K. Mildelangosch et al., PRESENCE AND PERSISTENCE OF HPV INFECTION AND P53 MUTATION IN CANCER OF THE CERVIX UTERI AND THE VULVA, International journal of cancer, 63(5), 1995, pp. 639-645
We studied 51 cervical carcinomas, among them 25 squamous-cell carcino
mas (SCC) and 26 cervical adenocarcinomas (AdCa), and 40 vulvar SCC fo
r the presence of HPV and mutant p53. HPV was detected by PCR, and p53
alterations by temperature-gradient gel electrophoresis/direct sequen
cing and immunohistochemistry. HPV, mostly type 16/18, was found in 80
.4% of the cervical tumors (92.0% of the SCC and 69.2% of the AdCa), b
ut in only 27.5% of vulvar carcinomas. In contrast, p53 mutations were
found in 7.8% and 52.5% of cervical and vulvar tumors respectively. M
utant p53 occurred in pre-invasive vulvar lesions, indicating that thi
s oncogenic factor is involved early in carcinogenesis. Further analys
is of recurrent/metastatic lesions of 9 cervical and 14 vulvar tumors
also showed remarkable differences: in cervical cancer, HPV was persis
tent, and p53 mutations absent, whereas in vulvar tumors, HPV was most
ly absent or not persistent, and the p53 mutation rate was very high (
78.6%). These observations suggest that HPV persistence is an importan
t event for the evolution and maintenance of cervical cancer, whereas
for vulvar cancers p53 mutation and not HPV activity is a central onco
genic event. (C) 1995 Wiley-Liss, Inc.