What is the consequence of nonfunctional p53 after radiation-induced DNA damage?

The correct answer highlights that when p53 is nonfunctional, cells can survive and proliferate despite experiencing DNA damage, such as that caused by radiation. p53 is often referred to as the "guardian of the genome" because it plays a crucial role in monitoring and responding to cellular stress, including DNA damage. Under normal circumstances, if DNA damage occurs, p53 can initiate a series of cellular responses: it can halt the cell cycle to allow for repair processes to take place, induce apoptosis if the damage is irreparable, or activate DNA repair mechanisms.

However, in cases where p53 is nonfunctional or mutated, the cell loses these critical regulatory pathways. This defect means that the cell does not respond properly to the DNA damage. Instead of undergoing cell cycle arrest for repair or apoptosis, these cells can continue to divide and proliferate, leading to the potential accumulation of more genetic errors and instability. This survival in the presence of DNA damage is a hallmark of cancerous cells that can contribute to tumorigenesis and resistance to therapies.

Although other options may suggest different outcomes related to p53 function, none accurately describe the situation where nonfunctional p53 leads to the unchecked survival and division of cells with damaged DNA.