Cervical cancer is the second largest cause of cancer-related death in women worldwide, and it occurs following persistent infection, sometimes for decades, with a specific subset of human papillomavirus (HPV) types, particularly types 16, 18, 33 and 42. Experimental studies show that the E6 and E7 genes of these high risk HPVs are oncogenes that deregulate key cell cycle controls. The E6 and E7 oncoproteins bind respectively to the p53 and Retinoblastoma (Rb) tumor suppressor proteins, which are involved in the regulation of growth control. The abnormalities in other cellular genes found in cervical cancer, including mutations in ras family of genes, and amplification in EGFR and ERBB2, may also play an important role in carcinogenesis and the aggressiveness of cervical tumors, although to date the role of most of these genetic abnormalities does not appear to be as important as the role of HPV.
