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UConn MCB 3211 - Exam 3 Review Questions 2020

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Review Questions List Exam 31. What is likely a major reason for the increase in cancer risk associated with age?2. Approximately how many rate-limiting steps are involved in cancer development? Approximately how long does eachstep take?3. Based on the rates of cigarette consumption and lung cancer development, provide an estimate for the time requiredfor lung cancer development?4. Is the increased risk of cancer with age due to the accumulation of mutations or an increased susceptibility of older individuals to carcinogens? 5. What is the difference between carcinoma and carcinoma in situ?6. Name the pre-cancerous lesions that form in the mouth, colon, prostate and breast.7. The Vogelgram envisions colon cancer proceeding through a series of stages, starting with tissue hyperplasia, followed by adenoma then carcinoma. Where are the APC, ras and p53 gene mutations on this pathway?8. Do the majority of colon cancers follow the pathway described by the Vogelgram? What type of mutation might substitute for a ras mutation? 9. What is the cancer risk associated with a DCIS lesion? What treatments are used to treat DCIS aggressively? 10. At each step of cancer progression, cells incur additional genetic or epigenetic changes. How do these changes influence their dynamics within the tissue?11. Most chemotherapeutic agents are tested and approved for use based on their ability to reduce tumor mass. Why might this approach to selecting chemotherapies be misguided?12. What does a fluorescent activated cell sorter do and how can it be used to demonstrate the existence of cancer stemcells?13. Name two cell surface markers that are sometimes used to isolate cancer stem cells. What experiment would you do to demonstrate that these markers are enriching the stem cell population of a cancer?14. Why is it useful to know that polyps are pre-neoplastic lesions in the colon? What is the evidence that they are pre-cancerous?15. Approximately how many mutations and/or epigenetic alterations are required to transform a human cell? How many for a mouse cell?16. Which transgenic mouse is more likely to develop a tumor, one with an oncogene expressed in a stem cell, or one with the oncogene expressed in differentiated cells?17. How does cancer risk in humans relate to the number of stem cell divisions in a tissue?18. What is the difference between a replicative and deterministic cancer?19. How does the cancer stem cell model influence the way we should think about cancer therapy?20. What type of cancer is likely to be more aggressive, one with many stem cells, or one with many differentiated cells?21. Suppose you had a mouse, a bottle of DMBA and a bottle of TPA. Describe exposure paradigms (using both DMBA and TPA) that would generate: a transient papilloma, a stable papilloma and a malignant carcinoma?22. How does an initiating agent differ from a tumor promoting agent?23. What is the difference between tumor promotion and tumor progression?24. What is the cellular target of TPA? Name three downstream cellular pathways activated by TPA. 25. Describe two lines of evidence that suggest that breast cancer development is promoted by estrogen and other hormones. 26. How is estrogen thought to increase breast cancer risk?27. Describe the interaction between aflatoxin and HBV on the development of hepatocellular carcinoma.28. How do TNF and NFkB interact to promote cancer development?29. What enzyme(s) do NSAIDs and coxibs inhibit? What product of this enzyme is particularly relevant to cancer promotion? 30. Why were Cox-2 inhibitors anticipated to have fewer side effects than NSAIDs for cancer prevention?31. Coxibs are thought to be dangerous because they increase the risk of: ______.32. When a stem cell undergoes asymmetric cell division, what are the two cell types typically formed?33. List three ways stem cells protect their genomic DNA. 34. What are the two main lineages derived from hematopoietic stem cells? List two differentiated cell types derived from each lineage.35. Some people believe that cancers form from mutated stem cells. What data from the study of CML supports this theory? 36. Many DNA polymerases have two catalytic activities. What are they? 37. What is the phenotype of a mouse in which the proof-reading activity of DNA polymerase has been eliminated through mutation?38. When a mistake occurs during DNA replication, it is important for the cell to identify which base is correct and which is incorrect. What clue is used by the repair machinery to determine which base(s) to remove?39. What is a microsatellite and how can they lead to random base insertions and deletions in the DNA sequence? 40. Some (but not all) cancers display microsatellite instability. How does this instability usually arise? 41. Many bases undergo deamination, but deamination of 5-methylcytosine is very frequent. What base is formed when 5-methylcytosine undergoes deamination?42. What products are formed from single electron reduction of O2 to H2O? 43. Name 3 sources of reactive oxygen species in living tissue.44. Would you expect a mouse with a deleted 8-oxo-deoxyguanosine glycosylase to have a higher or lower cancer risk?45. Compare how X rays and UV damage DNA. 46. What are the two major photoproducts formed by UV radiation?47. Many environmental agents can alkylate DNA. What is the specialized repair mechanism used by the cell to repair this type of damage?48. Many carcinogens enter the body as non-reactive pro-carcinogens. How do they become carcinogens? 49. Why do cytochrome P450 enzymes attach oxygen molecules to pro-carcinogens? 50. List three cytochrome P450 substrates that are thought to be human pro-carcinogens and indicate where they come from.51. Many dietary pro-carcinogens are absorbed by the small intestine. What is their next destination and where does most of their metabolism usually occur?52. What are phase I and phase II enzymes?53. What is glutathione and how do glutathione-S-transferases protect cells from carcinogens? 54. Name a cruciferous vegetable and one of its “active” ingredients with regard to cancer prevention.55. How does sulforaphane impact Keap1 and Nrf2 in the cell? What kind of proteins are Keap1 and Nrf2?56. Compare base excision DNA repair and nucleotide excision repair. What types of lesions are repaired by BER and which are repaired by NER?57. How many XP genes are there? Are XP individuals homozygous or heterozygous at a mutant XP locus?58. Most


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