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Pancreatic Neoplasms: HELP
Articles by Lawrence N. Kwong
Based on 2 articles published since 2010
(Why 2 articles?)
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Between 2010 and 2020, Lawrence N. Kwong wrote the following 2 articles about Pancreatic Neoplasms.
 
+ Citations + Abstracts
1 Article Integrative Genomic Analysis of Cholangiocarcinoma Identifies Distinct IDH-Mutant Molecular Profiles. 2017

Farshidfar, Farshad / Zheng, Siyuan / Gingras, Marie-Claude / Newton, Yulia / Shih, Juliann / Robertson, A Gordon / Hinoue, Toshinori / Hoadley, Katherine A / Gibb, Ewan A / Roszik, Jason / Covington, Kyle R / Wu, Chia-Chin / Shinbrot, Eve / Stransky, Nicolas / Hegde, Apurva / Yang, Ju Dong / Reznik, Ed / Sadeghi, Sara / Pedamallu, Chandra Sekhar / Ojesina, Akinyemi I / Hess, Julian M / Auman, J Todd / Rhie, Suhn K / Bowlby, Reanne / Borad, Mitesh J / Anonymous5350899 / Zhu, Andrew X / Stuart, Josh M / Sander, Chris / Akbani, Rehan / Cherniack, Andrew D / Deshpande, Vikram / Mounajjed, Taofic / Foo, Wai Chin / Torbenson, Michael S / Kleiner, David E / Laird, Peter W / Wheeler, David A / McRee, Autumn J / Bathe, Oliver F / Andersen, Jesper B / Bardeesy, Nabeel / Roberts, Lewis R / Kwong, Lawrence N. ·Departments of Surgery and Oncology, Arnie Charbonneau Cancer Institute, University of Calgary, Calgary, AB T2N 4N1, Canada. · Departments of Genomic Medicine, Melanoma Medical Oncology, Bioinformatics and Computational Biology, Pathology, and Translational Molecular Pathology, The University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA. · Human Genome Sequencing Center, Baylor College of Medicine, Houston, TX 77030, USA. · University of California Santa Cruz, Santa Cruz, CA 95064, USA. · The Eli and Edythe L. Broad Institute of Massachusetts Institute of Technology and Harvard University, Cambridge, MA 02142, USA; Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA 02215, USA. · Canada's Michael Smith Genome Sciences Centre, BC Cancer Agency, Vancouver, BC V5Z 4S6, Canada. · Center for Epigenetics, Van Andel Research Institute, Grand Rapids, MI 49503, USA. · Departments of Genetics and Pathology and Laboratory Medicine, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA; Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA. · Blueprint Medicines, 38 Sidney Street, Cambridge, MA 02139, USA. · Divisions of Gastroenterology and Hepatology and Laboratory Medicine and Pathology, Mayo Clinic College of Medicine, Rochester, MN 55905, USA. · Memorial Sloan Kettering Cancer Center, New York, NY 10005, USA. · University of Alabama at Birmingham, Birmingham, AL 35294, USA; HudsonAlpha Institute for Biotechnology, Huntsville, AL 35806, USA. · The Eli and Edythe L. Broad Institute of Massachusetts Institute of Technology and Harvard University, Cambridge, MA 02142, USA. · Departments of Genetics and Pathology and Laboratory Medicine, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA. · USC/Norris Comprehensive Cancer Center, University of Southern California, Los Angeles, CA 90033, USA. · Division of Hematology and Oncology, Mayo Clinic, Scottsdale, AZ 85054, USA. · Departments of Hematology and Oncology, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02114, USA. · Departments of Pathology and Oncology, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02114, USA. · National Cancer Institute, Bethesda, MD 20892, USA. · Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA. · Biotech Research and Innovation Centre, Department of Health and Medical Sciences, University of Copenhagen, Copenhagen 2200, Denmark. Electronic address: jesper.andersen@bric.ku.dk. · Departments of Pathology and Oncology, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02114, USA. Electronic address: bardeesy.nabeel@mgh.harvard.edu. · Divisions of Gastroenterology and Hepatology and Laboratory Medicine and Pathology, Mayo Clinic College of Medicine, Rochester, MN 55905, USA. Electronic address: roberts.lewis@mayo.edu. · Departments of Genomic Medicine, Melanoma Medical Oncology, Bioinformatics and Computational Biology, Pathology, and Translational Molecular Pathology, The University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA. Electronic address: lkwong@mdanderson.org. ·Cell Rep · Pubmed #28297679.

ABSTRACT: Cholangiocarcinoma (CCA) is an aggressive malignancy of the bile ducts, with poor prognosis and limited treatment options. Here, we describe the integrated analysis of somatic mutations, RNA expression, copy number, and DNA methylation by The Cancer Genome Atlas of a set of predominantly intrahepatic CCA cases and propose a molecular classification scheme. We identified an IDH mutant-enriched subtype with distinct molecular features including low expression of chromatin modifiers, elevated expression of mitochondrial genes, and increased mitochondrial DNA copy number. Leveraging the multi-platform data, we observed that ARID1A exhibited DNA hypermethylation and decreased expression in the IDH mutant subtype. More broadly, we found that IDH mutations are associated with an expanded histological spectrum of liver tumors with molecular features that stratify with CCA. Our studies reveal insights into the molecular pathogenesis and heterogeneity of cholangiocarcinoma and provide classification information of potential therapeutic significance.

