zur Hausen H
Deutsches Krebsforschungszentrum, Heidelberg, Federal Republic of Germany.
Cancer Res. 1989 Sep 1;49(17):4677-81.
Infections with specific types of human papillomaviruses (HPV) have emerged as necessary but not sufficient factors for the development, at least, of the majority of cervical, vulvar, penile, and perianal cancers. Evidence has accumulated for their causal role in the induction of anogenital premalignant lesions. Genetic events underlying the mechanism of anogenital carcinogenesis have become increasingly understood. A host cell-mediated intracellular control down-regulating specific HPV genes (E6, E7) in replicating normal cells appears to be interrupted in cancer cells, probably due to structural modifications of the respective host cell genes acquired in the course of HPV DNA persistence. Since genital HPV infections are ubiquitous, cofactors which modify controlling host cell genes are likely to determine the different geographic rates of cervical cancer incidence.
特定类型的人乳头瘤病毒(HPV)感染已成为至少大多数宫颈癌、外阴癌、阴茎癌和肛周癌发生的必要但非充分因素。已有证据表明它们在诱导肛门生殖器癌前病变中具有因果作用。肛门生殖器癌变机制背后的遗传事件已越来越为人所知。在复制的正常细胞中,宿主细胞介导的下调特定HPV基因(E6、E7)的细胞内控制似乎在癌细胞中被中断,这可能是由于在HPV DNA持续存在过程中获得的各自宿主细胞基因的结构修饰。由于生殖器HPV感染普遍存在,修饰宿主细胞控制基因的辅助因子可能决定宫颈癌发病率的不同地理差异。