[Oncogene of human papillomavirus].
Although certain types of human papillomavirus (HPV) have been supposed to be associated with carcinogenesis of cervix, a definitive conclusion has not yet been reported. To show that HPV is a causative agent of cervical cancer, we performed several lines of experiments and obtained the results described below. 1) In attempting to identify an activated oncogene(s), we showed that cellular DNAs from 8 cervical carcinomas induced transformation of NIH 3 T 3 cells and, in all cases, HPV sequences were retained in the secondary transformants. 2) Using a retrovirus vector system, we showed that HPV-16 had transforming activity for mouse or rat established cells. The transforming genes are located in the E6 and E7 ORF: the former governs tumorigenicity in nude mice and the latter influences cell growth properties such as saturation density, colony formation in soft ager and immortalization. These results strongly suggest that specific types of HPV are involved in carcinogenesis of the cervix. However, HPV only may not be sufficient to induce carcinomas, because even the E6 and E7 ORFs of HPV-16 could not transform rat primary cells immediately after infection, but could do so after a long latency. Evaluation of the change during the latency is very important to clarify the mechanism of cervical carcinogenesis.
Hakura
A
A
Dept. of Tumor Virology, Research Institute for Microbial Diseases, Osaka University.
Yutsudo
M
M
Inoue
H
H
Okamoto
Y
Y
Takami
Y
Y
D000818:Animals; D002455:Cell Division; D002470:Cell Survival; D002471:Cell Transformation, Neoplastic; D002472:Cell Transformation, Viral; D004273:DNA, Neoplasm / Q000235:genetics; D005260:Female; D005814:Genes, Viral; D006801:Humans; D051379:Mice; D009857:Oncogenes; D027383:Papillomaviridae / Q000235:genetics*; D051381:Rats; D014412:Tumor Virus Infections; D002583:Uterine Cervical Neoplasms / Q000209:etiology / Q000235:genetics
D004273:DNA, Neoplasm