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Pancreatic Neoplasms: HELP
Articles by Hai Li
Based on 3 articles published since 2009
(Why 3 articles?)
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Between 2009 and 2019, Hai Li wrote the following 3 articles about Pancreatic Neoplasms.
 
+ Citations + Abstracts
1 Article A precision oncology approach to the pharmacological targeting of mechanistic dependencies in neuroendocrine tumors. 2018

Alvarez, Mariano J / Subramaniam, Prem S / Tang, Laura H / Grunn, Adina / Aburi, Mahalaxmi / Rieckhof, Gabrielle / Komissarova, Elena V / Hagan, Elizabeth A / Bodei, Lisa / Clemons, Paul A / Dela Cruz, Filemon S / Dhall, Deepti / Diolaiti, Daniel / Fraker, Douglas A / Ghavami, Afshin / Kaemmerer, Daniel / Karan, Charles / Kidd, Mark / Kim, Kyoung M / Kim, Hee C / Kunju, Lakshmi P / Langel, Ülo / Li, Zhong / Lee, Jeeyun / Li, Hai / LiVolsi, Virginia / Pfragner, Roswitha / Rainey, Allison R / Realubit, Ronald B / Remotti, Helen / Regberg, Jakob / Roses, Robert / Rustgi, Anil / Sepulveda, Antonia R / Serra, Stefano / Shi, Chanjuan / Yuan, Xiaopu / Barberis, Massimo / Bergamaschi, Roberto / Chinnaiyan, Arul M / Detre, Tony / Ezzat, Shereen / Frilling, Andrea / Hommann, Merten / Jaeger, Dirk / Kim, Michelle K / Knudsen, Beatrice S / Kung, Andrew L / Leahy, Emer / Metz, David C / Milsom, Jeffrey W / Park, Young S / Reidy-Lagunes, Diane / Schreiber, Stuart / Washington, Kay / Wiedenmann, Bertram / Modlin, Irvin / Califano, Andrea. ·Department of Systems Biology, Columbia University, New York, NY, USA. · DarwinHealth Inc, New York, NY, USA. · Memorial Sloan Kettering Cancer Center, New York, NY, USA. · Institute for Systems Genetics, New York University Langone Medical Center, New York, NY, USA. · Department of Urology, Columbia University, New York, NY, USA. · Division of Pathology, European Institute of Oncology, Milan, Italy. · Broad Institute of Harvard and MIT, Cambridge, MA, USA. · Department of Pediatrics, Memorial Sloan Kettering Cancer Center, New York, NY, USA. · Cedars-Sinai Medical Center, Los Angeles, CA, USA. · Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, USA. · PsychoGenics Inc., Tarrytown, NY, USA. · Department of General and Visceral Surgery, Zentralklinik, Bad Berka, Germany. · Sulzberger Columbia Genome Center, Columbia University, New York, NY, USA. · Wren Laboratories, Branford, CT, USA. · Division of Hematology Oncology, Department of Medicine, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Korea. · Michigan Center for Translational Pathology, University of Michigan Medical School, Ann Arbor, MI, USA. · Department of Pathology, University of Michigan Medical School, Ann Arbor, MI, USA. · Comprehensive Cancer Center, University of Michigan Medical School, Ann Arbor, MI, USA. · Department of Neurochemistry, the Arrhenius Laboratories for Nat. Sci., Stockholm University, Stockholm, Sweden. · Laboratory of Molecular Biotechnology, Institute of Technology, University of Tartu, Tartu, Estonia. · Falconwood Foundation, New York, NY, USA. · Institute of Pathophysiology and Immunology, Medical University of Graz, Graz, Austria. · Department of Pathology, Columbia University, New York, NY, USA. · Department of Pathology, University Health Network, University of Toronto, Toronto, Canada. · Department of Pathology, Vanderbilt University Medical Center, Nashville, TN, USA. · Division of Colon and Rectal Surgery, State University of New York, Stony Brook, NY, USA. · Howard Hughes Medical Institute, University of Michigan Medical School, Ann Arbor, MI, USA. · Department of Urology, University of Michigan Medical School, Ann Arbor, MI, USA. · Imperial College London, London, UK. · Medical Oncology, National Center for Tumor Diseases Heidelberg, University Medical Center Heidelberg, Heidelberg, Germany. · Mount Sinai School of Medicine, New York, NY, USA. · Department of Surgery, New York-Presbyterian Hospital, Weill Cornell Medicine, New York, NY, USA. · Department of Chemistry and Chemical Biology, Harvard University, Cambridge, MA, USA. · Department of Internal Medicine, Division of Gastroenterology, Charite, Universitätsmedizin Berlin, Berlin, Germany. · Emeritus Professor Gastrointestinal Surgery, School of Medicine, Yale University, New Haven, Connecticut, USA. imodlin@irvinmodlin.com. · Department of Systems Biology, Columbia University, New York, NY, USA. califano@cumc.columbia.edu. · Department of Biomedical Informatics, Columbia University, New York, NY, USA. califano@cumc.columbia.edu. · Department of Biochemistry and Molecular Biophysics, Columbia University, New York, NY, USA. califano@cumc.columbia.edu. · J.P. Sulzberger Columbia Genome Center, Columbia University, New York, NY, USA. califano@cumc.columbia.edu. · Herbert Irving Comprehensive Cancer Center, Columbia University, New York, NY, USA. califano@cumc.columbia.edu. ·Nat Genet · Pubmed #29915428.

