These three areas of research have added needed details to our understanding of how cancer begins. The cell uses DNA repair systems to correct most of these genetic injuries. The cell begins proliferating faster than normal. This leads to a pre-cancerous growth such as an adenoma. At this point, the telomeres in these pre-cancer cells shorten with each cell division as usual.
Mutations continue to accumulate, and the cell begins growing out of control.
At some point, the genetic damage the cell has sustained should cause it to destroy itself by apoptosis. This is the first of two mortality checkpoints an early cancer cell faces. But mutations in tumor suppressor genes such as p53 prevent apoptosis from happening. At the same time, the telomeres in these cells continue to shorten. After about 50 cell divisions, the telomeres become critically short.