Lodish8e_Ch24_TestBank PDF

24 - 10 24 Cancer Section 24.1 1. Which of the following is a characteristic of malignant tumors? a. localized to tissue of origin b. metastatic c. well differentiated d. sense signals that restrict cell division Ans: b Question Type: Multiple choice Chapter: 24 Blooms: Understanding Difficulty:...

24 - 10 24 Cancer Section 24.1 1. Which of the following is a characteristic of malignant tumors? a. localized to tissue of origin b. metastatic c. well differentiated d. sense signals that restrict cell division Ans: b Question Type: Multiple choice Chapter: 24 Blooms: Understanding Difficulty: Moderate 2. Gain-of-function mutations in which of the following genes typify colorectal carcinomas? a. APC b. p53 c. K-ras d. all of the above Ans: c Question Type: Multiple choice Chapter: 24 Blooms: Remembering Difficulty: Easy 3. During metastasis, cells may undergo an epithelial-to-mesenchymal transition whereby there is a(n): a. increase in cell polarity. b. loss of cell-cell-adhesion. c. down-regulation in the expression of the Snail and Twist transcription factors. d. all of the above Ans: b Question Type: Multiple choice Chapter: 24 Blooms: Understanding Difficulty: Moderate 4. Which of the following promotes angiogenesis? a. EGF b. PDGF c. TGF d. VEGF Ans: d Question Type: Multiple choice Chapter: 24 Blooms: Remembering Difficulty: Easy 5. In females, all the cells in a tumor have the same inactive X chromosome. The reason for this is that: a. all of the cells in a tumor are derived from a single progenitor cell. b. all late-stage tumors have chromosome abnormalities. c. multiple mutations are required for tumor induction. d. many tumor-suppressor genes are on the X chromosome. Ans: a Question Type: Multiple choice Chapter: 24 Blooms: Applying Difficulty: Easy 6. Name the six fundamental properties of malignant tumors. Which of these properties are amenable to study in a cell culture model of cancer? Ans: Malignant tumors exhibit (1) self-sufficiency in growth signals; (2) insensitivity to antigrowth signals; (3) evasion of apoptosis; (4) limitless replicative potential; (5) sustained angiogenesis; and (6) tissue invasion and metastasis. The first four properties are amenable to study in a cell-culture model because they are autonomous properties of cancer cells. In contrast, sustained angiogenesis and tissue invasion and metastasis involve the interaction of cancer cells with other tissues and are better studied in vivo. Question Type: Essay Chapter: 24 Blooms: Applying Difficulty: Difficult 7. Leukemias are different from most other classes of cancers. Which of the fundamental properties of cancer cells are likely to be lacking in leukemias and why? Ans: Leukemias are derived from blood cells or their precursors and proliferate as individual cells in the blood rather than as solid tumors. Because they already exist in the circulation, leukemias do not need to promote angiogenesis and likewise do not need to escape their tissue of origin and metastasize, although some leukemias may do so. Question Type: Essay Chapter: 24 Blooms: Understanding Difficulty: Moderate 8. What is the multi-hit model of cancer? What data support this model? Ans: The multi-hit model proposes that multiple, successive mutations are required to produce a cancer cell. Many lines of evidence support this model, including the fact that tumor cells are clonally derived and possess the same genetic alterations. The increased incidence of cancer with age also supports the model. Finally, the cooperative effect of oncogenes in producing tumors in mice supports the model. Question Type: Essay Chapter: 24 Blooms: Analyzing Difficulty: Difficult 9. Describe the Warburg effect and how it applies to cancer cells. Ans: Otto Warburg described how cancer cells, regardless of the level of oxygen in their environment, produce large amounts of lactate as a result of using aerobic glycolysis to produce energy. Question Type: Essay Chapter: 24 Blooms: Understanding Difficulty: Easy 10. Which of the following is NOT a microscopic characteristic of tumor cells? a. high nuclear to cytoplasmic ratio b. greater percentage of mitotic cells c. larger size d. few specialized structures Ans: c Question Type: Multiple choice Chapter: 24 Blooms: Remembering Difficulty: Easy 11. 