At a simplistic level cancer is due to the accumulation of genetic mutations to key genes. Mutations may occur due to the effect of an external agent such as a carcinogen, or they may occur due to normal errors in DNA replication. Over a fixed period of time, the number of mutations that the cell accumulates will depend on the effect of external agents and on the number of cell cycles that the cell has gone through. Thus the rate of accumulation of mutations may be increased by either mutagenic or mitogenic influences.
The mutation may disable a gene so that it no longer provides its protective function. Or it may increase the activity of the gene and thus push the cell onto unchecked division. The disabling scenario is what happens in the case of tumor suppressor genes. The activating scenario is what happens in the case of oncogenes.
Other mechanisms are at work too. If a cell looses its ability to repair errors in DNA replication then the stage is set for malignant degeneration. Failure to recognise or repair errors inherent in DNA replication will result in a progressive accumulation of mutations that will effect tumor suppressors and oncogenes.