterologists (GE), and gynecologists (GYN) completed an electronic questionnaire consisting of 33 questions.
   Ninety percent of the physicians were from Germany and 10 % from Austria; 48 % of those were MO, 30 % were GYN, and 14 % were GE. Most physicians treated an average of 34 patients (pts)/year with MA. Twenty-six percent of these pts suffered from ovarian, 20 % from pancreatic, 17 % from gastric, and 14 % from colorectal cancer. The majority of the physicians associated MA with poor prognosis (92 %) and significant reduction in quality of life (87 %). One third felt that MA was a contraindication for full dosing of systemic chemotherapy. Paracentesis (PC) was performed in 70 % of pts with symptom relieve and quality of life being the main reasons. Almost half of the pts required 3-5 PC, 50 % even more than 5 PC during the course of their disease. Only 15 % of pts needed multiple PC per week; the majority (79 %) needed the procedure either once a week or every 14 days. In 61 % of pts, 3-5 L of ascites fluid was drained. Only in 8 %, 5 L and more were removed. Volume substitution with IV albumin was performed in 40 % of pts. Most pts (55 %) had to stay 1-3 h in a healthcare facility for the procedure. However, 21 % had to stay a parts per thousand yen1 day. While almost all physicians (89 %) performed a PC at some point in the treatment of MA, 75 % felt that a systemic chemotherapy and 55 % thought a concomitant diuretic therapy were a necessary adjunct. Seven percent of the pts received a targeted treatment with catumaxomab.
   Repeated PC is the main pillar of treatment of MA; its effect is only temporary and requires significant hospital resources. Further treatment strategies of MA have to be evaluated in prospective studies. Targeted therapies like catumaxomab and VEGF inhibitors should be integrated into these.
C1 [Jehn, C. F.; Lueftner, D.] Univ Hosp Charite, Dept Hematol Oncol & Tumor Immunol, Berlin, Germany.
   [Kuepferling, S.] Univ Med Berlin, Charite, Dept Gastroenterol Hepatol & Endocrinol, Berlin, Germany.
   [Oskay-Oezcelik, G.] MEOKlink, Berlin, Germany.
C3 Berlin Institute of Health; Free University of Berlin; Humboldt
   University of Berlin; Charite Universitatsmedizin Berlin; Berlin
   Institute of Health; Free University of Berlin; Humboldt University of
   Berlin; Charite Universitatsmedizin Berlin
RP Jehn, CF (corresponding author), Univ Hosp Charite, Dept Hematol Oncol & Tumor Immunol, Berlin, Germany.
EM Christian.Jehn@charite.de
OI Luftner, Diana/0000-0003-2511-9115
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NR 27
TC 20
Z9 22
U1 0
U2 6
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0941-4355
EI 1433-7339
J9 SUPPORT CARE CANCER
JI Support. Care Cancer
PD JUL
PY 2015
VL 23
IS 7
BP 2073
EP 2078
DI 10.1007/s00520-014-2557-9
PG 6
WC Oncology; Health Care Sciences & Services; Rehabilitation
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Health Care Sciences & Services; Rehabilitation
GA CJ1PI
UT WOS:000355255600029
PM 25528551
DA 2025-01-04
ER

PT J
AU Santha, S
   Ling, X
   Aljahdali, IAM
   Rasam, SS
   Wang, X
   Liao, JQ
   Wang, J
   Fountzilas, C
   Li, QY
   Qu, J
   Li, FZ
AF Santha, Sreevidya
   Ling, Xiang
   Aljahdali, Ieman A. M.
   Rasam, Sailee S.
