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

Jonas Cicenas1,2,3, Kotryna Kvederaviciute4, Ingrida Meskinyte5

  • 1Vetsuisse Faculty, Institute of Animal Pathology, University of Bern, Länggassstrasse 122, 3012 Bern, Switzerland. j.cicenas@mapkinases.eu.

Cancers
|April 29, 2017
PubMed

Insights

Pancreatic cancer has a high fatality rate and limited surgical options. This review details common genetic alterations in pancreatic cancer, crucial for understanding disease progression and developing targeted therapies.

Area of Science:

  • Oncology
  • Genetics
  • Cancer Research

Background:

  • Pancreatic cancer exhibits a high fatality rate, ranking as the fourth leading cause of cancer death in developed nations.
  • Surgical intervention, the primary treatment, is only feasible for 15-20% of patients at diagnosis, with survival rates below 30% post-surgery.
  • Genome instability is a hallmark of cancer, with approximately 97% of pancreatic cancers displaying significant gene derangements.

Purpose of the Study:

  • To review and describe the most frequent genetic alterations observed in pancreatic cancer.
  • To provide insights into the genomic landscape of pancreatic cancer.

Main Methods:

  • Literature review of studies focusing on genetic alterations in pancreatic cancer.
  • Analysis of reported gene derangements including point mutations, amplifications, deletions, translocations, and inversions.

Main Results:

  • Pancreatic cancer is characterized by widespread genomic instability.
  • Common genetic alterations include point mutations, amplifications, deletions, translocations, and inversions, affecting approximately 97% of tumors.

Conclusions:

  • Understanding frequent genetic alterations is critical for advancing pancreatic cancer research.
  • Identifying these alterations may pave the way for improved diagnostic and therapeutic strategies for pancreatic cancer.
Keywords:
BRCA1BRCA2CDKN2AKRASSMAD4TP53genetic variantmutationpancreatic cancer

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