title: [Papillomavirus and cancer].
abstract: Papillomaviruses are causative agents of benign tumor (papilloma) and are widely distributed in most of animals. The papillomaviruses are small DNA viruses grouped in the papovavirus family. The genomes of all papillomaviruses pce double stranded circular DNA of approximately 8 K. base pairs. Classification of the viruses is presently based on the host range and relatedness of the nucleic acids. In the case of human papillomavirus (HPV), more than 50 types have been isolated. The amount of information about the HPV has grown considerably in the last few years, and at present it has been considered that the specific types of HPV are involved in the development of human genital cancer and the skin cancer developed in the patients with EV (epidermodysplasia verruciformis). The reasons are; i) Epidemiological evidence distinctly indicates that cervical carcinoma and other high-grade lesions of female and male genital tracts derive from a sexually transmitted disease. ii) Many cervical carcinomas, most cell lines derived from the carcinoma and almost all skin tumors of EV patient contain specific types of HPV DNA (genital tumors; HPV-16, 18, 31, 33 and 25, skin tumor of EV patient; HPV-5, 8, 17 and 20). Moreover, genetic information of the viruses can be detected in the cancer cells. iii) Follow-up studies of HPV carriers suggested that HPV-16, 18 have high oncogenic potential. iv) Oncogenic functions (transformation and immortalization) can be detected in the early genetic region of HPV-16 DNA. v) Cottontail rabbit papillomavirus (CRPV) induces tumor in rabbit (and that almost all of these tumors contain CRPV DNA. When rabbits are infected with CRPV, benign papillomas are induced in 100% of the rabbits and the lesion are progressed to skin cancer at the frequency of 40-60%). In human cases, however, the presence of specific types of HPV does not seem to be sufficient to assure the development of benign tumors into carcinomas, since only a part of all such cases progress after latent period of several to several ten years. This emphasizes that other etiological agents or cofactors must be involved.
authors.affiliation: Dept. of Tumor Virology, Osaka University.
authors.forename: A
authors.initials: A
authors.lastname: Hakura
mesh_terms: D000818:Animals; D004279:DNA, Viral / Q000032:analysis; D004819:Epidermodysplasia Verruciformis / Q000209:etiology / Q000382:microbiology; D005260:Female; D005834:Genital Neoplasms, Male / Q000032:analysis / Q000209:etiology* / Q000382:microbiology; D006801:Humans; D008297:Male; D009857:Oncogenes; D010212:Papilloma / Q000032:analysis / Q000209:etiology* / Q000382:microbiology; D027383:Papillomaviridae / Q000145:classification / Q000235:genetics / Q000302:isolation & purification; D012878:Skin Neoplasms / Q000032:analysis / Q000209:etiology* / Q000382:microbiology; D014412:Tumor Virus Infections / Q000382:microbiology; D002583:Uterine Cervical Neoplasms / Q000032:analysis / Q000209:etiology* / Q000382:microbiology
chemical_list: D004279:DNA, Viral