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Transforming growth factor beta 2 (TGF-β2) is a secreted cytokine belonging to the TGF-beta superfamily that plays a pivotal role in regulating cell growth, differentiation, and immune responses [1, 4]. In the context of glioblastoma, TGF-β2 is frequently overexpressed and acts as a potent immunosuppressor, facilitating tumor escape from the immune system and promoting angiogenesis and invasion [2, 3]. The specific cellular phenotype described by high Ki67 and TGF-β2 expression identifies a highly proliferative and aggressive subset of glioblastoma cells that are often resistant to standard therapies [3]. Therapeutic strategies such as trabedersen (AP 12009), an antisense oligonucleotide, are designed to specifically target and downregulate TGF-β2 mRNA, thereby reducing protein levels and potentially restoring the anti-tumor immune response [2]. Clinical trials have utilized TGF-β2 and Ki67 levels as biomarkers to identify patients most likely to benefit from these targeted interventions [3]. Despite its potential, targeting TGF-β2 is complicated by its pleiotropic functions in normal physiology, including wound healing and tissue homeostasis, which necessitates careful monitoring for systemic safety concerns [1].
Antisense oligonucleotide-mediated inhibition of TGF-β2 mRNA translation and protein synthesis; Monoclonal antibody-mediated neutralization of the secreted protein
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