Jeffrey Trent

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Pancreatic cancer associated fibroblasts display normal allelotypes.

Kimberly Walter; Noriyuki Omura; Seung-Mo Hong; Margaret Griffith; Michael Goggins (Profiled Author: Michael Goggins)

Department of Pathology, The Sol Goldman Pancreatic Cancer Research Center, The Johns Hopkins Medical Institutions, Baltimore, Maryland 21231, USA.
Cancer biology & therapy 2008;7(6):882-8.

BACKGROUND: Recent studies have reported widespread copy number alterations and p53 mutations arising in cancer associated stromal cells. The aim of this study was to determine if pancreatic cancer associated fibroblasts display similar genetic alterations. DESIGN: Cancer-associated fibroblast cultures were established from 7 primary pancreatic adenocarcinomas. These fibroblasts and corresponding normal tissues when available were analyzed for genome-wide copy number changes using Affymetrix 250K SNP microarrays. Evidence of p53 protein expression, an indicator of p53 mutation was determined by immunohistochemical labeling of tissue microarrays containing 117 pancreatic ductal adenocarcinomas. RESULTS: Pancreatic cancer associated fibroblasts did not show any evidence of somatic copy number gains or losses. p53 protein expression was confined to invasive pancreatic adenocarcinoma cells and was not expressed in cancer-associated fibroblasts. CONCLUSIONS: We find no evidence that pancreatic cancer associated fibroblasts harbor somatic copy number changes or immunohistochemical evidence of p53 mutations.

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