Chapter 19: Problem 9
Define tumor-suppressor genes. Why is a mutated single copy of a tumor- suppressor gene expected to behave as a recessive gene?
Chapter 19: Problem 9
Define tumor-suppressor genes. Why is a mutated single copy of a tumor- suppressor gene expected to behave as a recessive gene?
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Get started for freeDescribe the steps by which the \(p 53\) gene responds to DNA damage and/or cellular stress to promote cell-cycle arrest and apoptosis. Given that \(p 53\) is a recessive gene and is not located on the X chromosome, why would people who inherit just one mutant copy of a recessive tumor-suppressor gene be at higher risk of developing cancer than those without the recessive gene?
How do normal cells and cancer cells differ in terms of cell-cycle regulation?
In this chapter, we focused on cancer as a genetic disease, with an emphasis on the relationship between cancer, the cell cycle, and DNA damage, as well as on the multiple steps that lead to cancer. (a) How do we know that malignant tumors arise from a single cell that contains mutations? (b) How do we know that cancer development requires more than one mutation? (c) How do we know that cancer cells contain defects in DNA repair?
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 \(13: 445-455\) ). (a) How might hypermethylation of the \(p 53\) 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. \(15(1): \mathrm{R} 4\) ), 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.
Distinguish between oncogenes and proto-oncogenes. In what ways can proto- oncogenes be converted to oncogenes?
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