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Part I - Describe DNA Mutations: Definition: Define a mutation. Are they good or bad? What types of mutations can occur in the DNA? What can cause a mutation? Can mutation be “fixed”? What are the requirements for normal cell division? What are the requirements for cancer cells to divide and grow? Define the difference between a benign tumor, a malignant tumor, and metastatic cancer. Part 2 – Describe DNA Damage: Definition: Define DNA damage. What are some causes of DNA damage? What affect does DNA damage have? Will replication proceed normally? If DNA damage is not repaired, what affect will it have? Can DNA damage be repaired? If DNA damage is not repaired, what affect will it have on the cell cycle (cell division)?

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Nestor Rutherford
Nestor RutherfordLv2
28 Sep 2019

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Related questions

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).

Cancer biologists use principles of evolution to understand the development of tumors. A population of cells can obtain a mutation after exposure to a carcinogen. In some of the cells, the mutation is not repaired by the cell’s DNA repair machinery and is retained in the genotype. Only a fraction of the cells retaining the mutation become cancerous and only a fraction of those cells have the ability to form a tumor – cells that grow much faster than normal body cells. From the perspective of a tumor-causing cell, what evolutionary processes are at work? From the perspective of the body harboring these tumor cells, what evolutionary processes are at work?

Cancer biologists use principles of evolution to understand the development of tumors. A population of cells can obtain a mutation after exposure to a carcinogen. In some of the cells, the mutation is not repaired by the cell’s DNA repair machinery and is retained in the genotype. Only a fraction of the cells retaining the mutation become cancerous and only a fraction of those cells have the ability to form a tumor – cells that grow much faster than normal body cells. From the perspective of a tumor-causing cell, what evolutionary processes are at work? From the perspective of the body harboring these tumor cells, what evolutionary processes are at work?

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