Abstract
The majority of cervix cancers are attributed to effects of HPV viral infection, which may cause cellular dysregulation via viral associated protein interaction with p53 and Rb resulting in p16 over-expression as a cellular compensatory mechanism. It is possible that alternate mechanisms of cervical carcinogenesis exist that are independent of the viral effects. These may include p53 mutation, or alteration of cell cycle regulators, such as over-expression of the p53 inhibitor MDM2.
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