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B7 homolog 3 receptor (B7-H3, CD276) is a type I transmembrane glycoprotein in the B7 family of immune modulators, encoded by the CD276 gene. It is primarily expressed at low levels in normal tissues (due to post-transcriptional silencing) but highly upregulated on many solid tumors, making it a prominent immune checkpoint and target in cancer immunotherapy[1][2][3]. B7-H3 suppresses T cell–mediated immune responses, facilitating tumor immune evasion, and also promotes tumorigenic processes such as migration, invasion, angiogenesis, and metabolic adaptation. Several antibody-based and cell therapy approaches are in clinical trials or development targeting B7-H3 for solid malignancies, with enoblituzumab and B7-H3–directed CAR T cells among the most advanced agents[1][3]. Biomarker studies support B7-H3 protein as a prognostic and predictive marker in cancer and a potential candidate for patient selection[2]. While B7-H3–targeted therapies hold promise for precision oncology, key safety considerations include the risk of off-tumor toxicity and immune-related complications[1][3].
Immune checkpoint blockade (antibody-based therapies block B7-H3 to enhance anti-tumor immune response); Antibody-directed cell cytotoxicity; CAR T cell–mediated lysis of B7-H3–expressing tumor cells; Targeted delivery of cytotoxins or radioisotopes
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