   Wang, Xue
   Liao, Jianqun
   Wang, Jue
   Fountzilas, Christos
   Li, Qingyong
   Qu, Jun
   Li, Fengzhi
TI Mutant Kras as a Biomarker Plays a Favorable Role in FL118-Induced
   Apoptosis, Reactive Oxygen Species (ROS) Production and Modulation of
   Survivin, Mcl-1 and XIAP in Human Bladder Cancer
SO CANCERS
LA English
DT Article
DE FL118; bladder cancer; apoptosis; survivin; Mcl-1; XIAP; mutant Kras;
   reactive oxygen species (ROS); proteomics analysis; human bladder tumor
   mouse models
ID DNA TOPOISOMERASE-I; P-GLYCOPROTEIN EXPRESSION; NF-KAPPA-B; CAMPTOTHECIN
   ANALOG; MOLECULAR-GENETICS; RESISTANCE PROTEIN; TARGETED THERAPIES; CELL
   APOPTOSIS; INHIBITOR; SENSITIVITY
AB Simple Summary
   FL118 is a novel orally available small molecule anticancer drug. We found that bladder cancer cells with a mutant Kras is highly sensitive to FL118-induced cell growth inhibition and cell death induction through inhibiting the anti-cancer cell death and drug resistance factors (survivin, Mcl-1, XIAP). In the Kras-mutation bladder cancer cells, FL118 can stimulate the reactive oxygen species (ROS) over-production for killing bladder cancer cells and inhibiting bladder cancer cell-established tumor growth. Elimination of mutant Kras by Kras-specific shRNA technology in mutant Kras-containing bladder cancer cell-established tumor decreased FL118 effectiveness to inhibit bladder cancer tumor growth. In this regard, mutant Kras is a potential favorable biomarker for FL118. This finding is significant because mutant Kras is known to be a formidable challenge treatment resistant factor in various types of cancer. Thus, FL118 could use mutant Kras as favorable biomarker for patient selection to carry out precision medicine.
   Tumor heterogeneity in key gene mutations in bladder cancer (BC) is a major hurdle for the development of effective treatments. Using molecular, cellular, proteomics and animal models, we demonstrated that FL118, an innovative small molecule, is highly effective at killing T24 and UMUC3 high-grade BC cells, which have Hras and Kras mutations, respectively. In contrast, HT1376 BC cells with wild-type Ras are insensitive to FL118. This concept was further demonstrated in additional BC and colorectal cancer cells with mutant Kras versus those with wild-type Kras. FL118 strongly induced PARP cleavage (apoptosis hallmark) and inhibited survivin, XIAP and/or Mcl-1 in both T24 and UMUC3 cells, but not in the HT1376 cells. Silencing mutant Kras reduced both FL118-induced PARP cleavage and downregulation of survivin, XIAP and Mcl-1 in UMUC3 cells, suggesting mutant Kras is required for FL118 to exhibit higher anticancer efficacy. FL118 increased reactive oxygen species (ROS) production in T24 and UMUC3 cells, but not in HT1376 cells. Silencing mutant Kras in UMUC3 cells reduced FL118-mediated ROS generation. Proteomics analysis revealed that a profound and opposing Kras-relevant signaling protein is changed in UMUC3 cells and not in HT1376 cells. Consistently, in vivo studies indicated that UMUC3 tumors are highly sensitive to FL118 treatment, while HT1376 tumors are highly resistant to this agent. Silencing mutant Kras in UMUC3 cell-derived tumors decreases UMUC3 tumor sensitivity to FL118 treatment. Together, our studies revealed that mutant Kras is a favorable biomarker for FL118 targeted treatment.
C1 [Santha, Sreevidya; Ling, Xiang; Aljahdali, Ieman A. M.; Liao, Jianqun; Li, Fengzhi] Roswell Pk Comprehens Canc Ctr, Dept Pharmacol & Therapeut, Elm & Carlton St, New York, NY 14263 USA.
   [Santha, Sreevidya; Ling, Xiang; Liao, Jianqun] Canget BioTekpharma LLC, New York, NY 14203 USA.
   [Aljahdali, Ieman A. M.] Roswell Pk Comprehens Canc Ctr, Dept Cellular & Mol Biol, New York, NY 14263 USA.
   [Rasam, Sailee S.] SUNY Buffalo, Jacobs Sch Med, Dept Biochem, New York, NY 14203 USA.
   [Wang, Xue; Qu, Jun] SUNY Buffalo, Sch Pharm, Dept Pharmaceut Sci, New York, NY 14214 USA.
   [Wang, Xue] Roswell Pk Comprehens Canc Ctr, Dept Cell Stress Biol, New York, NY 14263 USA.
   [Wang, Jue] Univ Arizona, Canc Ctr, Dept Interdisciplinary Oncol, Phoenix, AZ 85004 USA.
   [Fountzilas, Christos] Roswell Pk Comprehens Canc Ctr, Dept Med, New York, NY 14263 USA.
