Final answer:
The presence of a functional p53 protein prevents the progression to cancer after UV-induced DNA damage by repairing or eliminating damaged cells. If p53 is not affected by the damage, the cell maintains its ability to protect against the development of cancer.
Step-by-step explanation:
If chromosomes in a skin cell are damaged by ultraviolet radiation but the genes that affect p53 are not damaged, the cell may not necessarily become cancerous. The p53 protein is instrumental in halting the cell cycle to allow for DNA repair or for triggering programmed cell death (apoptosis) when the damage is irreparable. Given that the p53 protein is intact, it can still perform its role in DNA damage response, which includes activating other genes whose products participate in DNA repair, or initiating cell death if the damage cannot be repaired. Therefore, a functioning p53 can prevent the propagation of mutations and the potential development of cancerous cells.
However, should the p53 gene become mutated and lose its function, as seen in over 50 percent of human tumor cells, the consequences include the failure to arrest the cell cycle, the inability to correct DNA damage, and the lack of triggering apoptosis. This can lead to the proliferation of damaged cells and increase the risk of cancer development. Hence, the presence of a functional p53 protein plays a crucial role in preventing the progression to cancer after UV-induced DNA damage.