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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 ...
In July 2009, the FDA updated the labels of two anti-EGFR monoclonal antibody drugs (panitumumab and cetuximab) indicated for the treatment of metastatic colorectal cancer to include information about KRAS mutations. [14] This was the result of a study, which demonstrated lack of benefit with Panitumumab in patients who carried NRAS mutations. [6]
Because the G12C KRAS mutation is relatively common in some cancer types, 14% of non-small-cell lung cancer adenocarcinoma patients and 5% of colorectal cancer patients, [15] and sotorasib is the first drug candidate to target this mutation, there have been high expectations for the drug.
Accordingly, genetic testing to confirm the absence of KRAS mutations (and so the presence of the KRAS wild-type gene), is now clinically routine before the start of treatment with EGFR inhibitors. mCRC patients with wild-type KRAS tumors have been shown to benefit from a response rate of over 60% and a decreased risk for progression of over 40 ...
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]
Colon cancer is the second-leading cause of cancer deaths in the United States and is expected to kill more than 53,000 people in the nation in 2024, according to the American Cancer Society.
Colorectal PDX models are relatively easy to establish and the models maintain genetic similarity of primary patient tumor for about 14 generations. [21] In 2012, a study established 27 colorectal PDX models that did not diverge from their respective human tumors in histology, gene expression, or KRAS/BRAF mutation status. [22]
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. [3]
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