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Epidermal growth factor receptor (EGFR) mutation-derived tumor-associated antigens are specific protein variants resulting from somatic mutations in the EGFR gene that are uniquely or preferentially expressed by cancer cells. The most prominent example is EGFRvIII, a tumor-specific deletion mutant common in glioblastoma that creates a novel immunogenic junctional epitope not found in healthy tissues (Source: NIH, PubMed). Other neoantigens arise from point mutations like L858R or T790M in non-small cell lung cancer, which can be processed and presented by HLA molecules to trigger T-cell responses (Source: Nature Communications). These antigens serve as highly specific targets for immunotherapy, including therapeutic vaccines, CAR-T cells, and TCR-engineered T-cells, aiming to eliminate malignant cells while sparing normal cells expressing wild-type EGFR. In addition to their role as immunological targets, these mutated proteins often drive constitutive, ligand-independent signaling that promotes tumor growth and survival, making them dual targets for both immunotherapy and small-molecule kinase inhibitors (Source: Journal of Hematology & Oncology).
Induction of tumor-specific immune response, T-cell mediated cytotoxicity, Inhibition of oncogenic tyrosine kinase signaling, Antibody-dependent cellular cytotoxicity (ADCC)
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