Nunobiki Osamu, Ueda Masatsugu, Toji Eisaku, Yamamoto Michiko, Akashi Kyoko, Sato Naomi, Izuma Shinji, Torii Kiyo, Tanaka Ichiro, Okamoto Yoshiaki, Noda Sadamu
Department of Medical Technology, Kobe Tokiwa University, 6-2 2 chome, Ohtanicho, Nagataku, Hyogo, Kobe 653-0838, Japan.
Patholog Res Int. 2011;2011:364069. doi: 10.4061/2011/364069. Epub 2011 May 31.
It is widely accepted that specific human papillomavirus (HPV) types are the central etiologic agent of cervical carcinogenesis. However, a number of infected women do not develop invasive lesions, suggesting that other environmental and host factors may play decisive roles in the persistence of HPV infection and further malignant conversion of cervical epithelium. Although many previous reports have focused on HPV and environmental factors, the role of host susceptibility to cervical carcinogenesis is largely unknown. Here, we review the findings of genetic association studies in cervical carcinogenesis with special reference to polymorphisms of glutathione-S-transferase (GST) isoforms, p53 codon 72, murine double-minute 2 homolog (MDM2) gene promoter 309, and FAS gene promoter -670 together with HPV types including our recent research results.
特定的人乳头瘤病毒（HPV）类型是子宫颈癌发生的主要病因，这一点已被广泛接受。然而，许多感染HPV的女性并未发生浸润性病变，这表明其他环境和宿主因素可能在HPV感染的持续存在以及子宫颈上皮的进一步恶性转化中起决定性作用。尽管先前许多报告都聚焦于HPV和环境因素，但宿主易感性在子宫颈癌发生中的作用在很大程度上仍不清楚。在此，我们回顾子宫颈癌发生中基因关联研究的结果，特别提及谷胱甘肽-S-转移酶（GST）同工型、p53密码子72、鼠双微体2同源物（MDM2）基因启动子309和FAS基因启动子-670的多态性，以及HPV类型，包括我们最近的研究结果。
