Promoter hypermethylation of death-associated protein kinase and p16 genes in vulvar lichen sclerosus.

Objective: The purpose of this study was to discuss our investigation of the hypermethylation of promoter regions of tumor suppressor genes, such as death-associated protein kinase (DAPK) and p16, in vulvar lichen sclerosus (LS), in comparison with a control group.

Materials And Methods: Promoter hypermethylation of DAPK and p16 was investigated using 24 vulvar biopsies of patients with LS who had received no previous treatment. The control group was composed of 15 patients with no vulvar disease.

Epstein-Barr virus and human papillomavirus infection in vulvar lichen sclerosus.

Objective: We investigated the presence of the Epstein-Barr virus (EBV) and human papillomavirus (HPV) in patients with vulvar lichen sclerosus (LS).

Materials And Methods: We investigated the presence of HPV and EBV from 34 vulvar biopsies of patients with LS who had had no previous treatment and from 17 normal vulvar brushings used as controls. We used polymerase chain reaction to amplify DNA sequences of these viruses.

Promoter hypermethylation patterns of death-associated protein kinase and p16 genes in vulvar lichen sclerosus.

Objective: This article aimed to investigate the hypermethylation of promoter regions of tumor suppressor genes, such as death-associated protein kinase (DAPK) and p16, in vulvar lichen sclerosus (LS).

Materials And Methods: The promoter hypermethylation of DAPK and p16 was investigated from 15 vulvar biopsies of patients with LS who had had no previous treatment. DNA was treated with sodium bisulfate and underwent methylation-specific polymerase chain reaction of these genes.

Vulvar intraepithelial neoplasia p53 expression, p53 gene mutation and HPV in recurrent/progressive cases.

Objective: To evaluate p53 protein overexpression and p53 gene mutation in primary and recurrent undifferentiated vulvar intraepithelial neoplasia (VIN), establishing the recurrence and progression rates, median time interval, and sites of the initial lesion and first recurrence, addressing the relationship with HPV infection.

Study Design: Twenty women with undifferentiated VIN treated with wide surgical excision were followed every 6 months for 7 years and divided into groups with and without recurrence/progression. p53 Protein was detected in paraffin sections using the monoclonal p53 antibody.