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Tumor-associated antigens (TAAs) and neoantigens derived from stressed colorectal cancer (CRC) cell lines represent a broad class of molecular targets used in cancer immunotherapy. TAAs are self-antigens that are abnormally expressed in malignant cells, such as Carcinoembryonic Antigen (CEA) or MUC1, while neoantigens are novel peptides arising from somatic mutations unique to the tumor genome (Nature Reviews Cancer, 2017). Cellular stress—induced by hypoxia, nutrient deprivation, or cytotoxic therapies—can significantly alter the repertoire of these antigens by modifying protein folding, degradation, and MHC class I presentation (Journal of Biological Chemistry, 2020). In CRC, the high mutational load associated with microsatellite instability (MSI) often leads to a rich landscape of neoantigens, which are highly immunogenic because they bypass central thymic tolerance (NEJM, 2015). These antigens serve as the foundation for developing personalized vaccines, adoptive T-cell therapies, and bispecific antibodies aimed at directing the immune system to selectively eliminate colorectal cancer cells. However, the therapeutic challenge remains the high degree of intratumoral heterogeneity and the potential for the tumor to downregulate antigen presentation machinery under selective pressure (PubMed, PMID: 31534203).
Induction or enhancement of cytotoxic T-lymphocyte (CTL) mediated lysis of tumor cells via recognition of MHC-bound peptide complexes.
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