   [Li, Qingyong] Zhejiang Univ Technol, Coll Pharmaceut Sci, Hangzhou 310014, Peoples R China.
   [Li, Fengzhi] Roswell Pk Comprehens Canc Ctr, Dev Therapeut DT Program, New York, NY 14263 USA.
C3 Roswell Park Comprehensive Cancer Center; Roswell Park Comprehensive
   Cancer Center; State University of New York (SUNY) System; University at
   Buffalo, SUNY; State University of New York (SUNY) System; University at
   Buffalo, SUNY; Roswell Park Comprehensive Cancer Center; University of
   Arizona; Roswell Park Comprehensive Cancer Center; Zhejiang University
   of Technology; Roswell Park Comprehensive Cancer Center
RP Ling, X; Li, FZ (corresponding author), Roswell Pk Comprehens Canc Ctr, Dept Pharmacol & Therapeut, Elm & Carlton St, New York, NY 14263 USA.; Ling, X (corresponding author), Canget BioTekpharma LLC, New York, NY 14203 USA.; Li, FZ (corresponding author), Roswell Pk Comprehens Canc Ctr, Dev Therapeut DT Program, New York, NY 14263 USA.
EM sreevidya.gp@gmail.com; Xiang.Ling@RoswellPark.org;
   Ieman.Aljahdali@RoswellPark.org; saileesu@buffalo.edu;
   xwang79@buffalo.edu; Jian.Liao@RoswellPark.org;
   juewang@email.arizona.edu; Christos.Fountzilas@RoswellPark.org;
   liqy@zjut.edu.cn; junqu@buffalo.edu; fengzhi.li@roswellpark.org
RI Li, Fengzhi/GXF-0115-2022
OI Fountzilas, Christos/0000-0003-3837-5644; wang, xue/0000-0002-5267-6083;
   Li, Fengzhi/0000-0002-2299-7951
FU NIH [R21CA180764, R03CA182552, R44CA176937, P30CA016056]; 2020
   Pancreatic Cancer Action Network (PanCAN) Translational Research Grant
   [20-65-FENG]
FX This research work was sponsored in part by NIH Grants, R21CA180764,
   R03CA182552, R44CA176937 and P30CA016056 (NCI Cancer Center Core Support
   Grant) as well as the 2020 Pancreatic Cancer Action Network (PanCAN)
   Translational Research Grant (20-65-FENG).
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NR 83
TC 15
Z9 16
U1 1
U2 25
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2072-6694
J9 CANCERS
JI Cancers
PD NOV
PY 2020
VL 12
IS 11
AR 3413
DI 10.3390/cancers12113413
PG 25
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA OX5XB
UT WOS:000593636100001
PM 33217967
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Shen, LF
   Zhao, X
   Zhou, SH
   Lu, ZJ
   Zhao, K
   Fan, J
   Zhou, ML
AF Shen, Li-Fang
   Zhao, Xin
   Zhou, Shui-Hong
   Lu, Zhong-Jie
   Zhao, Kui
   Fan, Jun
   Zhou, Min-Li
TI <i>In vivo</i> evaluation of the effects of simultaneous inhibition of
   GLUT-1 and HIF-1α by antisense oligodeoxynucleotides on the
   radiosensitivity of laryngeal carcinoma using micro <SUP>18</SUP>F-FDG
   PET/CT
SO ONCOTARGET
LA English
DT Article
DE hypoxia-inducible factor 1 alpha; glucose transporter-1; antisense
   oligodeoxynucleotides; radiosensitivity; F-18-FDG micro PET/CT
ID HYPOXIA-INDUCIBLE FACTOR-1-ALPHA; HUMAN NASOPHARYNGEAL CARCINOMA;
   SQUAMOUS-CELL CARCINOMA; GLUCOSE-TRANSPORTER-1 EXPRESSION;
   COLORECTAL-CANCER; TARGETING HYPOXIA; ROI DEFINITION; FACTOR 1-ALPHA;
   TUMOR; RADIOTHERAPY
AB Purpose: Hypoxia-inducible factor 1a (HIF-1a) and glucose transporter-1 (GLUT-1) are two important hypoxic markers associated with the radioresistance of cancers including laryngeal carcinoma. We evaluated whether the simultaneous inhibition of GLUT-1 and HIF-1a expression improved the radiosensitivity of laryngeal carcinoma. We explored whether the expression of HIF-1a and GLUT-1 was correlated with 2 '-deoxy-2 '-[18F]fluoro-D-glucose (F-18-FDG) uptake and whether F-18-FDG positron emission tomography-computed tomography (PET/CT) was appropriate for early evaluation of the response of laryngeal carcinoma to targeted treatment in vivo.
