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mRNA-5671 also known as V941 is a cancer vaccine candidate developed by Moderna. [1] 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 ...
Patients who harbor an EGFR mutation have a 60% response rate to erlotinib. However, the mutation of KRAS and EGFR are generally mutually exclusive. [29] [30] [31] Lung cancer patients who are positive for KRAS mutation (and the EGFR status would be wild type) have a low response rate to erlotinib or gefitinib estimated at 5% or less. [29]
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. [7] [8] Sotorasib is an inhibitor of the RAS GTPase family. [4]
In recent years, significant research efforts have focused on finding effective inhibitors for the Kras-G12C mutation. For instance, sotorasib (Lumakras) became the first FDA-approved targeted therapy for the treatment of patients with NSCLC harboring the Kras-G12C mutation in 2021. [ 3 ]
There are typically three objectives applied to the treatment of lung cancer and can vary by patient or individual diagnosis: (1) curing lung cancer, (2) controlling lung cancer, and (3) being comfortable. [10]
About 2% of all lung cancers are non-carcinoma (mainly sarcoma, tumors of hematopoietic origin, or germ cell tumors. [5] These forms of lung cancer are usually treated differently from carcinomas. Because of the ubiquity of lung carcinomas, however, the term "lung cancer" generally refers to carcinomas in everyday clinical practice. [citation ...
Lewis lung carcinoma is a hypermutated Kras/Nras–mutant cancer with extensive regional mutation clusters in its genome. A tumor that spontaneously developed as an epidermoid carcinoma in the lung of a C57BL mouse. It was discovered in 1951 by Dr. Margaret Lewis of the Wistar Institute and became one of the first transplantable tumors. [1]
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 ...