Molecular characteristics of HRAS mutated non-small cell lung cancer


Asaad Trabolsi, MD1; Estelamari Rodriguez, MD, MPH1 Samuel A. Kareff, MD, MPH1; Michael Korn, MD2; Joanne Xiu, PhD2; Stephen Liu, MD3; Philip Walker, PhD2; Patrick C. Ma, MD4; Hirva Mamdani, MD5; Jorge Nieva, MD6; Hossein Borghaei, DO, MS7; Chadi Nabhan, MD MBA FACP2; Misako Nagasaka, MD8; Sonam Puri, MD9; Gilberto Lopes, MD


• 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.

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