Point mutations in DNA occur at a normal fixed rate. This is due to various things such as chemical reactions. This rate is increased by carcinogens and ionizing radiation. If a particular vital gene is mutated this may inactivate the gene or cause the gene to increase its activity (perhaps because it is resistant to degredation). The cell has an inbuilt machinery that repairs mistakes that are made when the cell replicates its DNA, if this machinery fails to perform its function, mutations accumulate. Process that result in increased mutation in these fashions cause cancer by mutageneisis. Another way of increasing the accumulation of mutations is by increasing cell turnover, this mitogenic effect is in part responsible for the `scar' cancers.
Abnormalities in the function of these genes, lead to the mutator phenotype or the replication error phenotype also termed microsattelite instability. These genes function is to notice errors in the replication of DNA and act to repair the damage. If they are defective, then damage accumulates. There are about six genes in this family, MSH1 (Hereditary non-polyposis coli, Lynch syndromes ), etc.
The function of these genes is poorly understood, but loss of their normal function leads to premature aging, cancers and impaired fertiliy. These genes include BLM (Bloom's syndrome), WRN (Werner's syndrome), RecQ4 (Rothmund-Thompson syndrome).
Methylation of DNA plays a role in tumorigenesis. The amount of methylation on promotor regions of the gene effects DNA activity. In addition methylation in the genes exons may result in subsequent mutation.