Background
• Alterations in the RAS pathway have been linked to tumorigenesis, cellular apoptosis, metabolism and angiogenesis. Mutations of KRAS in non-small cell lung cancer (NSCLC) are more frequent and well studied.
• Other family members such as HRAS remain under investigated, and RAS remains a challenging therapeutic target.
• HRAS has been indirectly targeted with tipifarnib, a farnesyltransferase inhibitor, rendering HRAS inactive in head and neck tumors.
• Here, we characterize the incidence, genomic landscape, and clinical context of HRAS alterations in NSCLC.