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Med Sci (Paris). 2013 Nov;29(11):991-7. doi: 10.1051/medsci/20132911015. Epub 2013 Nov 20.

[Kras oncogene and pancreatic cancer: thirty years after].

[Article in French]

Author information

  • 1Inserm UMR U1037, Centre de recherche sur le cancer de Toulouse, CHU Rangueil, 1, avenue Jean Poulhès, BP 84225, 31432 Toulouse Cedex 4, France - Service de gastroentérologie et nutrition, CHU Rangueil-Larrey, 1, avenue Jean Poulhès, TSA 50032, 31059 Toulouse, Cedex 9, France.

Abstract

Point mutations of the Kras oncogene induce in cancerous cells an uncontrolled increase of cell proliferation and invasiveness. Mutation of Kras appears early during the process of the pancreatic carcinogenesis and is the most frequent genetic alteration in pancreatic adenocarcinoma (75 to 95 % of cases) as well as in precancerous lesions such as PanIN and IMPN. These latter lesions and tumour microenvironment are reproduced in transgenic models developed in mice. These models are induced on the basis of Kras mutation (Pdx1-Cre ; Kras(G12D) mice) associated or not to the inactivation of tumour suppressor genes (TP53, DPC4, INK4A). Kras mutation assay is easily performed in human biological samples, especially in the cellular material sampled in pancreatic masses under endoscopic ultrasound by fine needle aspiration biopsy. In the near future, searching for Kras mutation could be useful in clinical practice either for positive diagnosis of pancreatic adenocarcinoma in case of unconclusive/doubtful cytopathological analysis or for the differential diagnosis with chronic pancreatitis especially in its pseudotumoural form.

© 2013 médecine/sciences – Inserm.

PMID:
24280502
[PubMed - indexed for MEDLINE]
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