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Pancreatic Neoplasms: HELP
Articles by Jay K. Kolls
Based on 2 articles published since 2010
(Why 2 articles?)
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Between 2010 and 2020, Jay K. Kolls wrote the following 2 articles about Pancreatic Neoplasms.
 
+ Citations + Abstracts
1 Article Immune Cell Production of Interleukin 17 Induces Stem Cell Features of Pancreatic Intraepithelial Neoplasia Cells. 2018

Zhang, Yu / Zoltan, Michelle / Riquelme, Erick / Xu, Hanwen / Sahin, Ismet / Castro-Pando, Susana / Montiel, Maria Fernanda / Chang, Kyle / Jiang, Zhengyu / Ling, Jianhua / Gupta, Sonal / Horne, William / Pruski, Melissa / Wang, Huamin / Sun, Shao-Cong / Lozano, Guillermina / Chiao, Paul / Maitra, Anirban / Leach, Steven D / Kolls, Jay K / Vilar, Eduardo / Wang, Timothy C / Bailey, Jennifer M / McAllister, Florencia. ·Department of Clinical Cancer Prevention, The University of Texas MD Anderson Cancer Center, Houston, Texas. · Department of Engineering, Texas Southern University, Houston, Texas. · Herbert Irving Comprehensive Cancer Center, Columbia University Medical Center, New York, New York. · Department of Molecular and Cellular Oncology, The University of Texas MD Anderson Cancer Center, Houston, Texas. · Department of Pathology, University of Texas MD Anderson Cancer Center, Houston, Texas. · Richard King Mellon Foundation Institute for Pediatric Research, Children's Hospital of Pittsburgh, Pittsburgh, Pennsylvania. · Division of Gastroenterology, Hepatology and Nutrition, Department of Internal Medicine, University of Texas Health Science Center, Houston, Texas. · Department of Immunology, University of Texas Health Sciences Center, Houston, Texas. · Department of Genetics, The University of Texas MD Anderson Cancer Center, Houston, Texas. · Center for Pancreatic Cancer Research, Memorial Sloan Kettering Cancer Center, New York, New York. · Department of Clinical Cancer Prevention, The University of Texas MD Anderson Cancer Center, Houston, Texas. Electronic address: fmcallister@mdanderson.org. ·Gastroenterology · Pubmed #29604293.

ABSTRACT: BACKGROUND & AIMS: Little is known about how the immune system affects stem cell features of pancreatic cancer cells. Immune cells that produce interleukin 17A (IL17A) in the chronically inflamed pancreas (chronic pancreatitis) contribute to pancreatic interepithelial neoplasia (PanIN) initiation and progression. We investigated the effects that IL17A signaling exerts on pancreatic cancer progenitor cells and the clinical relevance of this phenomena. METHODS: We performed studies with Mist1Cre;LSLKras;Rosa26mTmG (KC RESULTS: PanIN cells from KC CONCLUSIONS: In studies of mouse and human pancreatic tumors and precursors, we found that immune cell-derived IL17 regulated development of tuft cells and stem cell features of pancreatic cancer cells via increased expression of DCLK1, POU2F3, ALDH1A1, and IL17RC. Strategies to disrupt this pathway might be developed to prevent pancreatic tumor growth and progression.

2 Article Oncogenic Kras activates a hematopoietic-to-epithelial IL-17 signaling axis in preinvasive pancreatic neoplasia. 2014

McAllister, Florencia / Bailey, Jennifer M / Alsina, Janivette / Nirschl, Christopher J / Sharma, Rajni / Fan, Hongni / Rattigan, Yanique / Roeser, Jeffrey C / Lankapalli, Rachana H / Zhang, Hao / Jaffee, Elizabeth M / Drake, Charles G / Housseau, Franck / Maitra, Anirban / Kolls, Jay K / Sears, Cynthia L / Pardoll, Drew M / Leach, Steven D. ·Department of Oncology, Johns Hopkins University, Baltimore, MD 21205, USA; Division of Clinical Pharmacology, Department of Medicine, Johns Hopkins University, Baltimore, MD 21205, USA. · Department of Surgery and McKusick Nathans Institute of Genetic Medicine, Johns Hopkins University, Baltimore, MD 21205, USA. · Department of Oncology, Johns Hopkins University, Baltimore, MD 21205, USA. · Department of Pathology, The Sol Goldman Pancreatic Cancer Research Center, Johns Hopkins University, Baltimore, MD 21205, USA. · Department of Molecular Microbiology and Immunology, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD 21205, USA. · Department of Oncology, Johns Hopkins University, Baltimore, MD 21205, USA; Department of Pathology, The Sol Goldman Pancreatic Cancer Research Center, Johns Hopkins University, Baltimore, MD 21205, USA. · Richard King Mellon Foundation Institute for Pediatric Research, Children's Hospital of Pittsburgh, Pittsburgh, PA 15224, USA. · Department of Surgery and McKusick Nathans Institute of Genetic Medicine, Johns Hopkins University, Baltimore, MD 21205, USA. Electronic address: leachs@mskcc.org. ·Cancer Cell · Pubmed #24823639.

ABSTRACT: Many human cancers are dramatically accelerated by chronic inflammation. However, the specific cellular and molecular elements mediating this effect remain largely unknown. Using a murine model of pancreatic intraepithelial neoplasia (PanIN), we found that Kras(G12D) induces expression of functional IL-17 receptors on PanIN epithelial cells and also stimulates infiltration of the pancreatic stroma by IL-17-producing immune cells. Both effects are augmented by associated chronic pancreatitis, resulting in functional in vivo changes in PanIN epithelial gene expression. Forced IL-17 overexpression dramatically accelerates PanIN initiation and progression, while inhibition of IL-17 signaling using genetic or pharmacologic techniques effectively prevents PanIN formation. Together, these studies suggest that a hematopoietic-to-epithelial IL-17 signaling axis is a potent and requisite driver of PanIN formation.