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Review
. 2017 Apr 28;9(5):42.
doi: 10.3390/cancers9050042.

KRAS, TP53, CDKN2A, SMAD4, BRCA1, and BRCA2 Mutations in Pancreatic Cancer

Jonas Cicenas  1   2   3 , Kotryna Kvederaviciute  4 , Ingrida Meskinyte  5 , Edita Meskinyte-Kausiliene  6 , Aiste Skeberdyte  7 , Jonas Cicenas  8
Affiliations
Review

KRAS, TP53, CDKN2A, SMAD4, BRCA1, and BRCA2 Mutations in Pancreatic Cancer

Jonas Cicenas et al. Cancers (Basel). .

Abstract

Pancreatic cancer is a disease that has a very high fatality rate and one of the highest mortality ratios among all major cancers, remaining the fourth leading cause of cancer-related deaths in developed countries. The major treatment of pancreatic cancer is surgery; however, only 15-20% of patients are candidates for it at the diagnosis of disease. On the other hand, survival in patients, who undergo surgery, is less than 30%. In most cancers, genome stability is disturbed and pancreatic cancer is not the exception. Approximately 97% of pancreatic cancers have gene derangements, defined by point mutations, amplifications, deletions, translocations, and inversions. This review describes the most frequent genetic alterations found in pancreatic cancer.

Keywords: BRCA1; BRCA2; CDKN2A; KRAS; SMAD4; TP53; genetic variant; mutation; pancreatic cancer.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Mutations in the carcinogenesis of pancreatic adenocarcinoma. Pancreatic intraepithelial neoplasia (PanIN) grading.
Figure 2
Figure 2
Most frequent mutations in pancreatic cancer. KRAS mutations by the exons and TP53 mutations by protein domain.
See this image and copyright information in PMC

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