What if cellular growth and repair is 'forced' to occur repeatedly in a region where it wouldn't normally happen , if the biological area was 'healthier'. Could this more aggressive cellular growth and repair cause any apoptosis mechanisms to shut down permanently?
One long standing hypothesis of cancer formation is that it originates in a 'wound that never heals'. I was about to add that there is little hard evidence for wounding as a significant cause of cancers but Google found this fascinating report on Marjolin's Ulcers which I had never heard of. Whether it was the wound or a comorbid virus or something else.....
You may also want to search the current thinking of how a chemically inert 'irritant' - an asbestos fibre - can cause mesothelioma.
The definition of a tumor is a population of cells that:
2.. Does not exhibit apoptosis
3.. Does not differentiate
Additionally the two-hit hypothesis states that at least two genes need to be involved.
There are many genes, predominantly involved in the regulation of the cell cycle, that when their function is disrupted the cell exhibit uncontrolled replication. Attenuated expression or constitutive activation of the genes does not necessarily affect apoptosis. However, and to give you the quick answer – it depends on the gene involved. Some genes are involved both physiologies. Check out the protein AKT.