| Autor: |
Ueda, Yutaka, Enomoto, Takayuki, Miyatake, Takashi, Shroyer, Kenneth R, Yoshizaki, Tatsuo, Kanao, Hiroyuki, Ueno, Yuko, Sun, Hongbo, Nakashima, Ryuichi, Yoshino, Kiyoshi, Kimura, Toshihiro, Haba, Tomoko, Wakasa, Kenichi, Murata, Yuji |
| Zdroj: |
American Journal of Clinical Pathology; August 2004, Vol. 122 Issue: 2 p266-274, 9p |
| Abstrakt: |
To elucidate the pathogenesis of vulvar carcinomas, we studied clonality and human papillomavirus (HPV) infection in vulvar epithelial diseases. Monoclonal composition was demonstrated in all 9 invasive tumors (squamous cell carcinoma [SCC], 6; basal cell carcinoma, 1; malignant melanoma, 2), 15 of 20 cases of vulvar intraepithelial neoplasia (VIN), 7 of 9 cases of Paget disease, 2 of 6 cases of lichen sclerosus (LS), and 2 of 3 cases of squamous cell hyperplasia (SCH); high-risk type HPV was revealed in 5 of 6 SCCs and 17 of 20 VINs. These observations might imply that a subset of cases of LS and SCH result from a neoplastic proliferation, similar to VINs but not related to infection with high-risk type HPV. In 1 case of SCC with concurrent VIN 3 in an adjacent lesion, both lesions showed the same pattern of X chromosome inactivation and the presence of HPV-16 in episomal and integrated forms, suggesting that monoclonal expansion triggered by high-risk type HPV integration is an early event for carcinogenesis of HPV-associated SCC. |
| Databáze: |
Supplemental Index |
| Externí odkaz: |
|
