Cellular Origins of Pancreatic Cancer

Update item information
Identifier cellular_origins_of_pancreatic_cancer
Title Cellular Origins of Pancreatic Cancer
Creator Murtaugh, L.C.; Human Genetics; School of Medicine; University of Utah Health
Subject Diffusion of Innovation; Pancreatic Neoplasms; Blood Glucose; Biomarkers, Tumor; Acinar Cells; Pancrelipase; Pancreas, Exocrine; Pancreatic Ducts; Genetic Markers;Transcription Factors; Down-Regulation; Cell Differentiation; Carcinoma, Pancreatic Ductal; Models, Animal; Knowledge Discovery
Keyword Cancer
Image Caption Histological sections of mouse pancreas, stained for the acinar marker Cpa1 (blue) and the tumor marker Claudin18 (brown). Re-expressing Ptf1a in tumor cells causes them to revert back into normal acinar cells.
Description Our pancreas has two main functions, endocrine control of blood sugar and exocrine production of the enzymes that digest our food. These enzymes are synthesized by pancreatic acinar cells and transported to the intestine through a network of pancreatic duct cells. Pancreatic cancer, the third deadliest cancer in the U.S., was previously assumed, based on histology and gene expression, to arise from duct cells. However, research in the Murtaugh lab demonstrated that this cancer instead arises from fully differentiated acinar cells. This process requires a dramatic reprogramming of cellular function, resulting from the downregulation of the transcription factor Ptf1a, which is a rate-limiting step in pancreatic cancer development. The Murtaugh lab has found that reactivating Ptf1a in mouse and human pancreatic cancer induces re-differentiation and inhibits growth, and is pursuing this as a novel therapeutic approach.
Relation is Part of 50 Basic Science Discoveries in 5 Years- 2019
Publisher Spencer S. Eccles Health Sciences Library, University of Utah
Date Digital 2020
Date 2019
Type Image
Format image/jpeg
Rights Management Copyright © 2020, University of Utah, All Rights Reserved
Language eng
ARK ark:/87278/s6cc6pt1
References 1.) The acinar differentiation determinant PTF1A inhibits initiation of pancreatic ductal adenocarcinoma. Krah NM, De La O JP, Swift GH, Hoang CQ, Willet SG, Chen Pan F, Cash GM, Bronner MP, Wright CV, MacDonald RJ, Murtaugh LC. Elife. 2015 Jul;4. pii 07125. https://pubmed.ncbi.nlm.nih.gov/26151762/ 2.) Prevention and reversion of pancreatic tumorigenesis through a differentiation-based mechanism. Krah NM, Narayanan SM, Yugawa DE, Straley JA, Wright CVE, MacDonald RJ, Murtaugh LC. Dev Cell. 2019 Sep;50(6):744. https://pubmed.ncbi.nlm.nih.gov/31422917/.
Press Releases and Media Discovery of How Cells Override Genetic Changes Could Lead to New Approaches in Pancreatic Cancer Treatment https://healthcare.utah.edu/huntsmancancerinstitute/news/2019/08/discovery-of-how-cells-override-genetic-changes-could-lead-to-new-approaches-in-pancreatic-cancer-treatment.php
Setname ehsl_50disc
Date Created 2020-08-13
Date Modified 2020-11-17
ID 1589352
Reference URL https://collections.lib.utah.edu/ark:/87278/s6cc6pt1