ABSTRACT: We introduce and validate a new precision oncology framework for the systematic prioritization of drugs targeting mechanistic tumor dependencies in individual patients. Compounds are prioritized on the basis of their ability to invert the concerted activity of master regulator proteins that mechanistically regulate tumor cell state, as assessed from systematic drug perturbation assays. We validated the approach on a cohort of 212 gastroenteropancreatic neuroendocrine tumors (GEP-NETs), a rare malignancy originating in the pancreas and gastrointestinal tract. The analysis identified several master regulator proteins, including key regulators of neuroendocrine lineage progenitor state and immunoevasion, whose role as critical tumor dependencies was experimentally confirmed. Transcriptome analysis of GEP-NET-derived cells, perturbed with a library of 107 compounds, identified the HDAC class I inhibitor entinostat as a potent inhibitor of master regulator activity for 42% of metastatic GEP-NET patients, abrogating tumor growth in vivo. This approach may thus complement current efforts in precision oncology.

2 Article A panel of 13-miRNA signature as a potential biomarker for predicting survival in pancreatic cancer. 2016

Zhou, Xin / Huang, Zebo / Xu, Lei / Zhu, Mingxia / Zhang, Lan / Zhang, Huo / Wang, Xiaping / Li, Hai / Zhu, Wei / Shu, Yongqian / Liu, Ping. ·Department of Oncology, First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, China. · Department of Thoracic Surgery, The Affiliated Jiangning Hospital of Nanjing Medical University, Nanjing 210029, China. · Department of Pathology, Sir Run Run Hospital Affiliated With Nanjing Medical University, Nanjing 211166, China. · Department of Pathology, First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, PR China. · Cancer Center of Nanjing Medical University, Nanjing 210029, China. ·Oncotarget · Pubmed #27626307.

ABSTRACT: Some reports have evaluated the prognostic relevance of microRNAs (miRNAs) in patients with pancreatic cancer (PC). However, most studies focused on limited miRNAs with small number of patients. The aim of the study is to identify a panel of miRNA signature that could predict prognosis in PC with the data from The Cancer Genome Atlas (TCGA). A total of 167 PC patients with the corresponding clinical data were enrolled in our study. The miRNAs significantly associated with overall survival (OS) in PC patients were identified with Cox proportional regression model. A risk score formula was developed to evaluate the prognostic value of the miRNA signature in PC. Thirteen miRNAs were identified to be significantly related with OS in PC patients. Patients with high risk score suffered poor overall survival compared with patients who had low risk score. The multivariate Cox regression analyses showed that the miRNA signature could act as an independent prognostic indicator. In addition, the signature might serve as a predicator for treatment outcome. Our study identified a miRNA signature including 13 miRNAs which could serve as an independent marker in prognosis of PC.

