Hildesheim Allan, Wang Sophia S
Division of Cancer Epidemiology and Genetics, National Cancer Institute, 6120 Executive Blvd, Room 7062, EPS/MSC# 7234, Rockville, MD 20852, USA.
Virus Res. 2002 Nov;89(2):229-40. doi: 10.1016/s0168-1702(02)00191-0.
Infection with human papillomaviruses (HPV) is known to play a central role in the development of cervical cancer. Both host and viral genetic factors have been postulated to be important determinants of risk of HPV progression to neoplasia among infected individuals. In this report, we review epidemiological studies that have evaluated the role in cervical cancer pathogenesis of genetic variation in human leukocyte antigen (HLA) genes and in the HPV genome itself. A protective effect of HLA Class II DRB113/DBQ10603 alleles is the most consistent HLA finding in the published literature. A consistent association between HPV16 non-European variants and risk of disease is also evident from published work. These findings are discussed. Gaps in our understanding and future research needs are also discussed.
已知人乳头瘤病毒(HPV)感染在宫颈癌的发生发展中起着核心作用。宿主和病毒遗传因素均被认为是感染个体中HPV发展为肿瘤风险的重要决定因素。在本报告中,我们回顾了一些流行病学研究,这些研究评估了人类白细胞抗原(HLA)基因的遗传变异以及HPV基因组本身在宫颈癌发病机制中的作用。HLA II类DRB113/DBQ10603等位基因的保护作用是已发表文献中关于HLA最一致的发现。已发表的研究成果也明确显示,HPV16非欧洲变体与疾病风险之间存在稳定的关联。我们将对这些发现进行讨论。同时,也会讨论我们在认知上的差距以及未来的研究需求。