Cancer and the Cell Cycle

1) A base analog is a chemical that can bind in place of a nitrogenous base. But why is that a problem? It 5-bromouracil binds in place of thymine, for instance, and if it still binds to adenine, how can this cause a mutation?

2) In the Ames test, what do we know about cells from a stock that was his- that can now grow on minimal medium? If this stock has not been exposed to any putative mutagen, what does the number of these colonies growing on minimal medium represent? So, if we expose replicate samples to a chemical and get more colonies growing on minimal medium, what can we infer about the effect of the chemical? Why might we include liver enzymes?

3) Repair enzymes 'proofread' the DNA during the G1 and G2 periods of the cell cycle. They recognize and correct 'mismatched' base pairs, like A=G. How is the incorrect base identified?

4) UV radiation causes thymidine dimerization. How is this repaired?

5) More intense radiation can cause 'double-stranded breaks' in DNA. Curiously, the 'blunt ends' of the pieces are not just ligated back together. Instead, a rather complicated process is performed of using the identical sister chromatid (in G2, or the homolog in G1) to repair the lesion. What is the benefit of using this method, compared to just ligating blunt DNA ends together?

6) What genetic evidence exists that most tumors have proliferated from a single cell?

7) What are CDK's, how do they exert their effect, and what stimulates their activity? What is E2F and what does it do? Describe the pathway that activates E2F.

8) How do c-myc and p53 proteins influence the CDK-4 pathway?

9) What do the ras family of proteins do? How do they do it?

10) What are the relationships between proto-oncogenes and oncogenes?

11) describe two ways that viruses can cause cancer.