Vulvar Intraepithelial Neoplasia III: A Viral Disease of Undetermined Progressive Potential

Photodynamic therapy of vulvar and vaginal condyloma and intraepithelial neoplasia using topically applied 5‐aminolevulinic acid*

“…Similarly, in 59 patients with VIN III treated by surgical excision, Modesitt et al found that recurrence was associated with positive margins at the time of surgery, a history of genital warts, and multifocal disease [34]. The recurrence rate of 48% at 12 months for all patients in our study seems high, but comparable to rates in other published reports, which ranged from 26-48% [6,8,[34][35][36][37]. However, we included immunosuppressed patients into our study, multifocal disease was present in a high percentage of patients, and the mean age of our patients was low.…”

Immunohistochemical analysis of p53 in vulval intraepithelial neoplasia and vulval squamous cell carcinoma

“…Firstly, all VIN was assumed to be HPV-positive, irrespective of whether HPV detection was performed. This assumption is justified by our own data (Rosenthal et al, 2001) and that of others (Hording et al, 1995;Kohlberger et al, 1998), which indicates that 490% of VIN is HPV-positive. Secondly, 4'moderate staining' or 4'10% of nuclei staining positive' were taken to indicate aberrant p53 expression for IHC results, irrespective of the classification used in the original papers.…”

“…In cervical neoplasia, HPV E6 and E7 oncoproteins inhibit cell cycle arrest and apoptosis, allowing the proliferation of mutant clones. The almost universal presence of oncogenic HPV types in VIN and VIN-associated VSCC (Beckmann et al, 1991;Hording et al, 1995;Van Beurden et al, 1995;Rosenthal et al, 2001), along with the fact that HPV infection is associated with transcription of E6 and E7 in VIN III (Higgins et al, 1991;Jochmus et al, 1993;Van Beurden et al, 1995) and VSCC (Higgins et al, 1991;Park et al, 1991), suggests that HPV can also induce some cases of VSCC in a manner analogous to its effects in the cervix. If oncogenic HPV precipitates the accumulation of mutations throughout the genome in vulval neoplasia, then p53 mutations may occur.…”

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].…”