   Materials and Methods: To verify the above hypotheses, an in vivo model was applied by subcutaneously injecting Hep-2 (2 x 107/mL x 0.2 mL) and Tu212 cells (2 x 107/mL x 0.2 mL) into nude mice. The effects of HIF-1a antisense oligodeoxynucleotides (AS-ODNs) (100 mu g) and GLUT-1 AS-ODNs (100 mu g) on the radiosensitivity of laryngeal carcinoma were assessed by tumor volume and weight, microvessel density (MVD), apoptosis index (AI) and necrosis in vivo based on a full factorial (23) design. F-18-FDG-PET/CT was taken before and after the treatment of xenografts. The relationships between HIF-1a and GLUT-1 expression and 18F-FDG uptake in xenografts were estimated and the value of F-18-FDG-PET/CT was assessed after treating the xenografts.
   Results: 10 Gy X-ray irradiation decreased the weight of Hep-2 xenografts 8 and 12 days after treatment, and the weights of Tu212 xenografts 8 days after treatment. GLUT-1 AS-ODNs decreased the weight of Tu212 xenografts 12 days after treatment. There was a synergistic interaction among the three treatments (GLUT-1 AS-ODNs, HIF-1a AS-ODNs and 10Gy X-ray irradiation) in increasing apoptosis, decreasing MVD, and increasing necrosis in Hep-2 xenografts 8 days after treatment (p < 0.05) and in Tu212 xenografts 12 days after treatment (p < 0.001). Standardized uptake value (tumor/normal tissue)( SUVmaxT/N) did not show a statistically significant correlation with GLUT-1 and HIF-1a expression and therapeutic effect (necrosis, apoptosis).
   Conclusions: Simultaneous inhibition of HIF-1a and GLUT-1 expression might increase the radiosensitivity of laryngeal carcinoma, decreasing MVD, and promoting apoptosis and necrosis. F-18-FDG-PET/CT wasn't useful in evaluating the therapeutic effect on laryngeal cancer in this animal study.
C1 [Shen, Li-Fang; Zhou, Shui-Hong; Zhou, Min-Li] Zhejiang Univ, Coll Med, Affiliated Hosp 1, Dept Otolaryngol, Hangzhou, Zhejiang, Peoples R China.
   [Zhao, Xin; Zhao, Kui] Zhejiang Univ, Coll Med, Affiliated Hosp 1, Ctr PET CT, Hangzhou, Zhejiang, Peoples R China.
   [Lu, Zhong-Jie] Zhejiang Univ, Coll Med, Affiliated Hosp 1, Dept Radiotherapy, Hangzhou, Zhejiang, Peoples R China.
   [Fan, Jun] Zhejiang Univ, Coll Med, Affiliated Hosp 1, State Key Lab Diag & Treatment Infect Dis, Hangzhou, Zhejiang, Peoples R China.
C3 Zhejiang University; Zhejiang University; Zhejiang University; Zhejiang
   University
RP Zhou, SH (corresponding author), Zhejiang Univ, Coll Med, Affiliated Hosp 1, Dept Otolaryngol, Hangzhou, Zhejiang, Peoples R China.
EM zhouyunzhoush@163.com
FU National Natural Science Foundation of China [81172562, 81372903];
   Science and Technology Department of Zhejiang Province, China
   [2016C33144]
FX This research was supported by National Natural Science Foundation of
   China (No. 81172562 and 81372903), and Science and Technology Department
   of Zhejiang Province, China (No.2016C33144).
