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Applications of cell therapy in the treatment of virus-associated cancers
Nature Reviews Clinical Oncology ( IF 81.1 ) Pub Date : 2024-08-19 , DOI: 10.1038/s41571-024-00930-x
Keri Toner 1, 2 , Chase D McCann 1, 2 , Catherine M Bollard 1, 2
Affiliation  

A diverse range of viruses have well-established roles as the primary driver of oncogenesis in various haematological malignancies and solid tumours. Indeed, estimates suggest that approximately 1.5 million patients annually are diagnosed with virus-related cancers. The predominant human oncoviruses include Epstein–Barr virus (EBV), Kaposi sarcoma-associated herpesvirus (KSHV), hepatitis B and C viruses (HBV and HCV), human papillomavirus (HPV), human T-lymphotropic virus type 1 (HTLV1), and Merkel cell polyomavirus (MCPyV). In addition, although not inherently oncogenic, human immunodeficiency virus (HIV) is associated with immunosuppression that contributes to the development of AIDS-defining cancers (specifically, Kaposi sarcoma, aggressive B cell non-Hodgkin lymphoma and cervical cancer). Given that an adaptive T cell-mediated immune response is crucial for the control of viral infections, increasing research is being focused on evaluating virus-specific T cell therapies for the treatment of virus-associated cancers. In this Review, we briefly outline the roles of viruses in the pathogenesis of these malignancies before describing progress to date in the field of virus-specific T cell therapy and evaluating the potential utility of these therapies to treat or possibly even prevent virus-related malignancies.



中文翻译:


细胞疗法在治疗病毒相关癌症中的应用



多种病毒在各种血液恶性肿瘤和实体瘤中作为肿瘤发生的主要驱动因素具有明确的作用。事实上,据估计每年约有 150 万名患者被诊断患有与病毒相关的癌症。主要的人类肿瘤病毒包括EB病毒(EBV)、卡波西肉瘤相关疱疹病毒(KSHV)、乙型和丙型肝炎病毒(HBV和HCV)、人乳头瘤病毒(HPV)、人T淋巴细胞病毒1型(HTLV1)、和默克尔细胞多瘤病毒(MCPyV)。此外,虽然人类免疫缺陷病毒 (HIV) 本身不具有致癌性,但它与免疫抑制有关,从而导致艾滋病相关癌症(特别是卡波西肉瘤、侵袭性 B 细胞非霍奇金淋巴瘤和宫颈癌)的发生。鉴于适应性 T 细胞介导的免疫反应对于控制病毒感染至关重要,越来越多的研究集中在评估病毒特异性 T 细胞疗法用于治疗病毒相关癌症的情况。在这篇综述中,我们简要概述了病毒在这些恶性肿瘤发病机制中的作用,然后描述了病毒特异性 T 细胞治疗领域迄今为止的进展,并评估了这些疗法治疗甚至可能预防病毒相关恶性肿瘤的潜在效用。 。

更新日期:2024-08-19
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