3 research outputs found
Prognostic Properties of KRAS Gene Mutation Subtypes in Resected Pancreatic Cancer
Introduction Pancreatic ductal adenocarcinoma (PDAC) is an aggressive and therapy-resistant cancer with an overall 5-year survival rate of almost 12%, making it among the most lethal of all major cancers.1 PDAC has a distinct genomic profile, with somatic KRAS protooncogene mutations in ~90% of cases.2,3 Current literature has not reached a consensus on disease prognosis based on KRAS mutation subtype.2-5https://jdc.jefferson.edu/aoa_research_symposium_posters/1005/thumbnail.jp
The Clinical Implications of KRAS Mutations and Variant Allele Frequencies in Pancreatic Ductal Adenocarcinoma
The KRAS proto-oncogene is a major driver of pancreatic tumorigenesis and is nearly ubiquitously mutated in pancreatic ductal adenocarcinoma (PDAC). KRAS point mutations are detected in over 90% of PDAC cases, and these mutations have been shown to be associated with worse therapy response and overall survival. Pathogenic KRAS mutations are mostly limited to codons 12, 13 and 61, with G12D, G12V, G12R, Q61H, and G13D accounting for approximately 95% of the mutant cases. Emerging data have shown the importance of specific mutant subtypes, as well as KRAS variant allele frequency on clinical prognosis. Furthermore, novel technologies and therapies are being developed to target specific mutant subtypes, with encouraging early results. In this paper, we aim to review the recent studies regarding the relative impact of specific mutant KRAS subtypes on oncologic outcomes, the application of variant allele frequency in next generation sequencing analyses, and the ongoing research into therapies targeting specific mutant KRAS subtypes