2-hydroxyglutarate is produced in cancer cells: a. because cancer cells exhibit increased aerobic glycolysis. b. that have mutations in isocitrate dehydrogenase. c. to counteract all the lactate produced by aerobic glycolysis. d. all of the above Ans: b Question Type: Multiple choice Chapter: 24 Blooms: Understanding Difficulty: Moderate 12. Which of the following is NOT a role for the tumor microenvironment? a. tumor cells contain mutations b. interaction with immune cells c. neighboring cells relay information to cancer cells d. HCV-mediated inflammation Ans: a Question Type: Multiple choice Chapter: 24 Blooms: Understanding Difficulty: Moderate 13. Which of the following proteins involved in angiogenesis is paired correctly with its function? a. HIF – tyrosine kinase b. VEGF – receives a secreted signal to induce blood vessel growth c. oxygen sensor – transcription factor d. VEGF receptor – tyrosine kinase Ans: d Question Type: Multiple choice Chapter: 24 Blooms: Understanding Difficulty: Moderate 14. Which of the following interventions would NOT be likely to prevent tumor cells from metastasizing? a. inhibitors of adhesion molecules b. inhibitors of enzymes that degrade the basement membrane c. inhibitors of cell motility d. inhibitors of EGF Ans: a Question Type: Multiple choice Chapter: 24 Blooms: Understanding Difficulty: Moderate 15. A bone tumor sample appears to be heterozygous for a p53 mutation. The most likely explanation for this finding is: a. Mutated p53 is an oncogene. b. The p53 mutation is resulting in a dominant negative p53 protein. c. The p53 mutation is resulting in a premature stop codon, and no functional protein is made from that allele. d. There was a mistake in labeling the tissue sample—all tumors musts lack p53. Ans: b Question Type: Multiple choice Chapter: 24 Blooms: Understanding Difficulty: Moderate Section 24.2 16. Direct-acting carcinogens are those that: a. chemically react with nitrogen and phosphorous atoms in DNA. b. work in conjunction with cytochrome P-450 in the endoplasmic reticulum. c. are mainly reactive electrophiles. d. all of the above Ans: c Question Type: Multiple choice Chapter: 24 Blooms: Understanding Difficulty: Moderate 17. Telomerase: a. induces apoptosis. b. contains reverse transcriptase. c. is inactivated by Bcl-2. d. is active in all normal adult cells. Ans: b Question Type: Multiple choice Chapter: 24 Blooms: Understanding Difficulty: Moderate 18. Exposure to benzo(a)pyrene is most frequently associated with which type of cancer? a. lung cancer b. Burkitt’s lymphoma c. colorectal cancer d. breast cancer Ans: a Question Type: Multiple choice Chapter: 24 Blooms: Remembering Difficulty: Easy 19. The first line of defense against point mutations is: a. BRCA1. b. cytochrome P-450. c. DNA polymerase. d. MSH2. Ans: c Question Type: Multiple choice Chapter: 24 Blooms: Understanding Difficulty: Moderate 20. Describe the differences between direct-acting and indirect-acting carcinogens. Ans: Direct-acting carcinogens have reactive electrophiles that react with nitrogen and oxygen atoms in DNA. These modified nucleotides distort the normal pattern of base pairing. Indirect-acting carcinogens are generally unreactive, water- insoluble compounds. These compounds must first be converted to ultimate carcinogens by the introduction of electrophilic centers, usually by cytochrome P-450 enzymes in the liver. Question Type: Essay Chapter: 24 Blooms: Understanding Difficulty: Difficult 21. Which of the following is NOT evidence that smoking causes lung cancer? a. Epidemiological rates of lung cancer dramatically increased after more people started to smoke. b. Exposure of lung cells to the active carcinogen found in cigarettes causes mutations in p53. c. Mutations