To cause cancer, tumor suppressor genes require allele(s) to be mutated and therefore are considered The mutation results in a of function.
The Correct Answer and Explanation is:
Correct Answer:
To cause cancer, tumor suppressor genes require both alleles to be mutated and therefore are considered recessive. The mutation results in a loss of function.
Explanation
Tumor suppressor genes are a class of genes that regulate cell growth, division, and apoptosis (programmed cell death). Their primary role is to prevent the formation of tumors by ensuring cells do not grow uncontrollably or divide inappropriately. Examples include TP53, RB1, and BRCA1/BRCA2.
In contrast to oncogenes, which promote cancer when a single allele is activated (gain-of-function), tumor suppressor genes typically need both alleles to be inactivated or mutated to contribute to cancer. This is because the proteins they encode are involved in crucial protective functions, and having one working copy is usually sufficient to maintain control over the cell cycle. This concept is often referred to as Knudson’s “two-hit hypothesis.”
According to this hypothesis, the first “hit” may be an inherited germline mutation (as seen in many hereditary cancer syndromes), while the second “hit” could be a somatic mutation acquired during the person’s life. When both alleles are nonfunctional, the cell loses its ability to regulate growth and division, leading to increased cancer risk.
The mutations in tumor suppressor genes typically lead to a loss of function. This loss prevents the gene from carrying out its normal regulatory or repair functions. For example, mutations in the TP53 gene, known as the “guardian of the genome,” disable its ability to trigger DNA repair or apoptosis in cells with damaged DNA, allowing those cells to proliferate unchecked.
In summary, tumor suppressor genes are considered recessive at the cellular level because both alleles must be inactivated to lose function and contribute to tumorigenesis. The resulting loss of function removes critical control mechanisms that prevent uncontrolled cell growth, thereby facilitating the development of cancer.
