In a laboratory cell culture, many tumor cell lines divideuncontrollably. Some of

the cell lines have mutant tumor suppressor gene. Adding awild-type copy of this

tumor suppressor gene reduces the ability of the cell line todivide in culture.

Why would adding a wild type copy of a proto-oncogene to a tumorcell line with an

activated oncogene not have any effect on the uncontrolledgrowth of the cell line?

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Patrina SchowalterLv2

28 Sep 2019

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You are an oncologist with three patients:

Patient 1 has a tumor causing mutation in a pro-growth gene. The mutated protein allows the cell to grow without receiving growth signals from outside the cell. Is the mutated gene an oncogene or a tumor suppressor? Why? Which hallmark is the gene associated with?

Patient 2 has a tumor which contains a loss of function mutation in the P53 gene. How would you determine if it is a somatic or germ line mutation

Patient 3 has a tumor causing mutation in a gene called telomerase. The function of telomerase is to lengthen the ends of chromosomes. What hallmark is telomerase associated with? Is the mutation gain of function or loss of function? (Hint: to answer this question, you need to understand which hallmark telomere length is associated with)

You are interested in studying the origins of cancer and join a research lab to do so. You find that many cancer cell lines have mutations in the gene DRG1. You further investigate the mutations to DRG1 and find that some of the cell lines have mutations that affect expression of DRG1, so that no DRG1 mRNA is made in these cells, while other cell lines have mutations that lead the cells to produce a non-functional DRG1 protein.

a) Is DRG1 a proto-oncogene or a tumor suppressor? Explain your reasoning.

b) Your labmates propose several hypotheses about the possible role for DRG1 in normal cells. For each hypothesis, state whether or not you think it makes sense and explain your reasoning. a. DRG1 normally acts to repair DNA damage. b. DRG1 is a receptor for a mitogen (a signaling molecule that promotes cell division)

c. DRG1 is a receptor for a signaling molecule that causes apoptosis (programmed cell death).

1.) You are studying a particular type of cancer. You observe that the cells are expressing higher than normal levels of the activated version of the G protein Ras (ie, they contain more Ras-GTP than normal).

a.(2 pts) Further study shows that the one of the Ras genes has been mutated, would you classify this as the mutation of a tumor-suppressor gene or an oncogene?

b.(2 pts) Given your knowledge of the regulation of G proteins, suggest an explanation for how this mutant Ras protein results in more Ras-GTP than normal.

c.(2 pts) In a different cancer you also observe an increase in the activated form of Ras, however, in this case, the mutation has occurred in both copies of a gene encoding a protein that normally interacts with Ras. The mutant forms of the protein no longer interact with Ras and this leads to inappropriate growth. Since the mutation leads to cancer, would this loss of function be an example of an oncogene or a tumor-suppressor? Can you suggest a function for this protein?

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