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Pancreatic Neoplasms: HELP
Articles by Wei Shi
Based on 6 articles published since 2010
(Why 6 articles?)
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Between 2010 and 2020, Wei Shi wrote the following 6 articles about Pancreatic Neoplasms.
 
+ Citations + Abstracts
1 Article Definitive chemoradiotherapy and salvage chemotherapy for patients with isolated locoregional recurrence after radical resection of primary pancreatic cancer. 2019

Shi, Wei / Jiang, Rui / Liang, Fei / Yu, Genhua / Long, Jiang / Zhao, Jiandong. ·Department of Radiation Oncology, Fudan University Shanghai Cancer Center, Shanghai, People's Republic of China. · Department of Oncology, Shanghai Medical College, Shanghai, People's Republic of China. · Clinical Statistic Center, Shanghai Cancer Center and Shanghai Medical College, Fudan University, Shanghai, People's Republic of China. · Department of Radiation Oncology, Zhebei Mingzhou Hospital, Huzhou City, Zhejiang Province, People's Republic of China. · Department of Pancreatic Surgery, Fudan University Shanghai Cancer Center, Shanghai, People's Republic of China. ·Cancer Manag Res · Pubmed #31213918.

ABSTRACT:

2 Article Co-Delivery of Gemcitabine and Mcl-1 SiRNA via Cationic Liposome-Based System Enhances the Efficacy of Chemotherapy in Pancreatic Cancer. 2019

Wang, Yanbing / Gao, Fenghua / Jiang, Xingwei / Zhao, Xiao / Wang, Yu / Kuai, Qiyuan / Nie, Guangjun / He, Min / Pan, Yingjie / Shi, Wei / Ren, Suping / Yu, Qun. · ·J Biomed Nanotechnol · Pubmed #30890228.

ABSTRACT: Myeloid cell leukemia 1 (Mcl-1) overexpression is found in various human tumors and has emerged as a promising new target for pancreatic cancer treatment. Recent research has found that most pancreatic cancers develop resistance to the current first-line chemotherapeutic drug, gemcitabine (Gem), and high expression of Mcl-1 can reduce the sensitivity of pancreatic cancer cells to Gem chemotherapy. Therefore, novel strategies, such as combination therapy, to overcome resistance of Gem chemotherapy are needed urgently. Here, we employed a lipid-based delivery system (LPs) to codeliver Mcl-1 siRNA and Gem for pancreatic cancer treatment, named LP-Gem-siMcl-1. LP-Gem-siMcl-1 exhibited an increased cellular uptake, enhanced Mcl-1 down-regulation efficacy, and significant cytotoxicity in the human pancreatic carcinoma cell lines PANC-1 and BxPC-3. Furthermore, tumor inhibition

3 Article Cyclopamine treatment disrupts extracellular matrix and alleviates solid stress to improve nanomedicine delivery for pancreatic cancer. 2018

Zhang, Bo / Wang, Honglan / Jiang, Ting / Jin, Kai / Luo, Zimiao / Shi, Wei / Mei, Heng / Wang, Huafang / Hu, Yu / Pang, Zhiqing / Jiang, Xinguo. ·a Institute of Hematology , Union Hospital, Tongji Medical College, Huazhong University of Science & Technology , Wuhan , China. · b School of Pharmacy , Fudan University, Key Laboratory of Smart Drug Delivery, Ministry of Education , Shanghai , China. ·J Drug Target · Pubmed #29533111.

ABSTRACT: As one of the most intractable tumours, pancreatic ductal adenocarcinoma (PDA) has a dense extracellular matrix (ECM) which could increase solid stress within tumours to compress tumour vessels, reduce tumour perfusion and compromise nanomedicine delivery for PDA. Thus, alleviating solid stress represents a potential therapeutic target for PDA treatment. In this study, cyclopamine, a special inhibitor of the hedgehog signalling pathway which contributes a lot to ECM formation of PDA, was exploited to alleviate solid stress and improve nanomedicine delivery to PDA. Results demonstrated that cyclopamine successfully disrupted ECM and lowered solid stress within PDA, which increased functional tumour vessels and resulted in enhanced tumour perfusion as well as improved tumour nanomedicine delivery in PDA-bearing animal models. Therefore, solid stress within PDA represents a new therapeutic target for PDA treatment.