2 Article Synthetic vulnerabilities of mesenchymal subpopulations in pancreatic cancer. 2017

Genovese, Giannicola / Carugo, Alessandro / Tepper, James / Robinson, Frederick Scott / Li, Liren / Svelto, Maria / Nezi, Luigi / Corti, Denise / Minelli, Rosalba / Pettazzoni, Piergiorgio / Gutschner, Tony / Wu, Chia-Chin / Seth, Sahil / Akdemir, Kadir Caner / Leo, Elisabetta / Amin, Samirkumar / Molin, Marco Dal / Ying, Haoqiang / Kwong, Lawrence N / Colla, Simona / Takahashi, Koichi / Ghosh, Papia / Giuliani, Virginia / Muller, Florian / Dey, Prasenjit / Jiang, Shan / Garvey, Jill / Liu, Chang-Gong / Zhang, Jianhua / Heffernan, Timothy P / Toniatti, Carlo / Fleming, Jason B / Goggins, Michael G / Wood, Laura D / Sgambato, Alessandro / Agaimy, Abbas / Maitra, Anirban / Roberts, Charles W M / Wang, Huamin / Viale, Andrea / DePinho, Ronald A / Draetta, Giulio F / Chin, Lynda. ·Department of Genomic Medicine, The University of Texas MD Anderson Cancer Center, Houston, Texas 77030, USA. · Institute for Applied Cancer Science, The University of Texas MD Anderson Cancer Center, Houston, Texas 77030, USA. · European Institute of Oncology, Milano 20141, Italy. · Sun Yat-sen University Cancer Center, State Key Laboratory of Oncology in South China, Guangzhou, 510060, China. · Istituto di Patologia Generale, Universit├í Cattolica del Sacro Cuore, Rome 00168, Italy. · Graduate program in Structural and Computational Biology and Molecular Biophysics, Baylor College of Medicine, Houston, Texas 77030, USA. · Department of Pathology, The Sol Goldman Pancreatic Cancer Research Center, Johns Hopkins University, Baltimore, Maryland 21287, USA. · Department of Molecular and Cellular Oncology, The University of Texas MD Anderson Cancer Center, Houston, Texas 77030, USA. · Department of Translational Molecular Pathology, The University of Texas MD Anderson Cancer Center, Houston, Texas 77030, USA. · Department of Leukemia, The University of Texas MD Anderson Cancer Center, Houston, Texas 77030, USA. · Office of Technology Commercialization, The University of Texas MD Anderson Cancer Center, Houston, Texas 77030, USA. · Department of Cancer Systems Imaging, The University of Texas MD Anderson Cancer Center, Houston, Texas 77030, USA. · Department of Cancer Biology, The University of Texas MD Anderson Cancer Center, Houston, Texas 77030, USA. · Department of Experimental Therapeutics, The University of Texas MD Anderson Cancer Center, Houston, Texas 77030, USA. · ORBIT Platform, The University of Texas MD Anderson Cancer Center, Houston, Texas 77030, USA. · Department of Surgical Oncology, The University of Texas MD Anderson Cancer Center, Houston, Texas 77030, USA. · Department of Pathology, Friedrich Alexander University Erlangen-Nuremberg, University Hospital, Erlangen 91054, Germany. · Department of Pathology, The University of Texas MD Anderson Cancer Center, Houston, Texas 77030, USA. · Sheikh Ahmed Bin Zayed Al Nahyan Center for Pancreatic Cancer Research, The University of Texas MD Anderson Cancer Center, Houston, Texas 77030, USA. · Comprehensive Cancer Center and Department of Oncology, St Jude Children's Research Hospital, Memphis, Tennessee 77027, USA. ·Nature · Pubmed #28178232.

ABSTRACT: Malignant neoplasms evolve in response to changes in oncogenic signalling. Cancer cell plasticity in response to evolutionary pressures is fundamental to tumour progression and the development of therapeutic resistance. Here we determine the molecular and cellular mechanisms of cancer cell plasticity in a conditional oncogenic Kras mouse model of pancreatic ductal adenocarcinoma (PDAC), a malignancy that displays considerable phenotypic diversity and morphological heterogeneity. In this model, stochastic extinction of oncogenic Kras signalling and emergence of Kras-independent escaper populations (cells that acquire oncogenic properties) are associated with de-differentiation and aggressive biological behaviour. Transcriptomic and functional analyses of Kras-independent escapers reveal the presence of Smarcb1-Myc-network-driven mesenchymal reprogramming and independence from MAPK signalling. A somatic mosaic model of PDAC, which allows time-restricted perturbation of cell fate, shows that depletion of Smarcb1 activates the Myc network, driving an anabolic switch that increases protein metabolism and adaptive activation of endoplasmic-reticulum-stress-induced survival pathways. Increased protein turnover renders mesenchymal sub-populations highly susceptible to pharmacological and genetic perturbation of the cellular proteostatic machinery and the IRE1-╬▒-MKK4 arm of the endoplasmic-reticulum-stress-response pathway. Specifically, combination regimens that impair the unfolded protein responses block the emergence of aggressive mesenchymal subpopulations in mouse and patient-derived PDAC models. These molecular and biological insights inform a potential therapeutic strategy for targeting aggressive mesenchymal features of PDAC.