Karolina A. Kilowski, Martin F. Dietrich, Joanne Xiu, Nathaniel Jones, Matthew Powell, V. Galvan Turner, Britt Erickson, David Mutch, Premal Thaker, Adam ElNaggar, Don Dizon, Sarfraz Ahmad, Thomas J. Herzog, W. Michael Korn, Robert W. Holloway
KRAS mutant disease represents a frequent and genetically distinct group of epithelial ovarian cancers with minimal overlap to predictive markers of immunotherapy (MSI-H,TMB-H) and targeted therapy.
KRAS mutations infrequently overlap with other oncogenic drivers.
BRCA 1/2 mutations were mutually exclusive from KRAS mutations suggesting a separate treatment opportunity for recurrent disease or maintenance therapy.
Clinical trials evaluating subtype-specific KRAS inhibitors in ovarian tumors are warranted.