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A T cell receptor recognizing mutant KRAS peptide–MHC complex is a highly specific receptor (TCR) engineered or selected from T cells to bind to a peptide derived from a mutated form of KRAS (a common oncogenic driver), when this peptide is presented on the surface of cancer cells by a Class I MHC molecule such as HLA-A*11:01[2][3][5]. This recognition is the basis for targeted T cell therapies that can discriminate between mutant and wild-type KRAS, reducing off-target effects on healthy tissue. Enhanced-affinity TCRs or bispecific TCR-based molecules are under development to increase efficacy, though careful selection and screening is needed to mitigate cross-reactivity with self-antigens[5][6]. The primary therapeutic context is adoptive T cell therapy and targeted biologic drugs for cancers harboring actionable KRAS mutations where the relevant HLA allele is present.
Specific recognition of mutated KRAS peptide presented by MHC class I molecules (typically HLA-A*11:01)[2][3][5]. Induces cytotoxic T cell activation and killing of KRAS-mutant cancer cells when engaged by the engineered TCR or TCR-mimetic therapy[3][5][6]. May recruit endogenous T cells via bispecific formats (ImmTACs)[6].
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See how Gosset can support your research on T cell receptor recognizing mutant KRAS peptide–MHC complex (TCR recognizing mutant KRAS peptide–MHC complex (Note: There is no widely accepted short abbreviation specific for a mutant KRAS-recognizing TCR; researchers typically specify the particular TCR clone, e.g., "JDIa41b1" or "4TCR2" when relevant[2][3][5].)).