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Glioblastoma-associated antigens encompass a broad spectrum of molecular targets expressed on the surface of glioblastoma multiforme (GBM) cells, categorized into tumor-specific antigens (TSAs) and tumor-associated antigens (TAAs). TSAs, such as the Epidermal Growth Factor Receptor variant III (EGFRvIII), result from specific genetic mutations and are absent in normal tissues, while TAAs like IL-13Rα2, HER2, and EphA2 are overexpressed in tumors but may have low-level expression in healthy cells (Weller et al., 2017, Nature Reviews Clinical Oncology). These antigens play pivotal roles in driving tumor cell proliferation, survival, and invasion into the surrounding brain parenchyma, often acting as receptors for growth factors or signaling molecules (Ahmed et al., 2017, Journal of Clinical Oncology). They are the focus of various therapeutic strategies, most notably CAR-T cell therapies and therapeutic vaccines, which aim to harness the immune system to selectively destroy malignant cells (Brown et al., 2016, New England Journal of Medicine). Despite their potential, the clinical utility of targeting these antigens is often limited by the extreme intratumoral heterogeneity of GBM, leading to "antigen escape" where the tumor recurs from cells lacking the targeted molecule (O'Rourke et al., 2017, Science Translational Medicine).
Immunotherapeutic targeting of surface-expressed or mutated proteins to induce immune-mediated lysis of tumor cells via T-cell activation or antibody-dependent cellular cytotoxicity.
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