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The impact of KRAS mutations is heavily dependent on the order of mutations. Primary KRAS mutations generally lead to a self-limiting hyperplastic or borderline lesion, but if they occur after a previous APC mutation it often progresses to cancer. [18] KRAS mutations are more commonly observed in cecal cancers than colorectal cancers located in ...
K-Ras(G12C) inhibitor 6 is an irreversible inhibitor of oncogenic K-Ras(G12C), subverting the native nucleotide preference to favour GDP over GTP.Its family of inhibitors allosterically control GTP affinity and effector interactions by fitting inside a "pocket", or binding site, of mutant K-Ras.
Sotorasib, sold under the brand names Lumakras and Lumykras, is an anti-cancer medication used to treat non-small-cell lung cancer. [4] [5] It targets a specific mutation, G12C, in the protein K-Ras encoded by gene KRAS which is responsible for various forms of cancer.
It is a tetravalent vaccine that targets G12D, G12V, G13D or G12C driver mutations in the KRAS gene. [2] It is currently being evaluated for the treatment of either non-small cell lung cancer , colorectal cancers with microsatellite instability , or pancreatic adenocarcinoma , all with confirmed KRAS driver mutations.
The most common mutations are found at residue G12 in the P-loop and the catalytic residue Q61. The glycine to valine mutation at residue 12 renders the GTPase domain of Ras insensitive to inactivation by GAP and thus stuck in the "on state". Ras requires a GAP for inactivation as it is a relatively poor catalyst on its own, as opposed to other ...
BI 1701963 is an investigational drug that blocks KRAS activation by binding to SOS1 proteins. The drug is thought to be effective in cancers with a KRAS mutation. It has been tested in clinical trials alone and in combination with adagrasib. [1] [2] [3]
HCT116 cells have a mutation in codon 13 of the KRAS proto-oncogene, and are suitable transfection targets for gene therapy research. [2] The cells have an epithelial morphology and can metastasize in xenograft models. [1] When transducted with viral vectors carrying the p53 gene, HCT116 cells remain arrested in the G1 phase. [3]
If, through mutation, normal genes promoting cellular growth are up-regulated (gain-of-function mutation), they predispose the cell to cancer and are termed oncogenes. Usually, multiple oncogenes, along with mutated apoptotic or tumor suppressor genes , act in concert to cause cancer.