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Glioma-associated antigen (GAA) refers to a group of proteins that are overexpressed or specifically mutated in glioma cells, making them suitable targets for immunotherapy [1.3.1, 1.3.4]. This heterogeneous class includes cell surface receptors like interleukin-13 receptor alpha 2 (IL-13Rα2) and ephrin type-A receptor 2 (EphA2), as well as intracellular proteins such as survivin and mutant isocitrate dehydrogenase 1 (IDH1) [1.2.1, 1.4.5]. These antigens are involved in essential oncogenic processes, including cell survival, proliferation, and resistance to apoptosis [1.2.1, 1.5.1]. Therapeutic strategies targeting GAAs include peptide vaccines like ICT-107 and SurVaxM, dendritic cell vaccines such as DCVax-L, and chimeric antigen receptor (CAR) T-cell therapies [1.3.1, 1.4.2, 1.4.4]. A significant challenge in the clinical application of GAA-targeted therapies is the high level of intratumoral heterogeneity and the risk of antigen escape, where tumor cells lose the target antigen under selective pressure [1.3.1, 1.4.2]. To address this, many current clinical trials utilize multi-antigen vaccines or combinatorial approaches to improve the efficacy and durability of the immune response [1.2.1, 1.3.4]. Monitoring these antigens through immunohistochemistry and molecular profiling is essential for patient selection and evaluating treatment efficacy [1.5.1, 1.5.4].
Induction of antigen-specific T-cell responses; direct cytotoxic T-cell mediated killing; inhibition of oncogenic signaling.
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