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[人乳头瘤病毒诱导肿瘤发生机制研究的当前进展]

[Current advances in the mechanic studies of human papillomavirus-induced oncogenesis].

作者信息

Zhou Xiao-bo, Xu Ning-zhi

机构信息

Department of Cellular and Molecular Biology, Cancer Institute, CAMS and PUMC, Beijing 100021, China.

出版信息

Zhongguo Yi Xue Ke Xue Yuan Xue Bao. 2007 Oct;29(5):673-7.

Abstract

Human papillomavirus (HPV) is a common small DNA tumor virus that specifically infects squamous epithelial cells and causes benign or malignant epithelial lesions such as genital warts and cervical cancer. High-risk HPV is detected in specimens of more than 90% of cervical cancer. In the 7. 9 kb genome of HPV, E6 and E7 are the crucial viral oncoproteins that consistently maintained after viral integration into host cell genome. These two proteins interfere with cell proliferation and differentiation through interacting with important tumor suppressors including p53 and pRb. High-risk HPV E6/E7 also induces genomic instability, facilitating cell transformation.

摘要

人乳头瘤病毒(HPV)是一种常见的小型DNA肿瘤病毒,它特异性感染鳞状上皮细胞,并引起良性或恶性上皮病变,如尖锐湿疣和宫颈癌。超过90%的宫颈癌标本中可检测到高危型HPV。在HPV 7.9 kb的基因组中,E6和E7是关键的病毒癌蛋白,在病毒整合到宿主细胞基因组后持续存在。这两种蛋白通过与包括p53和pRb在内的重要肿瘤抑制因子相互作用,干扰细胞增殖和分化。高危型HPV E6/E7还会诱导基因组不稳定,促进细胞转化。

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