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The page below is a sample from the LabCE course Human Papillomavirus (HPV) and Molecular Testing for Cervical Cancer. Access the complete course and earn ASCLS P.A.C.E.-approved continuing education credits by subscribing online.

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Carcinogenesis of Cervical Cancer, continued

Numerous genetic events occur over a relatively long period of time that lead to the development of cervical carcinoma. The protein products of tumor suppressor genes are the regulators of cell growth, as discussed previously. Two intracellular protein products of tumor suppressor genes located within human cells are p53 and Rb. As noted earlier, protein products from HPV genes E6 and E7 bind to p53 and Rb, which results in unregulated cell growth. This unregulated growth prevents normal DNA repair, allowing for mutations to accumulate in the cell. As this process continues, it is postulated that a proto-oncogene becomes mutated, which in turn activates oncogenes.
The E2 gene in HPV controls the production of E6 and E7 in the normal viral life cycle. When the viral genome is integrated into host cells, the E2 gene is disturbed and uncontrolled production of E6 and E7 protein products occurs. This leads to a greater interaction and disabling of host cell tumor suppressor gene products. The genes E6 and E7 of HPV Types 16 and 18 have a greater affinity for tumor suppressor gene products than other HPV types. This explains the greater virulence associated with Types 16 and 18 and their association with 70% of cervical cancer.