QUESTION.19 Many mutations are found in cancer cells. In general, most mutations are likely to: A. Directly affect cell proliferation potential B. Have no effect on cellular phenotype C. Cause cell death QUESTION 20 Certain base changes can predominate in different cancers. What can these specific base changes reveal? A. This statement is not true, base changes are random in cancers. B. The base changes can point to specific environmental carcinogens causing the disease. C. Base changes are almost always the result of mismatch repair defects. QUESTION 21 Activating telomerase expression is the primary mechanism by which cancer cells achieve immortality. Based on PCAWG data, what is one way that this can occur? A. Mutations in non-coding DNA activate TERT expression B. By point mutations in ubiquitination sites stabilize the TERT protein C. Usually increasing telomerase RNA is sufficient
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QUESTION 48 Cellular protooncogenes can be activated to become cancer causing oncogenes by all of the following except mutagenesis total deletion of the gene chromosomal translocation gene amplification retroviral integration near the gene QUESTION 49 The life cycle of a retrovirus involves reverse transcription of the RNA genome into DNA and then integration into the host genome. The integrated form of the virus is referred to as repetitive viral DNA a latent virus a virion a provirus a long terminal repeat QUESTION 50 The oncogene ras is involved in many human cancers. We now know that in its non-oncogenic (protooncogene) form it functions as a transcription factor that induces cell division a receptor protein kinase a G-protein as part of the G-protein receptor pathway adenylate cyclase beta-catenin
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Cancer and Gene Regulation Why is a cell cycle control system needed for cell division? What happens when cells do NOT respond to the cell cycle control system and divide excessively? Tumor = Benign Tumor = Malignant Tumor = Metastasis = Oncogene = Proto-oncogene = Many proto-oncogenes code for growth factors = Tumor-Suppressor Genes = Accumulated mutations in proto-oncogenes and tumor-suppressor genes alters gene expression and aids in the development of malignant (cancerous) tumors. Mutations in proto-oncogenes converts them to over-active oncogenes. Explain how this alters the regulation of growth factors and leads to the development of cancer: Mutations in tumor-suppressor genes cause these genes to be inactivated. Explain how this alters the regulation of growth-inhibiting proteins and leads to the development of cancer:
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When cells are stimulated to divide, a. Proto-oncogenes are inactivated. b. Oncogenes become proto-oncogenes. c. Tumor suppressors are inactivated. d. Tumor suppressors are activated. 2. The proteins synthesized from proto-oncogenes, which often participate in signal cascades, are typically active a. Only in Golgi bodies. b. Only on the cell's surface. c. Throughout the cell. d. Only in the cell's nucleus. 3. If a cell's p53 genes are inactivated, the cell a. No longer makes proto-oncogenes. b. Stops dividing. c. Loses control over cell division. d. Activates tumor suppressors. 4. Malignant cancers often require that a single cell experience as many as four mutations; does a single mutation predispose a cell to a second or third? a. Yes, particularly if the first mutation depresses a DNA-correcting mechanism allowing subsequent injuries to remain uncorrected. b. Yes, initial mutations often lead to the construction of carcinogen receptors that pull harmful chemicals into the cell and accelerate the mutation process. c. No, each cell is uniformly at risk for mutation; if a cell has four mutations, it is likely that its neighbors have two or three. d. No, mutation is an entirely random process; carcinogens have no way of locating a previously damaged cell. 5. Which of the following statements about viruses is false? a. Viruses do not contain nucleic acid. b. Viruses can cause cancer. c. Viruses take over a cell's machinery to reproduce. d. Viruses can be used to destroy cancer cells. 6. When a mutant receptor protein no longer requires a growth factor to activate it, the result is a. Lack of protein products. b. Reduction in cell division. c. Extra binding sites. d. Uncontrolled cell division. 7. The p53 protein is critical to the regulation of the cell cycle because it a. Halts cell division when necessary, allowing the cell to repair damaged DNA. b. Causes cells with heavily damaged, unrepairable DNA to commit "suicide." c. Prevents the cell from dividing at inappropriate times. d. All of the above. 8. For proper cell division to occur, the activity of proto-oncogenes must be balanced by the activity of tumor suppressor genes.
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