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Cancer Biology genetics question:

A) Proto- oncogene, oncogene (should know at least 1 example andhow it acts)

B) tumor suppressor gene (should know at lease one example andhow it acts)

C) define benign tumor, malignant tumor, metastaste?

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Jarrod Robel
Jarrod RobelLv2
28 Sep 2019
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Related questions

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?

The Myc gene is a very important proto-oncogene that encodes the Myc transcription factor. The Myc gene is normally only expressed in response to the presence of growth factors, and once expressed the Myc protein promotes passage through the restriction point by activating the transcription of early cell cycle genes. As an indication of the importance of Myc, overexpression of the Myc protein is sufficient to cause tumorigenesis in many cell types. For example, Burkitt’s lymphoma is the result of a chromosomal translocation that leads to increased myc expression in B-lymphocytes.

(A) (3 pts) What is the restriction point, and which CDK complex is most directly activated by passage through the restriction point?

(B) (10 pts) Describe how activation of the CDK complex from part (A) leads to entry of cells into S-phase. Your answer must indicate the protein(s) that this CDK directly acts on, the proteins that directly stimulate S-phase entry, and the mechanism that prevents premature entry into S-phase.

(C) (8 pts) Indicate whether each protein you mention in part (B) is a proto-oncoprotein (e.g. a protein encoded by a proto-oncogene) or a tumor suppressor. You can incorporate this into your answer to part (B) if you choose.

(D) (4 pts) Why does the overexpression of Myc lead to cancer, for example Burkitt’s lymphoma?

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).

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