Document Type
Article
Publication Date
4-4-2024
Abstract
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.
Recommended Citation
Nusrat, Faria; Khanna, Akshay; Jain, Aditi; Jiang, Wei; Lavu, Harish; Yeo, Charles; Bowne, Wilbur; and Nevler, Avinoam, "The Clinical Implications of KRAS Mutations and Variant Allele Frequencies in Pancreatic Ductal Adenocarcinoma" (2024). Department of Surgery Faculty Papers. Paper 265.
https://jdc.jefferson.edu/surgeryfp/265
Creative Commons License
This work is licensed under a Creative Commons Attribution 4.0 License.
PubMed ID
38610868
Language
English
Comments
This article is the author's final published version in Journal of Clinical Medicine, Volume 13, Issue 7, April 2024, Article number 2103.
The published version is available at https://doi.org/10.3390/jcm13072103.
Copyright © 2024 by the authors