Abstract
RAS mutations are the most common oncogenic drivers in adenocarcinoma. KRAS is mutated in ∼30% of non-small cell lung cancer (NSCLC), majority of pancreatic adenocarcinomas and ∼40% of colorectal cancers (CRC). NF1 encodes the RAS GAP neurofibromin, functioning as an inhibitor of the MAPK pathway by facilitating the hydrolysis of RAS to its GDP-bound state. KRAS G13D is a recognised cycling mutant with NF1 GAP sensitivity, thus upstream co-mutation with NF1 is of importance to evaluate.
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have