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NR 56
TC 16
Z9 17
U1 0
U2 12
PU IMPACT JOURNALS LLC
PI ORCHARD PARK
PA 6666 E QUAKER ST, STE 1, ORCHARD PARK, NY 14127 USA
EI 1949-2553
J9 ONCOTARGET
JI Oncotarget
PD MAY 23
PY 2017
VL 8
IS 21
BP 34709
EP 34726
DI 10.18632/oncotarget.16671
PG 18
WC Oncology; Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Cell Biology
GA EV8RY
UT WOS:000402051700063
PM 28410229
OA Green Submitted, Green Published, gold
DA 2025-01-04
ER

PT J
AU Reel, PS
   Reel, S
   van Kralingen, JC
   Langton, K
   Lang, K
   Erlic, Z
   Larsen, CK
   Amar, L
   Pamporaki, C
   Mulatero, P
   Blanchard, A
   Kabat, M
   Robertson, S
   MacKenzie, SM
   Taylor, AE
   Peitzsch, M
   Ceccato, F
   Scaroni, C
   Reincke, M
   Kroiss, M
   Dennedy, MC
   Pecori, A
   Monticone, S
   Deinum, J
   Rossi, GP
   Lenzini, L
   McClure, JD
   Nind, T
   Riddell, A
   Stell, A
   Cole, C
   Sudano, I
   Prehn, C
   Adamski, J
   Gimenez-Roqueplo, AP
   Assié, G
   Arlt, W
   Beuschlein, F
   Eisenhofer, G
   Davies, E
   Zennaro, MC
   Jefferson, E
AF Reel, Parminder S.
   Reel, Smarti
   van Kralingen, Josie C.
   Langton, Katharina
   Lang, Katharina
   Erlic, Zoran
   Larsen, Casper K.
   Amar, Laurence
   Pamporaki, Christina
   Mulatero, Paolo
   Blanchard, Anne
   Kabat, Marek
   Robertson, Stacy
   MacKenzie, Scott M.
   Taylor, Angela E.
   Peitzsch, Mirko
   Ceccato, Filippo
   Scaroni, Carla
   Reincke, Martin
   Kroiss, Matthias
   Dennedy, Michael C.
   Pecori, Alessio
   Monticone, Silvia
   Deinum, Jaap
   Rossi, Gian Paolo
   Lenzini, Livia
   McClure, John D.
   Nind, Thomas
   Riddell, Alexandra
   Stell, Anthony
   Cole, Christian
   Sudano, Isabella
   Prehn, Cornelia
   Adamski, Jerzy
   Gimenez-Roqueplo, Anne-Paule
   Assie, Guillaume
   Arlt, Wiebke
   Beuschlein, Felix
   Eisenhofer, Graeme
   Davies, Eleanor
   Zennaro, Maria-Christina
   Jefferson, Emily
TI Machine learning for classification of hypertension subtypes using
   multi-omics: A multi-centre, retrospective, data-driven study
SO EBIOMEDICINE
LA English
DT Article
DE Machine learning; Multi-omics; Hypertension; Primary aldosteronism;
   Pheochromocytoma; paragan-glioma; Cushing syndrome; Biomarkers
ID PRIMARY ALDOSTERONISM; BLOOD-PRESSURE; ENDOCRINE; DIAGNOSIS; PREVALENCE;
   SOCIETY; METABOLOMICS
AB Background Arterial hypertension is a major cardiovascular risk factor. Identification of secondary hypertension in its various forms is key to preventing and targeting treatment of cardiovascular complications. Simplified diagnostic tests are urgently required to distinguish primary and secondary hypertension to address the current underdiagnosis of the latter.Methods This study uses Machine Learning (ML) to classify subtypes of endocrine hypertension (EHT) in a large cohort of hypertensive patients using multidimensional omics analysis of plasma and urine samples. We measured 409 multi-omics (MOmics) features including plasma miRNAs (PmiRNA: 173), plasma catechol O-methylated metabolites (PMetas: 4), plasma steroids (PSteroids: 16), urinary steroid metabolites (USteroids: 27), and plasma small metabolites (PSmallMB: 189) in primary hypertension (PHT) patients, EHT patients with either primary aldo-steronism (PA), pheochromocytoma/functional paraganglioma (PPGL) or Cushing syndrome (CS) and normoten-sive volunteers (NV). Biomarker discovery involved selection of disease combination, outlier handling, feature reduction, 8 ML classifiers, class balancing and consideration of different age-and sex-based scenarios. Classifica-tions were