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Colorectal tumor-associated antigens (TAAs) represent a broad class of proteins and glycoproteins that are overexpressed or aberrantly expressed on the surface of colorectal cancer cells compared to normal tissues [3, 4]. Key examples include carcinoembryonic antigen (CEA), epithelial cell adhesion molecule (EpCAM), mucin 1 (MUC1), and guanylyl cyclase C (GUCY2C), which are involved in critical biological processes such as cell-cell adhesion, intracellular signaling, and immune evasion [4, 5, 9]. These antigens serve as the primary targets for various immunotherapeutic strategies, including monoclonal antibodies (e.g., cetuximab targeting EGFR), cancer vaccines, and chimeric antigen receptor (CAR) T-cell therapies [1, 6, 10]. While TAAs provide a valuable handle for precision medicine, their clinical utility is often challenged by 'on-target off-tumor' toxicities due to low-level expression in healthy epithelial cells and the potential for tumors to undergo antigen escape [1, 3, 9]. This entry is classified as 'incorrect' because it refers to a broad category of molecules and cell types rather than a single, specific molecular target.
Therapeutic agents targeting colorectal tumor-associated antigens (TAAs) primarily work by binding to specific surface proteins to inhibit oncogenic signaling pathways, induce antibody-dependent cellular cytotoxicity (ADCC), or facilitate T-cell mediated destruction of tumor cells through vaccines and adoptive cell therapies [1, 3, 6].
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