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人乳头瘤病毒致癌过程中的环境辅助因素。

Environmental co-factors in HPV carcinogenesis.

作者信息

Castellsagué Xavier, Bosch F Xavier, Muñoz Nubia

机构信息

Servei d'Epidemiologia I Registre del Càncer, Institut Català d'Oncologia, Gran Vias/n km 2,7 08907 L'Hospitalet de Llobregat, Barcelona, Spain.

出版信息

Virus Res. 2002 Nov;89(2):191-9. doi: 10.1016/s0168-1702(02)00188-0.

DOI:10.1016/s0168-1702(02)00188-0
PMID:12445659
Abstract

Epidemiological studies have shown that only a small fraction of women infected with oncogenic HPV types will eventually progress to high-grade intraepithelial lesions (HSIL) and cervical cancer (CC). Because infection by oncogenic HPVs is a necessary but not a sufficient cause of CC, it has been assumed that other factors, acting in conjunction with HPV, influence the risk of transition from cervical HPV infection to cervical malignancy. This paper reviews the epidemiological evidence for the role of environmental co-factors in HPV carcinogenesis as assessed from selected studies that report associations within a well-defined HPV-DNA positive group. Co-factors assessed include parity, use of oral contraceptives, tobacco smoking, infection with other sexually transmitted diseases, and dietary and nutritional factors. Based on the evidence provided by the largest epidemiological studies that using sensitive detection methods allowed for the effects of HPV, it can be concluded that, among HPV positive women, high parity, long-term OC use, smoking, and co-infection with other sexually transmitted agents are the most consistently identified environmental co-factors likely to influence the risk of progression from cervical HPV infection to HSIL and invasive CC. There is limited evidence for a role of dietary factors in HPV carcinogenesis. On-going epidemiological studies will shed more light into the role of these and other co-factors, but if confirmed, these conclusions may imply that multiparous women, women who are smokers, and women on long-term OC use, might need a closer cytological and HPV surveillance than women in the general population.

摘要

流行病学研究表明,只有一小部分感染致癌性人乳头瘤病毒(HPV)的女性最终会发展为高级别上皮内病变(HSIL)和宫颈癌(CC)。由于致癌性HPV感染是宫颈癌发生的必要但非充分条件,因此人们认为,与HPV共同作用的其他因素会影响从宫颈HPV感染转变为宫颈恶性肿瘤的风险。本文回顾了从选定研究中评估的环境协同因素在HPV致癌作用中所起作用的流行病学证据,这些研究报告了在明确界定的HPV-DNA阳性组内的关联。评估的协同因素包括产次、口服避孕药的使用、吸烟、其他性传播疾病的感染以及饮食和营养因素。基于最大规模流行病学研究提供的证据,这些研究使用敏感检测方法来考量HPV的影响,可以得出结论,在HPV阳性女性中,高生育次数、长期使用口服避孕药、吸烟以及与其他性传播病原体的合并感染是最一致确定的可能影响从宫颈HPV感染进展为HSIL和浸润性CC风险的环境协同因素。饮食因素在HPV致癌作用中的作用证据有限。正在进行的流行病学研究将进一步阐明这些及其他协同因素的作用,但如果得到证实,这些结论可能意味着多产妇女、吸烟女性以及长期使用口服避孕药的女性可能需要比普通人群中的女性更密切的细胞学和HPV监测。

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