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CD30, also known as Tumor necrosis factor receptor superfamily member 8 (TNFRSF8), is a 120-kDa transmembrane glycoprotein that belongs to the tumor necrosis factor receptor (TNFR) superfamily [8, 10]. It was originally identified as the Ki-1 antigen on Reed-Sternberg cells of Hodgkin lymphoma [8, 16]. CD30 is highly expressed on the surface of malignant cells in classical Hodgkin lymphoma (cHL) and anaplastic large cell lymphoma (ALCL), while its expression in healthy tissues is restricted to a small subset of activated T and B lymphocytes [2, 10, 16]. This differential expression makes CD30 an ideal therapeutic target for antibody-based therapies, particularly antibody-drug conjugates (ADCs) like brentuximab vedotin [2, 3, 15]. Upon binding to CD30, these agents are internalized via receptor-mediated endocytosis, leading to the intracellular release of cytotoxic payloads that induce cell cycle arrest and apoptosis [1, 2, 4]. Beyond its role as a drug target, CD30 signaling activates the NF-kappa B pathway, influencing cell survival, proliferation, and the immune response [10, 14, 16]. Therapeutic strategies targeting CD30 also include chimeric antigen receptor (CAR) T-cell therapies and bispecific antibodies, which leverage the immune system to eliminate CD30-positive tumor cells [6, 9, 15].
Antibody-drug conjugate delivery, Antibody-dependent cellular cytotoxicity (ADCC), Receptor-mediated endocytosis, NF-kappa B signaling inhibition
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