CELLULAR AND MOLECULAR PATHOGENESIS OF CE RVICAL-CARCINOMA

There is now substantial evidence that specific human papillomavirus ( HPV) types are probably an etiological factor of cervical cancer and i ts precursors, Virus infection, viral genes expression emerge as neces sary but not sufficient for the cells transformation. The E6-E7 oncopr oteins of ''high risk'' (HPV 16-18) papillomaviruses bind specifically , and with high affinity, to cellular tumor suppressor gene products p 53 and pRb, in contrast to ''low risk'' (HPV 6-11) types. This bond di sturbs the cell cycle and results in chromosomal instability, aneuploi dy 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 ne oplasia and seem to be most important in the pathogenesis of cervical cancer precursors lesions and tumor progression.