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 :
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 protect cells from undergoing uncontrolled division. These genes typically function to regulate cell cycle checkpoints, promote apoptosis (programmed cell death), repair DNA damage, and prevent the formation of tumors. When tumor suppressor genes are mutated, their ability to control these processes is impaired, which can lead to uncontrolled cell growth and ultimately cancer.
However, for cancer to develop due to a mutation in a tumor suppressor gene, both alleles of the gene (one inherited from each parent) must be affected. This is because tumor suppressor genes follow a recessive model of inheritance. In this case, a mutation in a single allele of a tumor suppressor gene may not be enough to disrupt its function, as the other, non-mutated allele can still provide a functional copy of the gene. Only when both copies of the gene are mutated (leading to a loss of function in both alleles) does the tumor suppressor gene fail to perform its protective role.
For example, in the case of the p53 gene, a well-known tumor suppressor gene, an inherited mutation in one copy of the gene may not cause cancer immediately. However, if the second copy of the p53 gene acquires a mutation (often through environmental factors like UV radiation), the cell’s ability to repair DNA or undergo apoptosis becomes compromised. This loss of function in the tumor suppressor gene can lead to the accumulation of genetic mutations and promote the formation of cancer.
The recessive nature of tumor suppressor genes means that both alleles must be mutated for the gene’s function to be completely lost, which is why these genes are often referred to as “gatekeepers” in cancer development. This contrasts with oncogenes, which typically require only a single mutated allele to drive cancer formation.