Final answer:
Defective p53 fails to initiate apoptosis, allowing abnormal cells to divide and potentially lead to tumor formation.
Step-by-step explanation:
Mutations in the tumor suppressor gene, resulting in a defective p53, may fail to initiate apoptosis and lead to uncontrolled replication of cells with damaged DNA.
The p53 protein, coded for by the p53 gene, is a significant player at the G₁ checkpoint of the cell cycle where it monitors the DNA. If p53 detects damaged DNA, it usually triggers repair mechanisms or leads the cell towards programmed cell death, also known as apoptosis, to prevent the propagation of potential mutations that could lead to cancer. However, if the p53 protein is mutated, it may no longer function correctly. This defect prevents the initiation of DNA repair or apoptosis, consequently allowing cells with damaged DNA to proceed with cell division. The accumulation of such abnormal cells, with multiple mutations, often overtakes normal cellular growth, leading to tumor formation and contributing to the progression of cancer. The importance of p53 is further emphasized by the fact that this gene is found to be mutated in over half of all human cancers, underscoring its crucial role in maintaining cellular integrity and preventing tumor development.