[P53 protein and human papillomavirus oncogenes in carcinogenesis of the uterine cervix].

Human papillomavirus (HPV) DNA sequences are found in the majority (90%) of cervical tumors, and in cell lines derived from them. The products of the viral E6 and E7 oncogenes inactivate those from the p53 and Rb tumor suppressor genes. The p53 protein controls the entrance to the cell cycle. When DNA damage occurs, p53 levels are increased, resulting in cell arrest. This allows cells to repair the damage before replication occurs. Cells without p53 (either mutated or absent) will replicate their unrepaired DNA, increasing their genomic instability. In cells from cervical cancer the E6 protein will induce degradation of p53, so continuous expression of viral oncogenes will lead to genomic instability, that in turn will increase the risk of acquiring new mutations that probably contribute to cancer development.