4 Article A Concise Synthesis of Three Branches Derived from Polysaccharide RN1 and Anti-Pancreatic Cancer Activity Study. 2017

Cai, Deqin / Yao, Yanli / Tang, Yubo / Wang, Zheng / Shi, Wei / Huang, Wei / Ding, Kan. ·University of Chinese Academy of Sciences, No.19A Yuquan Road, Beijing 100049, China. deqincai2012@163.com. · Glycochemistry and Glycobiology Lab, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, 555 Zuchongzhi Road, Shanghai 201203, China. deqincai2012@163.com. · University of Chinese Academy of Sciences, No.19A Yuquan Road, Beijing 100049, China. yaoyanli1016@163.com. · Glycochemistry and Glycobiology Lab, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, 555 Zuchongzhi Road, Shanghai 201203, China. yaoyanli1016@163.com. · CAS Key Laboratory of Receptor Research, CAS Center for Excellence in Molecular Cell Science, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, 555 Zuchongzhi Road, Pudong, Shanghai 201203, China. yubotang1107@163.com. · Key Laboratory of Structure-Based Drug Design and Discovery, Ministry of Education, Shenyang Pharmaceutical University, Shenyang 110016, China. yubotang1107@163.com. · Glycochemistry and Glycobiology Lab, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, 555 Zuchongzhi Road, Shanghai 201203, China. wzheng92@mail.ustc.edu.cn. · Nano Science and Technology Institute, University of Science and Technology of China, 96 Jin Zhai Road, Hefei 230026, China. wzheng92@mail.ustc.edu.cn. · University of Chinese Academy of Sciences, No.19A Yuquan Road, Beijing 100049, China. hsw201204@163.com. · CAS Key Laboratory of Receptor Research, CAS Center for Excellence in Molecular Cell Science, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, 555 Zuchongzhi Road, Pudong, Shanghai 201203, China. hsw201204@163.com. · University of Chinese Academy of Sciences, No.19A Yuquan Road, Beijing 100049, China. huangwei@simm.ac.cn. · CAS Key Laboratory of Receptor Research, CAS Center for Excellence in Molecular Cell Science, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, 555 Zuchongzhi Road, Pudong, Shanghai 201203, China. huangwei@simm.ac.cn. · University of Chinese Academy of Sciences, No.19A Yuquan Road, Beijing 100049, China. dingkan@simm.ac.cn. · Glycochemistry and Glycobiology Lab, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, 555 Zuchongzhi Road, Shanghai 201203, China. dingkan@simm.ac.cn. ·Polymers (Basel) · Pubmed #30965840.

ABSTRACT: RN1, a polysaccharide from flowers of

5 Article Gemcitabine and CHK1 inhibition potentiate EGFR-directed radioimmunotherapy against pancreatic ductal adenocarcinoma. 2014