in p53 are found in the same codons in patients with lung cancer who smoke as in cultured cells treated with benzo(a)pyrene. d. Epidemiological rates of lung cancer in women increased years after the rates in men increased. Ans: d Question Type: Multiple choice Chapter: 24 Blooms: Applying Difficulty: Moderate 22. If colon cancers could be prevented by intervening in the earliest molecular changes during multi-hit progression, the molecule you would target for intervention would be: a. p53. b. Ras. c. APC. d. VEGF. Ans: c Question Type: Multiple choice Chapter: 24 Blooms: Understanding Difficulty: Easy D 23. Transgenic mice that express an activated oncogene like ras under the control of the TetOFF system are likely to undergo which of the following events when tetracycline is given? a. growth of tumors b. shrinkage of tumors c. no effect on tumors d. tumors become metastatic Ans: b Question Type: Multiple choice Chapter: 24 Blooms: Applying Difficulty: Moderate Section 24.3 24. Which of the following is(are) a tumor suppressor gene? a. APC b. ras c. Rb d. APC and Rb Ans: d Question Type: Multiple choice Chapter: 24 Blooms: Remembering Difficulty: Easy 25. Which of the following is a proto-oncogene? a. APC b. myc c. ptc1 d. Rb Ans: b Question Type: Multiple choice Chapter: 24 Blooms: Remembering Difficulty: Easy 26. Germ-line mutations in which of the following has(have) been implicated in hereditary cancers? a. HPV b. BRCA1 c. Rb d. BRCA1 and Rb Ans: d Question Type: Multiple choice Chapter: 24 Blooms: Remembering Difficulty: Easy 27. Hereditary cancers typically possess loss-of-heterozygosity in: a. proto-oncogenes. b. tumor-suppressor genes. c. both proto-oncogenes and tumor-suppressor genes. d. neither proto-oncogenes nor tumor-suppressor genes. Ans: b Question Type: Multiple choice Chapter: 24 Blooms: Applying Difficulty: Moderate 28. Nearly all malignant tumors possess a loss-of-function mutation in one or more cell cycle checkpoints. However, a loss of checkpoints is not a requisite characteristic of cancer cells per se. Explain this paradox. Ans: Because multiple mutations are required to produce the cancer phenotype, a loss of checkpoint function will greatly increase the likelihood that cancer-promoting mutations will develop. It is possible that these mutations could occur by chance, even with all checkpoint pathways intact. However, cancer would be a much less frequent event if mutations in checkpoint genes never occurred. Question Type: Essay Chapter: 24 Blooms: Analyzing Difficulty: Difficult 29. What are the differences and similarities between the transforming genes of retroviruses and those of DNA tumor viruses? Ans: The oncoproteins encoded by transducing retroviruses are derived from normal cell proteins, whereas those encoded by DNA viruses are required for viral replication. Indeed, the presence of oncogenes in transducing retroviruses renders these viruses defective (unable to replicate). Both types of viruses express oncoproteins from integrated genomes. Question Type: Essay Chapter: 24 Blooms: Applying Difficulty: Difficult 30. Describe gain-of-function and loss-of-function mutations with respect to cancer. Ans: A gain-of-function mutation converts a proto-oncogene into an oncogene. Such mutations are dominant. A loss-of- function mutation occurs in tumor-suppressor genes, abrogating their function in preventing cancer. Such mutations are recessive and require alteration of both alleles. Question Type: Essay Chapter: 24 Blooms: Understanding Difficulty: Moderate 31. How can DNA microarrays be used to detect gene amplifications in cancer cells? Ans: Using genomic DNA from cancer cells as probes and DNA microarrays containing fragments of normal genomic DNA, it is possible to tell the difference between amplified DNA and normal DNA. Amplified genes give stronger signals than do normal genes. Question Type: Essay Chapter: 24 Blooms: Applying Difficulty: Moderate 32. A patient with B cell leukemia donates some cancer cells for analysis. The cells do not