Molecular Pathology of Pancreatic Cancer

Ralph H. Hruban, Christine Iacobuzio-Donahue, Robb E. Wilentz, Michael Goggins, Scott E. Kern

Research output: Contribution to journalReview article

Abstract

Until recently, pancreatic cancer was a poorly understood disease. Research in the past decade has shown conclusively, however, that pancreatic cancer is primarily genetic in nature. Inactivation with a variety of tumor-suppressor genes such as p16, DPC4, and p53, coupled with activation of oncogenes such as K-ras, are a few of the mutations that trigger the growth of cancerous cells. Understanding these mutations is critical to a better understanding of familial pancreatic cancer and to the development of gene-based screening tests and therapies. In this article, we review the genetic alterations identified in pancreatic cancer and provide examples of how this information can be applied to patient care.

Original languageEnglish (US)
Pages (from-to)251-258
Number of pages8
JournalCancer Journal
Volume7
Issue number4
StatePublished - Jul 1 2001

Keywords

  • DPC4
  • K-ras
  • Oncogene
  • Pancreatic cancer
  • Tumor suppressor gene
  • p16
  • p53

ASJC Scopus subject areas

  • Oncology
  • Cancer Research

Fingerprint Dive into the research topics of 'Molecular Pathology of Pancreatic Cancer'. Together they form a unique fingerprint.

  • Cite this

    Hruban, R. H., Iacobuzio-Donahue, C., Wilentz, R. E., Goggins, M., & Kern, S. E. (2001). Molecular Pathology of Pancreatic Cancer. Cancer Journal, 7(4), 251-258.