Al-Ejeh, Fares / Pajic, Marina / Shi, Wei / Kalimutho, Murugan / Miranda, Mariska / Nagrial, Adnan M / Chou, Angela / Biankin, Andrew V / Grimmond, Sean M / Anonymous4220794 / Brown, Michael P / Khanna, Kum Kum. ·Authors' Affiliations: Signal Transduction Laboratory, QIMR Berghofer Medical Research Institute, Herston; Queensland Centre for Medical Genomics, Institute for Molecular Bioscience, The University of Queensland, St Lucia, Queensland; The Kinghorn Cancer Centre, Cancer Division, Garvan Institute of Medical Research; St Vincent's Clinical School, Faculty of Medicine, University of NSW; Department of Anatomical Pathology, SYDPATH, St Vincent's Hospital, Darlinghurst, New South Wales; Australian Pancreatic Cancer Genome Initiative, for the full list of contributors see http://www.pancreaticcancer.net.au/apgi/collaborators; Cancer Clinical Trials Unit, Royal Adelaide Hospital Cancer Centre, and Centre for Cancer Biology, SA Pathology; School of Medicine, University of Adelaide, Adelaide, Australia; and Wolfson Wohl Cancer Research Centre, Institute of Cancer Sciences, University of Glasgow, Glasgow, Scotland, United Kingdom Fares.Al-Ejeh@qimrberghofer.edu.au. · Authors' Affiliations: Signal Transduction Laboratory, QIMR Berghofer Medical Research Institute, Herston; Queensland Centre for Medical Genomics, Institute for Molecular Bioscience, The University of Queensland, St Lucia, Queensland; The Kinghorn Cancer Centre, Cancer Division, Garvan Institute of Medical Research; St Vincent's Clinical School, Faculty of Medicine, University of NSW; Department of Anatomical Pathology, SYDPATH, St Vincent's Hospital, Darlinghurst, New South Wales; Australian Pancreatic Cancer Genome Initiative, for the full list of contributors see http://www.pancreaticcancer.net.au/apgi/collaborators; Cancer Clinical Trials Unit, Royal Adelaide Hospital Cancer Centre, and Centre for Cancer Biology, SA Pathology; School of Medicine, University of Adelaide, Adelaide, Australia; and Wolfson Wohl Cancer Research Centre, Institute of Cancer Sciences, University of Glasgow, Glasgow, Scotland, United KingdomAuthors' Affiliations: Signal Transduction Laboratory, QIMR Berghofer Medical Research Institute, Herston; Queensland Centre for Medical Genomics, Institute for Molecular Bioscience, The University of Queensland, St Lucia, Queensland; The Kinghorn Cancer Centre, Cancer Division, Garvan Institute of Medical Research; St Vincent's Clinical School, Faculty of Medicine, University of NSW; Department of Anatomical Pathology, SYDPATH, St Vincent's Hospital, Darlinghurst, New South Wales; Australian Pancreatic Cancer Genome Initiative, for the full list of contributors see http://www.pancreaticcancer.net.au/apgi/collaborators; Cancer Clinical Trials Unit, Royal Adelaide Hospital Cancer Centre, and Centre for Cancer Biology, SA Pathology; School of Medicine, University of Adelaide, Adelaide, Australia; and Wolfson Wohl Cancer Research Centre, Institute of Cancer Sciences, University of Glasgow, Glasgow, Scotland, United Kingdom. · Authors' Affiliations: Signal Transduction Laboratory, QIMR Berghofer Medical Research Institute, Herston; Queensland Centre for Medical Genomics, Institute for Molecular Bioscience, The University of Queensland, St Lucia, Queensland; The Kinghorn Cancer Centre, Cancer Division, Garvan Institute of Medical Research; St Vincent's Clinical School, Faculty of Medicine, University of NSW; Department of Anatomical Pathology, SYDPATH, St Vincent's Hospital, Darlinghurst, New South Wales; Australian Pancreatic Cancer Genome Initiative, for the full list of contributors see http://www.pancreaticcancer.net.au/apgi/collaborators; Cancer Clinical Trials Unit, Royal Adelaide Hospital Cancer Centre, and Centre for Cancer Biology, SA Pathology; School of Medicine, University of Adelaide, Adelaide, Australia; and Wolfson Wohl Cancer Research Centre, Institute of Cancer Sciences, University of Glasgow, Glasgow, Scotland, United Kingdom. · Authors' Affiliations: Signal Transduction Laboratory, QIMR Berghofer Medical Research Institute, Herston; Queensland Centre for Medical Genomics, Institute for Molecular Bioscience, The University of Queensland, St Lucia, Queensland; The Kinghorn Cancer Centre, Cancer Division, Garvan Institute of Medical Research; St Vincent's Clinical School, Faculty of Medicine, University of NSW; Department of Anatomical Pathology, SYDPATH, St Vincent's Hospital, Darlinghurst, New South Wales; Australian Pancreatic Cancer Genome Initiative, for the full list of contributors see http://www.pancreaticcancer.net.au/apgi/collaborators; Cancer Clinical Trials Unit, Royal Adelaide Hospital Cancer Centre, and Centre for Cancer Biology, SA Pathology; School of Medicine, University of Adelaide, Adelaide, Australia; and Wolfson Wohl Cancer Research Centre, Institute of Cancer Sciences, University of Glasgow, Glasgow, Scotland, United KingdomAuthors' Affiliations: Signal Transduction Laboratory, QIMR Berghofer Medical Research Institute, Herston; Queensland Centre for Medical Genomics, Institute for Molecular Bioscience, The University of Queensland, St Lucia, Queensland; The Kinghorn Cancer Centre, Cancer Division, Garvan Institute of Medical Research; St Vincent's Clinical School, Faculty of Medicine, University of NSW; Department of Anatomical Pathology, SYDPATH, St Vincent's Hospital, Darlinghurst, New South Wales; Australian Pancreatic Cancer Genome Initiative, for the full list of contributors see http://www.pancreaticcancer.net.au/apgi/collaborators; Cancer Clinical Trials Unit, Royal Adelaide Hospital Cancer Centre, and Centre for Cancer Biology, SA Pathology; School of Medicine, University of Adelaide, Adelaide, Australia; and Wolfson Wohl Cancer Research Centre, Institute of Cancer Sciences, University of Glasgow, Glasgow, Scotland, United KingdomAuthors' Affiliations: Signal Transduction Laboratory, QIMR Berghofer Medical Research Institute, Herston; Queensland Centre for Medic ·Clin Cancer Res · Pubmed #24838526.

