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Define tumor-suppressor genes. Why is a mutated single copy of a tumor- suppressor gene expected to behave as a recessive gene?

Short Answer

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Answer: A mutated single copy of a tumor-suppressor gene is expected to behave as a recessive gene because the presence of a functional copy of the gene can still keep cell growth under control, preventing uncontrolled cell growth and cancer development. The functional gene can perform its role in suppressing uncontrolled cell division even if one copy is mutated. Thus, both copies must be mutated for the tumor-suppressor gene to completely lose its function and result in the uncontrolled cell growth characteristic of cancer.

Step by step solution

01

Definition of Tumor-Suppressor Genes

Tumor-suppressor genes are a class of genes that play a crucial role in preventing the uncontrolled growth of cells, which can lead to the formation of tumors. These genes are involved in regulating the cell cycle, DNA repair, and cell death, among other important cellular processes. When functioning properly, tumor-suppressor genes act as a safeguard against the development of cancer by keeping cell division in check and promoting the repair of damaged DNA.
02

Understanding Mutated Tumor-Suppressor Genes

Each individual inherits two copies of every gene, one from the mother and one from the father. When one of the copies of a tumor-suppressor gene undergoes a mutation, it loses its normal function. However, the presence of a functional copy of the gene can still keep the cell growth under control. This is because the protein encoded by the functional copy of the gene can perform its role in suppressing uncontrolled cell division.
03

Behavior of Mutated Tumor-Suppressor Genes as Recessive Genes

In genetics, a trait is considered recessive when it is only expressed when an individual has two copies of the mutated gene, while a dominant trait is expressed even if there is only one mutated gene. In the case of a mutated single copy of a tumor-suppressor gene, it is expected to behave as a recessive gene because the presence of a functional copy of the gene prevents the uncontrolled cell growth and the development of cancer. The reason behind this behavior is the mechanism through which tumor-suppressor genes work. Since they function to restrain cell division, the functional gene can still carry out this role even if one copy is mutated. Thus, both copies must be mutated for the tumor-suppressor gene to completely lose its function and result in the uncontrolled cell growth that is characteristic of cancer. This is why a mutated single copy of a tumor-suppressor gene behaves as a recessive trait.

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Most popular questions from this chapter

Those who inherit a mutant allele of the RB1 gene are at risk for developing a bone cancer called osteosarcoma. You suspect that in these cases, osteosarcoma requires a mutation in the second RB1 allele, and you have cultured some osteosarcoma cells and obtained a cDNA clone of a normal human RBI gene. A colleague sends you a research paper revealing that a strain of cancer-prone mice develop malignant tumors when injected with osteosarcoma cells, and you obtain these mice. Using these three resources, what experiments would you perform to determine (a) whether osteosarcoma cells carry two RB1 mutations, (b) whether osteosarcoma cells produce any pRB protein, and (c) if the addition of a normal RB1 gene will change the cancer-causing notential of astensarcama cells?

How are epigenetic changes associated with cancer? What kind of epigenetic changes may be required for a normal cell to become malignant?

Radiotherapy (treatment with ionizing radiation) is one of the most effective current cancer treatments. It works by damaging DNA and other cellular components. In which ways could radiotherapy control or cure cancer, and why does radiotherapy often have significant side effects?

Mutations in tumor-suppressor genes are associated with many types of cancers. In addition, epigenetic changes (such as DNA methylation) of tumor-suppressor genes are also associated with tumorigenesis (Otani et al., 2013. Expert Rev Mol Diagn 13:445455 ). (a) How might hypermethylation of the p53 gene promoter influence tumorigenesis? (b) Knowing that tumors release free DNA into certain surrounding body fluids through necrosis and apoptosis (Kloten et al., 2013. Breast Cancer Res. 15(1):R4 ), outline an experimental protocol for using human blood as a biomarker for cancer and as a method for monitoring the progression of cancer in an individual.

Explain why many oncogenic viruses contain genes whose products interact with tumor-suppressor proteins.

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