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Molecular biology of head and neck tumorigenesis: the role of p53 expression and genetic instability.

Head and neck cancers progress as multistep tumorigenesis through accumulation of genetic instability. The p53 tumor-suppressor gene encodes a cell-cycle checkpoint protein that functions in the G1 phase of the cell cycle. When DNA damage is incurred, p53 transactivates a number of downstream genes whose products, with diverse biologic activities, contribute to the cellular response to DNA damage. One major p53-mediated function in response to DNA damage is to induce the G1 cell-cycle arrest, or delay, which probably allows time for the cell to repair DNA damage prior to S-phase entry. In cell lacking of p53 function, a condition of genetic instability results from checkpoint loss (Fig. 4.). These events occur early from ANL to SCC and increase gradually through multistep tumorigenesis. Due to the potential role of p53 expression and genetic instability, both might be useful biomarkers in assessing the risk of head and neck tumorigenesis.