Human papillomavirus (HPV) infection has been implicated to be an important causative factor for the development of cervical carcinoma. P53 gene mutation is common in human malignancies, and it is suggested that p53 function is inactivated either by complex formation with HPV E6 product or by gene mutation in cervical carcinoma. Forty-six cervical carcinoma samples were evaluated for the presence of mutations in p53,p21WAF1 and p16INK4a genes with polymerase chain reaction (PCR), single stranded conformational polymorphism (SSCP) analysis and DNA sequencing. The status of HPV infection in tumor tissues was analysed by PCR. Forty-two of 46 cervical mobility-shifted band in PCR-SSCP analysis of p53, p21WAF1 and p16INK4a mutational inactivation. But it remains to be determined whether disruption of the 3’UTR of p16INK4a mRNA leads to an increased risk for cervical carcinomas.