The KRAS mutational spectrum and its clinical implications in pancreatic cancer

Luigi Perelli; Giannicola Genovese; Giulio F Draetta

doi:10.1016/j.ccell.2024.08.001

The KRAS mutational spectrum and its clinical implications in pancreatic cancer

Cancer Cell. 2024 Sep 9;42(9):1494-1496. doi: 10.1016/j.ccell.2024.08.001. Epub 2024 Aug 29.

Authors

Luigi Perelli¹, Giannicola Genovese², Giulio F Draetta³

Affiliations

¹ Department of Genomic Medicine, The University of Texas, MD Anderson Cancer Center, Houston, TX, USA; Department of Genitourinary Medical Oncology, Division of Cancer Medicine, The University of Texas, MD Anderson Cancer Center, Houston, TX, USA. Electronic address: lperelli@mdanderson.org.
² Department of Genomic Medicine, The University of Texas, MD Anderson Cancer Center, Houston, TX, USA; Department of Genitourinary Medical Oncology, Division of Cancer Medicine, The University of Texas, MD Anderson Cancer Center, Houston, TX, USA.
³ Department of Genomic Medicine, The University of Texas, MD Anderson Cancer Center, Houston, TX, USA. Electronic address: gdraetta@mdanderson.org.

PMID: 39214093
DOI: 10.1016/j.ccell.2024.08.001

Abstract

In this issue of Cancer Cell, McIntyre et al. show that specific mutations in the KRAS proto-oncogene shape clinical progression of pancreatic ductal adenocarcinoma (PDAC). Importantly, they find that the KRAS^G12R mutation is enriched in early-stage PDAC, and it is characterized by distinctly activated molecular programs.

MeSH terms

Carcinoma, Pancreatic Ductal* / genetics
Carcinoma, Pancreatic Ductal* / pathology
Humans
Mutation*
Pancreatic Neoplasms* / genetics
Pancreatic Neoplasms* / pathology
Proto-Oncogene Mas*
Proto-Oncogene Proteins p21(ras)* / genetics

Substances

Proto-Oncogene Mas
MAS1 protein, human
Proto-Oncogene Proteins p21(ras)
KRAS protein, human