Although most human pancreatic carcinomas are thought to arise in the small pancreatic ducts, early attempts to develop pancreatic carcinomas in GEM produced acinar tumors. These early studies utilized the EL-1 (elastase) promoter with oncogenes such as Kras, Hras, and TGF-α. Since different promoters target different cell types in various stages of development, in 2004 NCI sponsored an international workshop to standardize the phenotypic nomenclature of GEM pancreatic neoplasms (Hruban et al, 2006). In the last decade, several new GEM models have been developed which produce ductal adenocarcinomas. Among these, expression of an endogenous allele of oncogenic Kras produced ductal adenocarcinomas with a short latency (Tuveson and Hingorani, 2005).
Core Signaling Pathways in Human Pancreatic Cancers Revealed by Global Genomic Analyses. Sian Jones et al, Science 321:pp1801-1806, 26 Sept 2008, DOI:10.1126science.1164368
Distinct Populations of Cancer Stem Cells Determine Tumor Growth and Metastatic Activity in Human Pancreatic Cancer, Hermann, Patrick C. et al, Stem Cell, 2007, DOI10.1016/j.stem2007.06.002
High proportion of large genomic STK11 deletions in Peutz-Jeghers syndrome. Aretz S. et al. Hum Mutat. 2005;26:513–9.
Genotype-phenotype correlations in Peutz-Jeghers syndrome. Amos CI , et al .J Med Genet. 2004;41:327–33
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