evaluated using balanced accuracy, sensitivity, specificity, AUC, F1, and Kappa score.Findings Complete clinical and biological datasets were generated from 307 subjects (PA=113, PPGL=88, CS=41 and PHT=112). The random forest classifier provided -92% balanced accuracy (-11% improvement on the best mono-omics classifier), with 96% specificity and 0.95 AUC to distinguish one of the four conditions in multi-class ALL -ALL comparisons (PPGL vs PA vs CS vs PHT) on an unseen test set, using 57 MOmics features. For discrimination of EHT (PA + PPGL + CS) vs PHT, the simple logistic classifier achieved 0.96 AUC with 90% sensitivity, and -86% specificity, using 37 MOmics features. One PmiRNA (hsa-miR-15a-5p) and two PSmallMB (C9 and PC ae C38:1) features were found to be most discriminating for all disease combinations. Overall, the MOmics-based classi-fiers were able to provide better classification performance in comparison to mono-omics classifiers.Interpretation We have developed a ML pipeline to distinguish different EHT subtypes from PHT using multi-omics data. This innovative approach to stratification is an advancement towards the development of a diagnostic tool for EHT patients, significantly increasing testing throughput and accelerating administration of appropriate treatment.Funding European Union's Horizon 2020 Research and Innovation Programme under Grant Agreement No. 633983, Clinical Research Priority Program of the University of Zurich for the CRPP HYRENE (to Z.E. and F.B.), and Deutsche Forschungsgemeinschaft (CRC/Transregio 205/1).Copyright (c) 2022 The Authors. Published by Elsevier B.V. This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/)
C1 [Reel, Parminder S.; Reel, Smarti; Nind, Thomas; Cole, Christian; Jefferson, Emily] Univ Dundee, Sch Med, Div Populat Hlth & Genom, Dundee DD2 4BF, Scotland.
   [van Kralingen, Josie C.; Robertson, Stacy; MacKenzie, Scott M.; McClure, John D.; Riddell, Alexandra; Davies, Eleanor] Univ Glasgow, BHF Glasgow Cardiovasc Res Ctr, Sch Cardiovasc & Metab Hlth, Glasgow G12 8TA, Lanark, Scotland.
   [Langton, Katharina; Peitzsch, Mirko; Eisenhofer, Graeme] Tech Univ Dresden, Inst Clin Chem & Lab Med, Univ Hosp Carl Gustav Carus, Dresden, Germany.
   [Lang, Katharina; Taylor, Angela E.; Arlt, Wiebke] Univ Birmingham, Coll Med & Dent Sci, Inst Metab & Syst Res, Birmingham, W Midlands, England.
   [Lang, Katharina; Arlt, Wiebke] Birmingham Hlth Partners, Ctr Endocrinol Diabet & Metab, Birmingham, W Midlands, England.
   [Lang, Katharina; Arlt, Wiebke] Univ Hosp Birmingham NHS Fdn Trust, Queen Elizabeth Hosp Birmingham, Dept Endocrinol, Birmingham, W Midlands, England.
   [Erlic, Zoran; Beuschlein, Felix] Univ Spital Zurich USZ, Klin Endokrinol Diabetol & Klin Ernahrung, Zurich, Switzerland.
   [Erlic, Zoran; Beuschlein, Felix] Univ Zurich UZH, Zurich, Switzerland.
   [Larsen, Casper K.; Amar, Laurence; Gimenez-Roqueplo, Anne-Paule; Zennaro, Maria-Christina] Univ Paris Cite, PARCC, INSERM, F-75006 Paris, France.
   [Amar, Laurence] Hop Europ Georges Pompidou, Assistance Publ Hop Paris, Unite Hypertens Arterielle, Paris, France.
   [Pamporaki, Christina; Eisenhofer, Graeme] Tech Univ Dresden, Dept Med 3, Univ Hosp Carl Gustav Carus, Dresden, Germany.
   [Mulatero, Paolo; Pecori, Alessio; Monticone, Silvia] Univ Torino, Dept Med Sci, Div Internal Med, Turin, Italy.
   [Mulatero, Paolo; Pecori, Alessio; Monticone, Silvia] Univ Torino, Dept Med Sci, Hypertens Unit, Turin, Italy.
   [Blanchard, Anne] Hop Europ Georges Pompidou, Ctr Invest Clin 9201 Paris, Assistance Publ Hop Paris, Paris, France.
