Oct 30, 2019 · The two other KRAS contenders, Amgen’s AMG 510 and Mirati’s MRTX849, have produced some promising early clinical results in non-small cell lung cancer (NSCLC). Jul 16, 2015 · Therefore, we characterized glutamine metabolism genes in mutant vs wild-type KRAS NSCLC both in vitro and in vivo, demonstrated the necessity of ME1 in mutant, but not wild-type, KRAS cell lines, and demonstrated that ME1 gene expression is a predictive marker in the treatment response to radiation therapy in a cohort NSCLC patients. Crucially, KRASG12C is a mutant form of the guanosine triphosphatase (GTPase) KRAS. Collectively, inhibitors targeting KRASG12C are a promising new class of oncogene-specific therapeutics for the treatment of tumors driven by the mutant protein. Besides, these KRASG12C inhibitors react with the mutant cysteine residue. This invention relates to methods comprising administering a FAK inhibitor and an immunotherapeutic agent such as anti-PD-1 or anti-PD-L1; that are useful in the treatment of abnormal cell growth, such as cancer, in mammals, especially humans. Although both antibody and small molecule inhibitors of EGFR and PI3K show clinical benefit in subsets of lung cancer patients, tumors that harbor KRAS mutations have proven refractory to treatment, and no small molecule inhibitors of KRAS yet exist. Mar 14, 2019 · Working in cell lines and mouse models of lung cancer, a team led by Don Gibbons, M.D., Ph.D., associate professor of Thoracic/Head & Neck Medical Oncology, demonstrated how the KRAS-driven lung cancer cells defeat treatment by switching from stable, stationary cells into a type of mobile, resistant cell associated with embryonic development.