Pancreatic cancer

Anirban Maitra, Ralph H. Hruban

Research output: Chapter in Book/Report/Conference proceedingChapter

Abstract

The past two decades have witnessed an explosion in our understanding of pancreatic cancer, and it is now clear that pancreatic cancer is a disease of inherited (germ-line) and somatic gene mutations. The genes mutated in pancreatic cancer include KRAS2, p16/CDKN2A, TP53, and SMAD4/DPC4, and these are accompanied by a substantial compendium of genomic and transcriptomic alterations that facilitate cell cycle deregulation, cell survival, invasion, and metastases. Pancreatic cancers do not arise de novo, and three distinct precursor lesions have been identified. Experimental models of pancreatic cancer have been developed in genetically engineered mice, which recapitulate the multistep progression of the cognate human disease. Although the putative cell of origin for pancreatic cancer remains elusive, minor populations of cells with stem-like properties have been identified that appear responsible for tumor initiation, metastases, and resistance of pancreatic cancer to conventional therapies.

Original languageEnglish (US)
Title of host publicationAnnual Review of Pathology
Subtitle of host publicationMechanisms of Disease
EditorsAbul Abbas, Stephen Galli, Peter Howley
Pages157-188
Number of pages32
DOIs
StatePublished - 2008

Publication series

NameAnnual Review of Pathology: Mechanisms of Disease
Volume3
ISSN (Print)1553-4006
ISSN (Electronic)1553-4014

Keywords

  • Adenocarcinoma
  • Carcinoma
  • Genetics
  • Mouse model
  • Pancreas
  • Precursor
  • Stem cell
  • Targeted therapy

ASJC Scopus subject areas

  • Pathology and Forensic Medicine

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