CONCEPTS - Study Questions.docx

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Department
Biochemistry
Course
Biochemistry 4450A
Professor
Caroline Schild- Poulter
Semester
Fall

Description
CONCEPTS – Study Questions Lecture 3: Cancer Genes I – Viruses and RB 1. What is an oncogene? How are they created? In humans, how are most oncogenes created? 2. What is a proto-oncogene? How are they activated? How do they gain the ability to become activated? 3. What are the prefixes given to proto-oncogenes and oncogenes? What do they mean? 4. What is a tumor suppressor gene? How do mutations affect these genes? Are viruses able to cause the same result as the mutation? What other effects cause their loss of function? 5. What is the typical function of tumor suppressor genes? 6. Which viruses are able to create tumors in humans? What is the name of the proteins they carry that do this? How do they create tumors? 7. How were viral proteins used to determine important cell targets? What were the proteins used and which virus did they come from? What were the important cellular targets? 8. What are the 4 characteristics of nearly all cancer cells? 9. How do cancer cells differ from normal cells when grown in a petri dish? What do normal cells undergo that cancer cells do not? 10. What type of growth signal occurs in normal cells that is absent from cancer cells and what is the result? 11. What happens to cancer cells when they’re grown without firm attachment? How does this differ from normal cells? Why do they differ? 12. What is the restriction point? Why is it important? When do normal cells pass the restriction point? How does this differ from cancer cells? 13. How can normal cells be transformed into cancer cells? What occurs in the transformed cells? 14. What is the importance of pRB in cell cycle entry? Which entry point does it control? What occurs in normal cells at this point? 15. What are p16 and p21? How do they affect pRB? 16. What are the pathway components of the RB pathway in cancer? What mutations occur in each component? What types of mutations are these? 17. What viral protein can directly inhibit RB? What is the most common way to remove RB function? 18. Why is understanding RB function in cancer important? 19. What proteins does RB bind to? What does it inhibit? What happens when it’s phosphorylated? 20. Which gene is mutated to remove RB function? How does this occur? What is the role of cre? 21. What cell state does loss of RB all the cell to escape? 22. What are the implications of restoring RB function? Lecture 4: Cancer Genes 2 – Ras and p53 1. What cancer syndrome is caused by inherited p53 mutations? 2. How does the mouse model for cancer differ from humans in respect to p53 function? 3. Which gene is the most mutated gene in cancer cells? Why is it the most mutated gene? 4. What is the function of p53? How is it activated? What are the types of signals that activate p53? 5. What is the function of MDM2? How is it inhibited? What occurs to p53 to prevent its binding to MDM2? 6. How is p53 turned off (attenuated)? What types of feedback mechanisms are used? 7. What are the targets of p53? What is the cellular response to p53 binding these targets? Which targets result in each cellular response? 8. What is the importance of p21 to p53 function? How does this relate to RB function? 9. What is the importance of mitochondrial proteins? How do they aid in p53’s function? 10. What are the mitochondrial proteins? 11. What proteins are suppressed by p53 function? Why are these proteins suppressed? 12. What parts of the cell does p53 bind? 13. How is p53 altered to either become activated or deactivated? 14. What are the ways p53 can be inactivated by the cell? Which cancers typically use each method? What is the effect of that type of inactivation? Which mutation is the most common on found in cancer? 15. What does p14 ARFusually tell p53 to do? 16. What is a potential target site for chemotherapy drugs in MDM2? Why would this be a good target site? Why is it not useful in every type of cancer? 17. When was v-Ras first identified? What did this work lead to? When was Ras identified as an oncogene? 18. What percentage of cancer cells have mutated Ras? How does the oncogenetic form of Ras differ from the proto-oncogenic form? Does the mutation have to occur in both copies of the gene? 19. How does Ras contribute to cell growth? How does it start signal transduction? 20. Which 2 key residues are often mutated in oncogenetic Ras? What does this mutation cause Ras to do? How does each mutation aid in the constant activation of Ras? Lecture 5: Multistage Progression in Cancer 1. Why do most cancers occur in old age? 2. What does the age-specific aspect of cancer depend on? How does each contribute to cancer development? 3. What are the two types of genetic events that lead to cancer? Which types of genes does each of these events occur in? What are the types of events that create these changes? What is an example of a gene that undergoes each type of change? How does each occur? 4. What is the Philadelphia chromosome? What is it the primary cause of? What is the result of the Philadelphia chromosome? 5. What is abl? What is bcr? Why is the bcr-abl gene important to cancer but the abl-bcr gene unimportant? Which chromosome contains the bcr-abl gene? Which contains the able-bcr gene? 6. How does the fusion of chromosomes 9 and 22 differ between CML and ALL? 7. Why do drugs that target bcr-abl have a high success rate? 8. How does the activation of abl kinase cause leukemia? 9. What is retinoblastoma? What is it caused by? What are the two types of retinoblastoma? What percentage of retinoblastomas have no family history? What percentage have family members with retinoblast
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