   [Kabat, Marek] Natl Inst Cardiol, Dept Hypertens, Warsaw, Poland.
   [Ceccato, Filippo; Scaroni, Carla] Azienda Osped Univ Padova, Dipartimento Med DIMED, UOC Endocrinol, Padua, Italy.
   [Reincke, Martin; Kroiss, Matthias; Beuschlein, Felix] LMU Munchen, Klinikum Univ Munchen, Med Klin & Poliklin 4, Munich, Germany.
   [Kroiss, Matthias] Univ Klinikum Wurzburg, Core Unit Clin Mass Spectrometry, Clin Chem & Lab Med, Wurzburg, Germany.
   [Kroiss, Matthias] Univ Klinikum Wurzburg, Med Klin & Poliklin 1, Schwerpunkt Endokrinol Diabetol, Wurzburg, Germany.
   [Kroiss, Matthias] Univ Wurzburg, Comprehens Canc Ctr Mainfranken, Wurzburg, Germany.
   [Dennedy, Michael C.] Natl Univ Ireland, Discipline Pharmacol & Therapeut, Sch Med, Galway 33, Ireland.
   [Deinum, Jaap] Radboud Univ Nijmegen Med Ctr, Dept Med, Sect Vasc Med, Nijmegen, Netherlands.
   [Rossi, Gian Paolo; Lenzini, Livia] Univ Padua, Internal & Emergency Med ESH Specialized Hyperten, Dept Med DIMED, Padua, Italy.
   [Stell, Anthony] Univ Melbourne, Dept Comp & Informat Syst, Melbourne, Vic, Australia.
   [Sudano, Isabella] Univ Hosp Zurich, Cardiol, Univ Heart Ctr, Zurich, Switzerland.
   [Sudano, Isabella] Univ Zurich, Zurich, Switzerland.
   [Prehn, Cornelia] Helmholtz Zentrum Munchen, German Res Ctr Environm Hlth, Metabol & Prote Core MPC, Neuherberg, Germany.
   [Adamski, Jerzy] Helmholtz Zentrum Munchen, Inst Expt Genet, German Res Ctr Environm Hlth, Ingolstadter Landstr 1, D-85764 Neuherberg, Germany.
   [Adamski, Jerzy] Natl Univ Singapore, Yong Loo Lin Sch Med, Dept Biochem, 8 Med Dr, Singapore 117597, Singapore.
   [Adamski, Jerzy] Univ Ljubljana, Fac Med, Inst Biochem, Vrazov Trg 2, Ljubljana 1000, Slovenia.
   [Gimenez-Roqueplo, Anne-Paule; Zennaro, Maria-Christina] Hop Europ Georges Pompidou, Assistance Publ Hop Paris, Serv Genet, F-75015 Paris, France.
   [Assie, Guillaume] Univ Paris, CNRS, INSERM, Inst Cochin, F-75014 Paris, France.
   [Assie, Guillaume] Hop Cochin, Assistance Publ Hop Paris, Ctr Rare Adrenal Dis, Dept Endocrinol, F-75014 Paris, France.
   [Arlt, Wiebke] Univ Hosp Birmingham NHS Fdn Trust, NIHR Birmingham Biomed Res Ctr, Birmingham, W Midlands, England.
   [Arlt, Wiebke] Univ Birmingham, Birmingham, W Midlands, England.
   [Jefferson, Emily] Univ Glasgow, Inst Hlth & Wellbeing, Glasgow G12 8RZ, Lanark, Scotland.