ABSTRACT: PURPOSE: To develop effective combination therapy against pancreatic ductal adenocarcinoma (PDAC) with a combination of chemotherapy, CHK1 inhibition, and EGFR-targeted radioimmunotherapy. EXPERIMENTAL DESIGN: Maximum tolerated doses were determined for the combination of gemcitabine, the CHK1 inhibitor PF-477736, and Lutetium-177 ((177)Lu)-labeled anti-EGFR antibody. This triple combination therapy was investigated using PDAC models from well-established cell lines, recently established patient-derived cell lines, and fresh patient-derived xenografts. Tumors were investigated for the accumulation of (177)Lu-anti-EGFR antibody, survival of tumor-initiating cells, induction of DNA damage, cell death, and tumor tissue degeneration. RESULTS: The combination of gemcitabine and CHK1 inhibitor PF-477736 with (177)Lu-anti-EGFR antibody was tolerated in mice. This triplet was effective in established tumors and prevented the recurrence of PDAC in four cell line-derived and one patient-derived xenograft model. This exquisite response was associated with the loss of tumor-initiating cells as measured by flow cytometric analysis and secondary implantation of tumors from treated mice into treatment-naïve mice. Extensive DNA damage, apoptosis, and tumor degeneration were detected in the patient-derived xenograft. Mechanistically, we observed CDC25A stabilization as a result of CHK1 inhibition with consequent inhibition of gemcitabine-induced S-phase arrest as well as a decrease in canonical (ERK1/2 phosphorylation) and noncanonical EGFR signaling (RAD51 degradation) as a result of EGFR inhibition. CONCLUSIONS: Our study developed an effective combination therapy against PDAC that has potential in the treatment of PDAC.

6 Article Silibinin causes apoptosis and cell cycle arrest in some human pancreatic cancer cells. 2011

Ge, Yakun / Zhang, Yuanxin / Chen, Yunpeng / Li, Quanshun / Chen, Jun / Dong, Ying / Shi, Wei. ·Key Laboratory for Molecular Enzymology & Engineering of the Ministry of Education, School of Life Science, Jilin University, Changchun 130023, China · E-Mails: yakunge@126.com (Y.G.) · zhangyuanxin@126.com (Y.Z.) · qsli06@mails.jlu.edu.cn (Q.L.). ·Int J Mol Sci · Pubmed #21954330.

ABSTRACT: Silibinin, an effective anti-cancer and chemopreventive agent in various epithelial cancer models, has been reported to inhibit cancer cell growth through mitogenic signaling pathways. However, whether it can inhibit human pancreatic carcinoma growth and what are the underlying mechanisms is still not well elucidated. Here, we evaluated the inhibitory proliferation effects of Silibinin in pancreatic carcinoma growth and examined whether Silibinin modulates cell cycle and apoptosis. Our results indicate that Silibinin effectively inhibited the pancreatic carcinoma AsPC-1, BxPC-3 and Panc-1 cells' proliferation and caused apoptosis. Silibinin induced a decrease in S phase and cell cycle arrest in G1 phase in AsPC-1 cells, but had no obvious changes in BxPC-3 and Panc-1 cell cycle. Furthermore, these results suggest that Silibinin might be a candidate chemopreventive agent for pancreatic carcinoma therapy.