Why is the mutation of both copies of the p53 gene critical in cancer development?

The mutation of both copies of the p53 gene is critical in cancer development primarily because it enables uncontrolled cell proliferation. The p53 protein is often referred to as the "guardian of the genome" due to its essential role in regulating the cell cycle and maintaining genomic stability. When functioning properly, p53 can induce cell cycle arrest, allowing time for DNA repair, or initiate apoptosis when damage is irreparable.

In the case where both copies of the p53 gene are mutated, the protector function of p53 is lost. This loss of function means that cells with damaged DNA can bypass checkpoints and continue to divide uncontrollably, contributing to tumorigenesis. Without the ability of p53 to halt the cycle or trigger programmed cell death in response to damage or stress signals, cells can accumulate additional mutations that lead to more aggressive cancer phenotypes.

The other choices do not accurately reflect the consequence of p53 mutations in cancer. Enhancing DNA repair mechanisms or increasing cellular responses to stress would actually be protective functions against cancer, while supporting healthy cell apoptosis is also a protective mechanism that is compromised when p53 is mutated.