Inactivation of two tumor suppressor gene products, P53 and pRb, either by complex formation with the E6 and E7 proteins of oncogenic Human papilloma virus (HPV) or by mutations of the two tumor suppressor genes is known as an important step in carcinogenesis of the uterine cervix. Some experiments with established cervical cancer ceIl lines have confirmed this hypothesis. The present study was designed to clarify the association between p53 mutation and oncogenic HPV infection in primary carcinomas of the uterine cervix. Thirty primary cervical cancer tissues were examined for the presence of HPV DNA by polymerase chain re- action (PCR) with Ll consensus primers, HPV type 16 specific primers, and type 18 specific primers. With LI consensus primers, 25 (83%) of 30 were positive, with HPV type 16 specific primers, 16 (53%) were positive, and with HPV type 18 specific primers, 5 (17%) were positive. Mutations in the highly conserved regions of p53 gene were further examined by PCR-single strand conformation polymorphism (SSCP) and direct sequencing method. Point mutation was detected in only one case which was positive for HPV type 18. The mutation was an AAA to TAA transversion at codon 101 of exon 4, resulted in nonsense mutation. These observations suggest thst, in contrast to data derived from established cervical carcinoma cell lines, inactivation of the P53 gene by sllelic losses or by point mutations is infrequent in clinical samples of carcinomas tissues of the uterine cervix irrespective of the presence or absence of HPV infection.
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