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The KRAS G12V neoantigen presented by HLA-A*11:01 is a mutant peptide derived from the KRAS oncogene, containing a glycine-to-valine substitution at codon 12 (G12V).[1][2][5] This mutation is a common driver in cancers such as pancreatic ductal adenocarcinoma, colorectal cancer, and lung cancer. When processed and presented by the MHC class I molecule HLA-A*11:01 on the tumor cell surface, the KRAS G12V peptide (notably the 9-mer sequence VVGAVGVGK) forms a neoantigen that can be specifically recognized by cytotoxic T lymphocytes (CTLs) via tumor-specific T cell receptors (TCRs).[1][2][5][6][8] This specificity enables the rational design of TCR-engineered cell therapies directed at mutant KRAS-expressing tumors in patients who carry the HLA-A*11:01 allele. Clinical studies highlight both strong immunogenicity and the need to avoid autoimmunity through cross-reactivity with similar self-peptides such as RAB7B.[4][7] The prevalence of KRAS G12V in certain cancers makes this peptide-HLA complex a compelling target for precision immunotherapy.[1][4][5]
Immune-mediated cytotoxicity: Engineered T cells expressing TCRs specific for KRAS G12V/HLA-A*11:01 recognize and kill tumor cells presenting this neoantigen. Cancer immunotherapy: Targeting of tumor cells by enhancing or redirecting T cell responses against the mutant peptide/MHC complex.
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