Presentation at the precongres curse: vulvar disease A, presided by prof J. Borenstein
The female genital tract, a continuum of squamous epithelium from the vulva to the cervix, is commonly infected by human papillomavirus. The outcome of HPV infection depends on the immune response, the viral genotype (low-risk or high-risk/oncogenic) and the site of infection (the cervical and anal squamo-columnar junction is more susceptible to HPV disease). The key role of HPV in most cancers of the female lower genital tract has been firmly established biologically and epidemiologically
Review: High-risk human papillomavirus infection usually is seen at one anatomic site in an individual. Rarely, infection at multiple anatomic sites of the female lower genital tract in the same individual is encountered either simultaneously and/or at a later date. Multisubtype infection and infection by rare hrHPV subtypes are common in multifocal dysplasia involving multiple anatomic sites of the female lower genital tract
Women with a history of grade 3 CIN had increased risks of cancer of the vagina (6·74), vulva (2·22), and anus (4·68). Among women with a history of cervical cancer or grade 3 CIN, the incidence rates of anal cancer ranged from 0.8 to 63.8 per 100,000 person-years, and in the general population, the incidence rates ranged from 0.55 to 2.4 per 100,000 person-years.
Squamous cell carcinomas (SCCs) of the vulva develop through human papilloma virus (HPV)-associated or HPV-independent pathways, but the relationship between pathogenesis, classification, and prognosis of these tumors is controversial. HPV-associated neoplasms present in younger women and are associated with usual vulvar intraepithelial neoplasia (VIN), distinct histologic subtypes, and diffuse expression of the cell cycle protein p16 (INK4a). In contrast, HPV-independent vulvar SCCs occur in older women and harbor frequent TP53 somatic mutations. Histologically, non–HPV-associated vulvar SCCs have been associated with differentiated VIN and lichen sclerosus
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