Conclusions:
- 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.