1. Suppose you identified a new gene and suspect that it may be an oncogene. What are some characteristics that you would look for and how would you test for them?
2. What role have viruses played in the discovery of oncogenes and what roles do they currently have in cancer research?
3. Imagine you are a cancer researcher and you want to create tumors in a mouse to test some potential anti-cancer compounds. What types of genes would you want to mutate? What are their functions and how would you turn them into oncogenes?
4. What are some ways in which oncogenes can be inactivated?
5. How can inactivating one oncogene cause tumor regression? Why would this not necessarily cure cancer?
6. What kinds of effects would you expect an effective anti-cancer compound to have on oncogenes?
7. What sort of things act on proto oncogenes to turn them into oncogenes? What are the sources of these mutations? Does this depend on the type of cancer?
8. What methods do viral infections cause the transformation of normal cells?
9. How does prolonged viral infection result in increased rates of cancer?
10. Explain the experimental rational of a colony-forming assay. What are the advantages and limitations of implementing this protocol when trying to identify potential oncogenes?
11. Suppose you identify a tumor that appears 'oncogene addicted' to the KRAS oncogene. How would you design your therapeutic if the oncogene addiction had resulted from i) genetic streamlining ii) oncogene shock iii) synthetic lethality?
12. Design an experimental assay in which you prove that a tumour is oncogene addicted as a result of genetic streamlining.
13. Propose advantages and disadvantages for drug designing based upon oncogene addiction hypotheses.