Molecular pathology of pancreatic cancer.
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.
Hruban
R H
RH
Department of Pathology, The Johns Hopkins Medical Institutions, Baltimore, Maryland, USA.
Iacobuzio-Donahue
C
C
Wilentz
R E
RE
Goggins
M
M
Kern
S E
SE
D004272:DNA, Mitochondrial / Q000235:genetics*; D016147:Genes, Tumor Suppressor / Q000502:physiology*; D006801:Humans; D009857:Oncogenes / Q000502:physiology*; D010190:Pancreatic Neoplasms / Q000201:enzymology / Q000235:genetics* / Q000473:pathology
D004272:DNA, Mitochondrial