KRASstatus

KRASstatus refers to the mutational status of the KRAS gene in a tumor. KRAS encodes a small GTPase that transduces signals from growth factor receptors to cell proliferation pathways. Activating KRAS mutations lead to continuous signaling, promoting oncogenesis and potentially affecting treatment responses. In clinical practice, KRAS status is treated as a biomarker that can be predictive of therapy response and, in some contexts, provides prognostic information. Testing can be performed on tumor tissue or circulating tumor DNA from blood samples. Common testing methods include next-generation sequencing panels, PCR-based assays, and targeted sequencing designed to detect mutations in codons 12, 13, and 61, with G12C, G12D, and G12V among the most frequent variants.

In colorectal cancer, KRAS status is crucial for guiding therapy with anti-EGFR monoclonal antibodies. Tumors with wild-type KRAS are more likely to respond to cetuximab or panitumumab, whereas activating KRAS mutations predict resistance, guiding treatment choices. In non-small cell lung cancer, KRAS mutations are among the most common alterations; historically linked to poorer outcomes, but recent approvals of KRAS G12C inhibitors have begun to change the treatment landscape for patients with this specific mutation. In pancreatic cancer, KRAS mutations are highly prevalent, and while there are limited approved targeted therapies, KRAS status remains important for prognosis and for eligibility in clinical trials.

Limitations include intratumoral heterogeneity and the varying predictive value of different KRAS mutations across cancer types. Ongoing research aims to expand targeted options and refine how KRAS status informs personalized treatment strategies.