contain the usual chromosomal translocations associated with leukemia. Instead, a sporadic mutation seems to have arisen in a certain gene, followed by loss of heterozygosity in the second copy. This gene product is most likely: a. Ras. b. Rb. c. VEGF. d. telomerase. Ans: b Question Type: Multiple choice Chapter: 24 Blooms: Applying Difficulty: Moderate 33. Cancer genome analysis has been utilized for all the following applications, except: a. to identify which patients are good candidates for molecularly targeted drugs. b. to identify cancerous cells in a biopsy based on morphological characteristics. c. to identify driver mutations. d. to identify the link between chromothripsis and aggressive neuroblastoma. Ans: b Question Type: Multiple choice Chapter: 24 Blooms: Applying Difficulty: Moderate Section 24.4 34. Ras is a: a. growth factor. b. kinase. c. phosphatase. d. none of the above Ans: d Question Type: Multiple choice Chapter: 24 Blooms: Understanding Difficulty: Easy 35. Src is a: a. growth factor. b. kinase. c. phosphatase. d. transcription factor. Ans: b Question Type: Multiple choice Chapter: 24 Blooms: Understanding Difficulty: Easy 36. A loss-of-function mutation in _____ would have the same effect as a gain-of-function mutation in Ras. a. Crk b. Csk c. Myc d. NF1 Ans: d Question Type: Multiple choice Chapter: 24 Blooms: Applying Difficulty: Moderate 37. Burkitt’s lymphoma results from the overproduction of: a. Fos. b. Myc. c. Ras. d. Src. Ans: b Question Type: Multiple choice Chapter: 24 Blooms: Remembering Difficulty: Easy 38. What renders erbB and her2 oncogenic? What are their normal proto-oncogene counterparts? Ans: ErbB and her2 both encode constitutively active receptor tyrosine kinases. That is, they encode proteins that transduce a growth-promoting signal even in the absence of ligand binding. ErbB is a mutant form of the EGF receptor, and Neu is a mutant form of the Her2 receptor. ErbB possesses a deletion in the extracellular domain; Neu possesses a point mutation. Both mutant receptors dimerize and become active as kinases in the absence of ligand. Question Type: Essay Chapter: 24 Blooms: Understanding Difficulty: Moderate 39. Explain how the chemotherapeutic drug Gleevec works in the treatment of myelogenous leukemia. Ans: Gleevec specifically targets the fusion protein Abl kinase that is present in CML cells. It inhibits Abl kinase activity and is highly lethal to CML cells but does not inhibit normal tyrosine kinase activity. Question Type: Essay Chapter: 24 Blooms: Understanding Difficulty: Moderate Section 24.5 40. Which of the following proteins belong to the control system that regulates cells past a certain point in late G1 (START)? a. CDK4 b. cyclin B c. Rb d. CDK4 and Rb Ans: d Question Type: Multiple choice Chapter: 24 Blooms: Understanding Difficulty: Moderate 41. A gain-of-function mutation in _____ will bypass restriction point controls. a. cyclin D b. p16 c. Rb d. cyclin D and p16 Ans: a Question Type: Multiple choice Chapter: 24 Blooms: Applying Difficulty: Moderate 42. The human papillomavirus E7 protein inhibits the function of: a. p53. b. Rb. c. PDGF receptor. d. all of the above Ans: b Question Type: Multiple choice Chapter: 24 Blooms: Remembering Difficulty: Easy 43. MicroRNAs are a new class of oncogenic factors because they function: a. as tumor suppressors. b. as oncogenes. c. to induce errors during DNA replication. d. as tumor suppressors and as oncogenes. Ans: d Question Type: Multiple choice Chapter: 24 Blooms: Understanding Difficulty: Moderate 44. Mutation of p53 is described as a dominant-negative mutation. Describe the mechanism by which this mutation causes the dominant-negative phenotype. Ans: Mutation of p53 is a dominant mutation because the active protein is a tetramer of identical subunits; the presence of even one defective subunit in the complex abrogates its function. It is a negative mutation because the normal function of the protein is lost. Question Type: Essay Chapter: 24 Blooms: Analyzing Difficulty: Moderate