Abstract
Classic Kaposi’s sarcoma (CKS) is a cutaneous neoplasm of endothelial origin, caused by chronic human herpes virus-8 (HHV-8) infection combined with an impaired immune function status. Systemic treatment of CKS is based on chemotherapy (CT), resulting in 30%–50% of transient responses. There is a strong clinical need to assess the efficacy of new drugs for treatment of CKS. Pilot studies of anti-programmed cell death protein 1 (PD1) antibodies in CKS have shown promising results. Beside immunodeficiency status, HHV8 viral genes contribute to tumorigenesis through the VEGF signaling pathways.
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