Final answer:
Tumors with normal TP53 alleles are more effective targets for radiation therapy due to the p53 protein's role in the DNA damage response, which can halt the cell cycle or initiate apoptosis. Abnormal TP53 alleles found in many cancer cells lead to resistance against the cell-killing effects of radiation by failing to halt proliferation or trigger cell death.
Step-by-step explanation:
Tumors with normal TP53 alleles are more likely to be killed by radiation therapy compared to tumors with abnormal TP53 alleles. This is due to the role of the p53 protein in DNA damage response. Normally, p53 activates genes that halt the cell cycle for DNA repair, or initiate cell death if the damage is irreparable. However, mutated p53, as found in cancer cells, fails to stop cell proliferation or trigger apoptosis. As a result, cancer cells with abnormal TP53 alleles tend to accumulate mutations and might resist radiation therapy more than cells with normal TP53 alleles, which would undergo apoptosis when confronted with the DNA damage caused by radiation.
Radiotherapy is an effective cancer treatment because it uses the high sensitivity of rapidly reproducing cancer cells to radiation to cause damage at multiple sites, preventing these cells from surviving or replicating properly. Enhancement of the therapeutic ratio, which is the ratio of abnormal cells killed to normal cells killed, is a central goal in radiotherapy. Techniques such as geometrically concentrating radiation in the tumor increase this ratio, thereby potentiating the treatment's effectiveness against tumors with normal p53 protein function.