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Molecular studies and therapeutic targeting of Kaposi's sarcoma herpesvirus (KSHV/HHV-8) oncogenesis

机译:Kaposi的肉瘤疱疹病毒(KSHV / HHV-8)肿瘤发生的分子研究和治疗靶向

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摘要

Kaposi's sarcoma herpesvirus or human herpesvirus-8 (KSHV/HHV-8) is the etiological agent of Kaposi's sarcoma (KS), an AIDS-defining angioproliferative neoplasm that continues to be a major global health problem and, of primary effusion lymphoma (PEL), a rare incurable B-cell lymphoma. This review describes the research from our laboratory and its collaborators to uncover molecular mechanisms of viral oncogenesis in order to develop new patho-genesis-based therapies to the KSHV-induced AIDS malignancies KS and PEL. They include the discovery of the viral angiogenic oncogene G protein-coupled receptor (vGPCR), the development of mouse models of KSHV and oxidative stress-induced KS, the identification of the role of Racl-induced ROS in viral oncogenesis of KS and the development of novel therapeutic approaches able to target both latent and lytic oncogenic KSHV infection.
机译:Kaposi的肉瘤疱疹病毒或人类疱疹病毒-8(KSHV / HHV-8)是Kaposi的肉瘤(KS)的病因,艾滋病定义血管升压肿瘤,该肿瘤持续是主要的全球健康问题,初级活力淋巴瘤(PEL) ,一种罕见的B细胞淋巴瘤。 本综述描述了我们实验室及其合作者的研究,以发现病毒肿瘤发生的分子机制,以便为KSHV诱导的艾滋病恶性肿瘤KS和PEL开发基于疾病的基础疗法。 它们包括发现病毒血管生成的癌基因G蛋白偶联受体(VGPCR),显影的小鼠模型的KSHV和氧化应激诱导的Ks,鉴定RACL诱导的ROS在病毒的致癌中的作用和发展的作用 一种能够瞄准潜在和裂解致癌的KSHV感染的新型治疗方法。

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