[Cellular and molecular pathogenesis of cancer of the cervix]

There is now substantial evidence that specific human papillomavirus (HPV) types are probably an etiological factor of cervical cancer and its precursors. Virus infection, viral genes expression emerge as necessary but not sufficient for the cells transformation. The E6-E7 oncoproteins of "high risk" (HPV 16-18) papillomaviruses bind specifically, and with high affinity, to cellular tumor suppressor gene products p53 and pRb, in contrast to "low risk" (HPV 6-11) types. This bond disturbs the cell cycle and results in chromosomal instability, aneuploidy and is the probably starting point of the integration of viral DNA to the host genome. These endogenous modifications are reported to the morphological and colposcopical events of cervical intraepithelial neoplasia and seem to be most important in the pathogenesis of cervical cancer precursors lesions and tumor progression.