Distinguish between oncogenes and proto-oncogenes. In what ways can proto-oncogenes be converted to oncogenes?

How do translocations such as the Philadelphia chromosome contribute to cancer?

If a cell suffers damage to its DNA while in S phase, how can this damage be repaired before the cell enters mitosis?

Explain why many oncogenic viruses contain genes whose products interact with tumor-suppressor proteins.

Part of the Ras protein is associated with the plasma membrane, and part extends into the cytoplasm. How does the Ras protein transmit a signal from outside the cell into the cytoplasm? What happens in cases where the ras gene is mutated?

Describe the steps by which the TP53 gene responds to DNA damage and/or cellular stress to promote cell-cycle arrest and apoptosis. Given that TP53 is a recessive gene and is not located on the X chromosome, why would people who inherit just one mutant copy of a recessive tumor-suppressor gene be at higher risk of developing cancer than those without the recessive gene?

Of the two classes of genes associated with cancer, tumor-suppressor genes and oncogenes, mutations in which group can be considered gain-of-function mutations? In which group are the loss-of-function mutations? Explain.