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1. If the stability of p53 is increased due to a mutation, what effect would you anticipate on cell cycle progression? 2. Can you provide a molecular mechanism that might contribute to the elevation of cyclin D levels? 3. Do you think that the deletion or inactivation of p16 would lead to comparable abnormalities as the overexpression of cyclin D?

1. If the stability of p53 is increased due to a mutation, what effect would you anticipate on cell cycle progression? 2. Can you provide a molecular mechanism that might contribute to the elevation of cyclin D levels? 3. Do you think that the deletion or inactivation of p16 would lead to comparable abnormalities as the overexpression of cyclin D?

Biology 2e
Biology 2e
2nd Edition
ISBN:9781947172517
Author:Matthew Douglas, Jung Choi, Mary Ann Clark
Publisher:Matthew Douglas, Jung Choi, Mary Ann Clark
Chapter5: Structure And Function Of Plasma Membranes
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Instructions: Provide essay-type responses that are well-organized, thorough, and demonstrate a deep understanding of the clinical case and related medical concepts. Use clear and concise language, and support your ideas with relevant and reliable sources of information. Some references are provided in the picture.

CLINICAL CASE STUDY 1: Checkpoints, Cancer, and Proliferation The cell cycle involves the coordination of cell growth with cell division, which is regulated by distinct proteins that are synthesized and degraded at different stages. The cell cycle also has checkpoints that pause molecular activity to ensure that each stage is complete before moving forward. Defective checkpoints can lead to uncontrolled cell division and mutations, resulting in tumor formation. p53 is a commonly mutated tumor-suppressor gene that normally functions in checkpoint control during the cell cycle. When DNA damage signals are detected, a cascade of kinase activities lead to phosphorylation and stabilization of p53. This results in an increase in active p53, which binds to promoter sequences and controls gene expression of other proteins, such as p21. Increased levels of p21 inhibit the activity of cyclin/CDK complexes, which halts the cell cycle. The p16 protein is another important cell cycle inhibitor that inhibits the Cyclin D/Cdk1 complex, which is required to pass the restriction point and progress into Sphase. Overexpression of cyclin D can cause premature progression through the restriction point and increase cell proliferation, which is found in some tumors, including breast tumors and B-cell tumors that affect antibody production. Guide Questions: 1. If the stability of p53 is increased due to a mutation, what effect would you anticipate on cell cycle progression? 2. Can you provide a molecular mechanism that might contribute to the elevation of cyclin D levels? 3. Do you think that the deletion or inactivation of p16 would lead to comparable abnormalities as the overexpression of cyclin D? Where can I find additional information? Tomasini, R., T.W. Mak and G. Melino, The impact of p53 and p73 on aneuploidy and cancer. Trends in cell biology, 2008. 18: p. 244-252. 2. Oren M, Rotter V. Mutant p53 gain-of-function in cancer. Cold Spring Harb Perspect Biol. 2010;2(2):a001107. doi:10.1101/cshperspect.a001107
Transcribed Image Text:CLINICAL CASE STUDY 1: Checkpoints, Cancer, and Proliferation The cell cycle involves the coordination of cell growth with cell division, which is regulated by distinct proteins that are synthesized and degraded at different stages. The cell cycle also has checkpoints that pause molecular activity to ensure that each stage is complete before moving forward. Defective checkpoints can lead to uncontrolled cell division and mutations, resulting in tumor formation. p53 is a commonly mutated tumor-suppressor gene that normally functions in checkpoint control during the cell cycle. When DNA damage signals are detected, a cascade of kinase activities lead to phosphorylation and stabilization of p53. This results in an increase in active p53, which binds to promoter sequences and controls gene expression of other proteins, such as p21. Increased levels of p21 inhibit the activity of cyclin/CDK complexes, which halts the cell cycle. The p16 protein is another important cell cycle inhibitor that inhibits the Cyclin D/Cdk1 complex, which is required to pass the restriction point and progress into Sphase. Overexpression of cyclin D can cause premature progression through the restriction point and increase cell proliferation, which is found in some tumors, including breast tumors and B-cell tumors that affect antibody production. Guide Questions: 1. If the stability of p53 is increased due to a mutation, what effect would you anticipate on cell cycle progression? 2. Can you provide a molecular mechanism that might contribute to the elevation of cyclin D levels? 3. Do you think that the deletion or inactivation of p16 would lead to comparable abnormalities as the overexpression of cyclin D? Where can I find additional information? Tomasini, R., T.W. Mak and G. Melino, The impact of p53 and p73 on aneuploidy and cancer. Trends in cell biology, 2008. 18: p. 244-252. 2. Oren M, Rotter V. Mutant p53 gain-of-function in cancer. Cold Spring Harb Perspect Biol. 2010;2(2):a001107. doi:10.1101/cshperspect.a001107
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