P53 PROTEIN OVEREXPRESSION IS COMMON AND INDEPENDENT OF HUMAN-PAPILLOMAVIRUS INFECTION IN SQUAMOUS-CELL CARCINOMA OF THE VULVA

Citation
Mj. Kagie et al., P53 PROTEIN OVEREXPRESSION IS COMMON AND INDEPENDENT OF HUMAN-PAPILLOMAVIRUS INFECTION IN SQUAMOUS-CELL CARCINOMA OF THE VULVA, Cancer, 80(7), 1997, pp. 1228-1233
Citations number
36
Categorie Soggetti
Oncology
Journal title
CancerACNP
ISSN journal
0008543X
Volume
80
Issue
7
Year of publication
1997
Pages
1228 - 1233
Database
ISI
SICI code
0008-543X(1997)80:7<1228:PPOICA>2.0.ZU;2-T
Abstract
BACKGROUND, Human papillomavirus (HPV) infection and p53 abnormalities might both play a role in the carcinogenesis of subtypes of squamous cell carcinoma of the vulva. In this study, the authors investigated t he prevalence of and the relationship between p53 overexpression and H PV infection in patients with vulvar carcinoma. METHODS, Immunohistoch emical methods for the detection of p53 protein and consensus primer p olymerase chain reaction (PCR) were used, followed by direct sequencin g of the PCR product for the evaluation of HPV subtype infection. Sixt y-six patients with squamous cell carcinoma of the vulva were availabl e for this study. RESULTS, DO7, an anti-p53 monoclonal antibody, showe d p53 overexpression in 35 carcinomas (53%). Consensus primer PCR show ed HPV infection in 12 carcinomas (18%). No significant association wa s observed between p53 overexpression or HPV infection and tumor subty pe. Approximately 57% of the HPV negative carcinomas and 33% of the HP V positive carcinomas had p53 overexpression. With regard to the patie nts with DO7 positivity in greater than or equal to 50% of the nuclei only, significantly more HPV negative carcinomas were DO7 positive com pared with HPV positive carcinomas (41% vs. 0%, respectively; P = 0.01 8). No relation was found between either HPV infection or p53 overexpr ession and disease free survival. CONCLUSIONS, p53 overexpression is c ommon in both HPV positive and HPV negative carcinomas of the vulva. T hese findings indicate that these two both play a role in the pathogen esis of vulvar carcinoma, but do not influence disease free survival.