Human papillomavirus and vulval intra-epithelial neoplasia

Presence and type of oncogenic human papillomavirus in classic and in differentiated vulvar intraepithelial neoplasia and keratinizing vulvar squamous cell carcinoma

“…In classic vulvar intraepithelial neoplasia, a HPV positivity of 66.1% was reported confirming the high presence of HPVs in this histological type of lesions. The prevalence of HPV positivity in vulvar intraepithelial neoplasias and vulvar squamous cell carcinoma (from 31% up to 90%), reported in the literature [Park et al, 1991;Hording et al, 1995;Sun et al, 1996;Trimble et al, 1996;Hildesheim et al, 1997;Iwasawa et al, 1997;Kagie et al, 1997;Gastrell and McConnell, 2001;Hart, 2001;McNally et al, 2002;Engelman et al, 2003] has a broad range and the values differ greatly from one study to another: HPV has been searched for in various geographical regions, in subjects with different immunological status, sometimes unregarding the histological type of vulvar lesions, studying classic and differentiated vulvar intraepithelial neoplasias and vulvar squamous cell carcinoma together, and using methodologies (serology, histology, in situ hybridization, PCR) with different sensitivities and sometimes directed to detect only the presence of HPV 16. In the present study, the predominant HPV type found in classic vulvar intraepithelial neoplasia was HPV 16 (81.8%), with 35, 33, and 52 types rarely found and sometimes in concomitance with the presence of 16 HPV type; this finding is in accordance with the majority of reports [Hording et al, 1995;Trimble et al, 1996;Gastrell and McConnell, 2001;Hart, 2001;Engelman et al, 2003].…”

Inactivation of the CDKN2A and the p53 tumour suppressor genes in external genital carcinomas and their precursors

“…The role of the p53 gene has been extensively studied in EGC 5–12 . In EGC associated with oncogenic HPV infection, inactivation of the p53 protein occurs through binding with HPV E6 protein and subsequent degradation.…”

High‐risk human papillomavirus infection of the genital tract of women with a previous history or current high‐grade vulvar intraepithelial neoplasia

“…Nevertheless, VIN lesions tend to recur in up to 50% of women regardless of treatment modality [Herod et al, 1996]. Positive excision margins, multifocality of VIN, and persistent vulvar HPV infection have been proposed as risk factors for recurrence of VIN-3 [Modesitt et al, 1998;Gastrell and McConnell, 2001]. We hypothesize that women who have been treated for VIN should have a lower detection rate of vulvar HPV DNA than women who have active lesions, but should have a higher rate than women with no history of VIN.…”