C3 University of Dundee; University of Glasgow; Technische Universitat
   Dresden; Carl Gustav Carus University Hospital; University of
   Birmingham; University of Birmingham; University of Zurich; Universite
   Paris Cite; Institut National de la Sante et de la Recherche Medicale
   (Inserm); Assistance Publique Hopitaux Paris (APHP); Universite Paris
   Cite; Hopital Universitaire Europeen Georges-Pompidou - APHP; Hopital
   Universitaire Saint-Louis - APHP; Technische Universitat Dresden; Carl
   Gustav Carus University Hospital; University of Turin; University of
   Turin; Assistance Publique Hopitaux Paris (APHP); Universite Paris Cite;
   Hopital Universitaire Europeen Georges-Pompidou - APHP; Hopital
   Universitaire Saint-Louis - APHP; Institute of Cardiology - Poland;
   University of Padua; Azienda Ospedaliera - Universita di Padova;
   University of Munich; University of Wurzburg; University of Wurzburg;
   University of Wurzburg; Radboud University Nijmegen; University of
   Padua; University of Melbourne; University of Zurich; University Zurich
   Hospital; University of Zurich; Helmholtz Association; Helmholtz-Center
   Munich - German Research Center for Environmental Health; Helmholtz
   Association; Helmholtz-Center Munich - German Research Center for
   Environmental Health; National University of Singapore; University of
   Ljubljana; Assistance Publique Hopitaux Paris (APHP); Universite Paris
   Cite; Hopital Universitaire Saint-Louis - APHP; Hopital Universitaire
   Europeen Georges-Pompidou - APHP; Centre National de la Recherche
   Scientifique (CNRS); Universite Paris Cite; Institut National de la
   Sante et de la Recherche Medicale (Inserm); Assistance Publique Hopitaux
   Paris (APHP); Universite Paris Cite; Hopital Universitaire Saint-Louis -
   APHP; Hopital Universitaire Cochin - APHP; University of Birmingham;
   University of Birmingham; University of Glasgow
RP Reel, PS; Jefferson, E (corresponding author), Univ Dundee, Sch Med, Div Populat Hlth & Genom, Dundee DD2 4BF, Scotland.; Zennaro, MC (corresponding author), Univ Paris Cite, PARCC, INSERM, F-75006 Paris, France.; Zennaro, MC (corresponding author), Hop Europ Georges Pompidou, Assistance Publ Hop Paris, Serv Genet, F-75015 Paris, France.; Jefferson, E (corresponding author), Univ Glasgow, Inst Hlth & Wellbeing, Glasgow G12 8RZ, Lanark, Scotland.
EM p.s.reel@dundee.ac.uk; maria-christina.zennaro@inserm.fr;
   erjefferson@dundee.ac.uk
RI Rossi, Giuseppe/G-7838-2012; Langton, Katharina/AAY-4085-2020;
   Eisenhofer, Graeme/AAU-9829-2021; GIMENEZ-ROQUEPLO,
   Anne-Paule/T-6752-2018; Cole, Christian/AFD-8166-2022; Zennaro,
   Maria-Christina/IZP-8913-2023; Amar, Laurence/LUW-8846-2024; Ceccato,
   Filippo/K-1316-2018; Peitzsch, Mirko/LWK-6489-2024; Beuschlein,
   Felix/N-1282-2018; Erlic, Zoran/AAA-5680-2020; Kroiss,
   Matthias/B-4785-2014; MacKenzie, Scott/S-8459-2018; Arlt,
   Wiebke/B-6310-2009
OI Erlic, Zoran/0000-0001-6953-9133; Prehn, Cornelia/0000-0002-1274-4715;
   Jefferson, Emily/0000-0003-2992-7582; Kroiss,
   Matthias/0000-0002-7628-3161; Assie, Guillaume/0000-0001-9590-0906;
   MacKenzie, Scott/0000-0002-4593-4101; Pamporaki,
   Christina/0000-0003-0772-1604; Zennaro,
   Maria-Christina/0000-0001-5449-9191; Arlt, Wiebke/0000-0001-5106-9719;
   Reel, Parminder Singh/0000-0001-7796-1457; Stell,
   Anthony/0000-0003-4819-9883; Cole, Christian/0000-0002-2560-2484;
   Riddell, Alexandra/0000-0003-4566-8680
FU European Union [633983]; Deutsche Forschungsgemeinschaft [CRC/Transregio
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FX European Union's Horizon 2020 Research and Innovation Programme under
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   Deutsche Forschungsgemeinschaft (CRC/Transregio 205/1).
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NR 49
TC 28
Z9 29
U1 1
U2 26
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
SN 2352-3964
J9 EBIOMEDICINE
JI EBioMedicine
PD OCT
PY 2022
VL 84
AR 104276
DI 10.1016/j.ebiom.2022.104276
EA SEP 2022
PG 15
WC Medicine, General & Internal; Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine; Research & Experimental Medicine
GA 5J5AO
UT WOS:000869053500011
PM 36179553
OA Green Published, Green Accepted, gold
DA 2025-01-04
ER

EF