3 Article Alisertib induces cell cycle arrest and autophagy and suppresses epithelial-to-mesenchymal transition involving PI3K/Akt/mTOR and sirtuin 1-mediated signaling pathways in human pancreatic cancer cells. 2015

Wang, Feng / Li, Hai / Yan, Xiao-Gang / Zhou, Zhi-Wei / Yi, Zhi-Gang / He, Zhi-Xu / Pan, Shu-Ting / Yang, Yin-Xue / Wang, Zuo-Zheng / Zhang, Xueji / Yang, Tianxing / Qiu, Jia-Xuan / Zhou, Shu-Feng. ·Department of Hepatobiliary Surgery, General Hospital, Ningxia Medical University, Yinchuan, People's Republic of China ; Department of Pharmaceutical Sciences, College of Pharmacy, University of South Florida, Tampa, FL, USA. · Department of Colorectal Surgery, General Hospital, Ningxia Medical University, Yinchuan, People's Republic of China. · Department of Oncological Surgery, The First People's Hospital of Yinchuan, Yinchuan, People's Republic of China. · Department of Pharmaceutical Sciences, College of Pharmacy, University of South Florida, Tampa, FL, USA. · Department of General Surgery, Changqing Yangehu Hospital, Yinchuan, People's Republic of China. · Guizhou Provincial Key Laboratory for Regenerative Medicine, Stem Cell and Tissue Engineering Research Center and Sino-US Joint Laboratory for Medical Sciences, Guiyang Medical University, Guiyang, People's Republic of China. · Department of Oral and Maxillofacial Surgery, The First Affiliated Hospital of Nanchang University, Nanchang, People's Republic of China. · Department of Hepatobiliary Surgery, General Hospital, Ningxia Medical University, Yinchuan, People's Republic of China. · Research Center for Bioengineering and Sensing Technology, University of Science and Technology Beijing, Beijing, People's Republic of China. · Department of Internal Medicine, University of Utah and Salt Lake Veterans Affairs Medical Center, Salt Lake City, UT, USA. ·Drug Des Devel Ther · Pubmed #25632225.

ABSTRACT: Pancreatic cancer is the most aggressive cancer worldwide with poor response to current therapeutics. Alisertib (ALS), a potent and selective Aurora kinase A inhibitor, exhibits potent anticancer effects in preclinical and clinical studies; however, the effect and underlying mechanism of ALS in the pancreatic cancer treatment remain elusive. This study aimed to examine the effects of ALS on cell growth, autophagy, and epithelial-to-mesenchymal transition (EMT) and to delineate the possible molecular mechanisms in human pancreatic cancer PANC-1 and BxPC-3 cells. The results showed that ALS exerted potent cell growth inhibitory, pro-autophagic, and EMT-suppressing effects in PANC-1 and BxPC-3 cells. ALS remarkably arrested PANC-1 and BxPC-3 cells in G2/M phase via regulating the expression of cyclin-dependent kinases 1 and 2, cyclin B1, cyclin D1, p21 Waf1/Cip1, p27 Kip1, and p53. ALS concentration-dependently induced autophagy in PANC-1 and BxPC-3 cells, which may be attributed to the inhibition of phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt)/mammalian target of rapamycin (mTOR), p38 mitogen-activated protein kinase (p38 MAPK), and extracellular signal-regulated kinases 1 and 2 (Erk1/2) but activation of 5'-AMP-dependent kinase signaling pathways. ALS significantly inhibited EMT in PANC-1 and BxPC-3 cells with an increase in the expression of E-cadherin and a decrease in N-cadherin. In addition, ALS suppressed the expression of sirtuin 1 (Sirt1) and pre-B cell colony-enhancing factor/visfatin in both cell lines with a rise in the level of acetylated p53. These findings show that ALS induces cell cycle arrest and promotes autophagic cell death but inhibits EMT in pancreatic cancer cells with the involvement of PI3K/Akt/mTOR, p38 MAPK, Erk1/2, and Sirt1-mediated signaling pathways. Taken together, ALS may represent a promising anticancer drug for pancreatic cancer treatment. More studies are warranted to investigate other molecular targets and mechanisms and verify the efficacy and safety of ALS in the treatment of pancreatic cancer.