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EB 病毒诱导 B 细胞肿瘤发生的机制。

Mechanisms of B-Cell Oncogenesis Induced by Epstein-Barr Virus.

机构信息

Department of Life Sciences, Presidency University, Kolkata, West Bengal, India

Department of Otorhinolaryngology-Head and Neck Surgery, and the Tumor Virology Program, Abramson Comprehensive Cancer Center, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, Pennsylvania, USA

出版信息

J Virol. 2019 Jun 14;93(13). doi: 10.1128/JVI.00238-19. Print 2019 Jul 1.

DOI:10.1128/JVI.00238-19
PMID:30971472
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6580952/
Abstract

Epstein-Barr virus (EBV) is a ubiquitous gammaherpesvirus which asymptomatically infects the majority of the world population. Under immunocompromised conditions, EBV can trigger human cancers of epithelial and lymphoid origin. The oncogenic potential of EBV is demonstrated by infection and transformation of quiescent B cells into lymphoblastoid cell lines (LCLs). These cell lines, along with primary infection using genetically engineered viral particles coupled with recent technological advancements, have elucidated the underlying mechanisms of EBV-induced B-cell lymphomagenesis.

摘要

爱泼斯坦-巴尔病毒(EBV)是一种广泛存在的γ疱疹病毒,无症状感染世界上大多数人口。在免疫功能低下的情况下,EBV 可引发上皮和淋巴来源的人类癌症。EBV 的致癌潜能通过感染和将静止的 B 细胞转化为淋巴母细胞系(LCL)来证明。这些细胞系,以及使用遗传工程病毒颗粒进行原发性感染,并结合最近的技术进步,阐明了 EBV 诱导的 B 细胞淋巴瘤发生的潜在机制。

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本文引用的文献

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Cell Death Dis. 2018 May 22;9(6):605. doi: 10.1038/s41419-018-0668-9.
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PI3Kδ activates E2F1 synthesis in response to mRNA translation stress.PI3Kδ 通过响应 mRNA 翻译应激激活 E2F1 的合成。
Nat Commun. 2017 Dec 13;8(1):2103. doi: 10.1038/s41467-017-02282-w.
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Tetraspanin CD63 Bridges Autophagic and Endosomal Processes To Regulate Exosomal Secretion and Intracellular Signaling of Epstein-Barr Virus LMP1.
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