KRAS Gene, in Visit Clinic

KRAS encodes a small GTPase that acts as a molecular switch in cell signalling, controlling cell growth, division, differentiation and survival through pathways such as MAPK and PI3K. When mutated, KRAS can become permanently active, driving uncontrolled cell proliferation and contributing to cancers (especially pancreatic, colorectal and lung). KRAS status guides diagnosis, prognosis and targeted treatment decisions.

KRAS stands for Kirsten rat sarcoma viral oncogene homolog. It encodes a small GTPase of the RAS family involved in cell signaling pathways that regulate proliferation, differentiation, and survival. Mutations in KRAS are common oncogenic drivers in cancers such as colorectal, lung, and pancreatic cancer, where constitutive activation promotes uncontrolled growth and affects therapy response and prognosis.

KRAS is an oncogene whose activating mutations are commonly linked to several cancers, most notably pancreatic ductal adenocarcinoma (seen in about 90% of cases), colorectal cancer (around 30–50%), and non‑small cell lung adenocarcinoma (about 20–30%). KRAS mutations also occur in biliary, endometrial and ovarian cancers and influence prognosis and treatment choices.

KRAS itself isn’t simply good or bad: the normal KRAS protein is essential for cell growth and signaling. However, when KRAS acquires certain mutations it becomes oncogenic, driving uncontrolled cell proliferation and contributing to cancers (particularly pancreatic, colorectal, and lung). Mutant KRAS can worsen prognosis and complicate therapy, so its clinical impact depends on whether it’s normal or mutated.

A KRAS mutation itself cannot be "cured" as a genetic alteration, but cancers driven by certain KRAS variants can sometimes be controlled. Targeted drugs (for specific KRAS types), chemotherapy, surgery, and immunotherapy may shrink tumors or prolong survival. Outcomes depend on KRAS subtype, cancer type, stage and resistance; research continues on newer targeted therapies and combinations.

Most KRAS mutations are acquired (somatic) during a person’s life and are not present at birth; they commonly occur in cancers such as lung, colorectal, and pancreatic tumors. Rarely, people can be born with a germline KRAS mutation—these inherited variants are uncommon and cause developmental syndromes (RASopathies). Genetic testing and family history can clarify inheritance.