Molecular genetic basis of pancreatic adenocarcinoma

Werner Hilgers, Scott E. Kern

Research output: Contribution to journalReview articlepeer-review

Abstract

Pancreatic ductal adenocarcinoma is a complex genetic disease. As might be expected for a malignancy that is rather homogeneous in clinical presentation and behavior, a distinct subset of genes are found to be genetically inactivated in a majority of the tumors. A yet larger subset of genes experiences genetic inactivation at much lower frequencies. The latter subset could solely reflect a somewhat trivial genetic heterogeneity of the tumor, but more likely will represent the initial insights into pathways whose more widespread importance will be shown in future work. Familial pancreatic cancer susceptibility underlies a significant fraction of the overall incidence. Genetic testing is feasible for many of the causative genes, although the clinical utility remains unsettled. The precursor lesion for pancreatic cancer shares some of the genetic lesions of the more advanced invasive stage, and follows a stepwise progression model both histologically and genetically.

Original languageEnglish (US)
Pages (from-to)1-12
Number of pages12
JournalGenes Chromosomes and Cancer
Volume26
Issue number1
DOIs
StatePublished - Sep 1999

ASJC Scopus subject areas

  • Genetics
  • Cancer Research

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