Distinguish between tumor suppressor genes and proto-oncogenes. What are their normal functions in cell proliferation?

Distinguish between tumor suppressor genes and proto-oncogenes. What are their normal functions in cell proliferation? How do they work to suppress or promote tumor formation? Which class of genes requires mutations at both loci in a diploid organism, and which class requires only one copy to be mutated? Which genes are proto-oncogenes in the growth factor controlled pathway? What kind of mutations (gain-of-function or loss-of-function) in these genes can cause hyper-proliferation? Why do loss-of-function mutations of tumor suppressor genes drive cells towards cancer? Understand why P53 and Rb are classified as tumor suppressors. How does P53 activity prevent DNA replication in the presence of DNA damage? In the colorectal tumor syndrome that begins with the loss of the Adenomatous Polyposis Coli (APC) gene, a common sequence of mutations often follows: the loss of APC leads to large numbers of polyps, the ras protein is mutated, the p53 protein function is lost. Briefly explain how this series of changes can contribute to the development of benign polyps into malignant tumors. (Note: The Adenomatous Polyposis Coli (APC) gene is different from the Anaphase Promoting Complex (also called APC) gene!!) How does developing more sensitive and more accurate detection techniques help to fight cancer? What is the genetic cause for CML? Why is Gleevec effective in treating CML? One of the major break-throughs in cancer treatment is the development of anti-immune-checkpoint antibodies. Explain how this type of antibodies help to eliminate cancer cells in certain types of cancer, such as metastatic melanoma. What are the main environmental and lifestyle factors that influence the incidence of cancer?