Onkológia 5/2010

Etiopathogenesis of cervical cancer

The authors have outlined the structure of HPV virus, mechanisms of its entry into the cell, structure of its genome, as well as the function of single genes. The oncogenic potential of „high-risk“ HPV is given by two small protein’s E6 and E7. These proteins are small, but very promiscuous and they are able to interact with bright spectrum of cell regulatory proteins involved in the cell cycle regulation. The critical moment for malignant transformation of infected cell seems to be the integration of a part of viral genome containing these two genes into the genome of infected cell. The integration is realized probably by a mechanism of non homologous recombination. Major part of viral genome involved in the regulation of these two oncogenes is lost. Uncontrolled over expression of these two oncogenes block the activities of many cell regulatory proteins, in the first line the Rb1 and p53 tumor suppressors genes. The lost of the cell cycle control results in instability of cells genome, accumulation of next mutations and finally malignant transformation.

Keywords: human papillomavirus (HPV), E6–E7 oncogenes, viral genome integration, cell cycle deregulation.