Final answer:
Null mutations in p53 or DNA damage suppressor genes can lead to the survival of cells that would normally undergo apoptosis, hence contributing to the development of cancers by allowing these cells to divide and accumulate further mutations.
Step-by-step explanation:
Null mutations in either p53 or DNA damage suppressor genes lead to the survival of cells that would normally die. The p53 protein is critically involved in several cellular processes at the G₁ checkpoint; it activates genes involved in halting the cell cycle to allow for DNA repair and triggers apoptosis when damage is irreparable. Mutated p53 genes interfere with these processes, resulting in the propagation of cells with DNA errors, contributing to tumor growth and cancer development.
A functional p53 protein acts to prevent the proliferation of potentially cancerous cells by inducing apoptosis when DNA damage is detected and cannot be repaired. However, a mutated or damaged p53 gene can result in cells ignoring genetic aberrations, allowing these cells to continue dividing and accumulating additional mutations. These conditions foster the development of cancers, as seen in various human tumors where p53 mutations are prevalent.
DNA damage suppressor genes also play a crucial role in maintaining genetic integrity, operating as recessive alleles. When mutated, these genes can further contribute to the survival and proliferation of abnormal cells. As a result, cells with both oncogenes and non-functional tumor suppressor genes accumulate rapidly, leading to unchecked cell division and tumor growth.