Adaptieve mechanismen in kankercellen

Cancer cells exhibit a mutator phenotype characterized by defective DNA repair mechanisms that lead to higher than normal mutation rates. Their tolerance to mutations even in the critical cell cycle genes confer them with survival advantages over normal cells. 

For example, normal cells stop dividing once they contact another cell, in a phenomenon known as contact inhibition. However, some cells can mutate to overcome contact inhibition and pile up on top of each other, forming a tumor mass. 

Nonetheless, these tumor cells cannot continue to proliferate forever. At some point, they may undergo replicative cell senescence, a phenomenon where cells stop dividing after a certain number of cell divisions. 

Thus, some tumor cells mutate further to overcome this hurdle and become cancerous. First, they increase their rate of cell division to compensate for the loss of cells due to cell senescence. Secondly, they can evade apoptosis, resulting in the prolonged survival of old and damaged cells.

The tumor grows, the cells in the interior of a large tumor receive less oxygen - a phenomenon called hypoxia. This limits the ability of the cells to grow and can trigger cell necrosis inside the