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The Follicle-stimulating hormone receptor (FSHR) is a G protein-coupled receptor traditionally associated with reproductive functions in the ovaries and testes (UniProt P23945). Recent clinical research has revealed that FSHR is also expressed on the luminal surface of endothelial cells in the neo-vasculature of many solid tumors, while remaining absent from healthy tissues and normal blood vessels (Ghinea et al., NEJM, 2010). This unique expression pattern makes FSHR a highly specific target for anti-angiogenic therapies and targeted drug delivery across a broad spectrum of cancers, including prostate, breast, and lung malignancies (Siraj et al., Journal of Pathology, 2013). Therapeutic approaches currently under investigation include monoclonal antibodies, antibody-drug conjugates, and CAR-T cell therapies designed to disrupt tumor blood supply or eliminate FSHR-positive cells (Perales-Puchalt et al., Clinical Cancer Research, 2017). By targeting the tumor microenvironment specifically, these strategies aim to provide potent anti-tumor activity with reduced systemic side effects compared to traditional chemotherapy.
Targeted cell lysis via CAR-T cells, inhibition of angiogenesis, or delivery of cytotoxic payloads via antibody-drug conjugates (Ghinea et al., 2010; Perales-Puchalt et al., 2017).
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