P53 point mutations in initial superficial bladder cancer occur only in tumors from current or recent cigarette smokers.

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Abstract
Mutations of the p53 tumor suppressor gene are present in approximately 50% of all human cancers and are the most frequent genetic alteration known in human cancers. The p53 protein can also be inactivated by mechanisms other than mutation, for example by complexing with viral or cellular proteins such as MDM2. It is clear that the malfunction of this protein plays a central role in the development of cancer. p53 acts as a transcription factor and is implicated in the regulation of the cell cycle and consequently in growth control (1). The current view of the p53 role in the cell suggests that it acts as the guardian of the genome, sensing damage or potential damage to the DNA and invoking a protective response either by blocking the cell cycle or by inducing apoptosis in the affected cell. Expression of high levels of wild-type p53 arrests the cell cycle in G0/G1 phase in response to DNA damage, allowing more time for DNA repair mechanisms. Loss of this gene function allows the propagation of cells with genetic damage and is a key step in the development of neoplasia (2).

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