CAMPBELL BIOLOGY IN FOCUS-TEXT,AP ED.
3rd Edition
ISBN: 9780136811206
Author: Urry
Publisher: SAVVAS L
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Chapter 16.3, Problem 1CC
Summary Introduction
To discuss:
How mutation in protein coding genes functioning in apoptosis can lead to cancer.
Introduction:
Apoptosis is defined as the programmed cell death (PCD). It is a process, which only occurs in multi-cellular organisms. The cells undergoing PCD include blebbing, fragmentation of DNA (deoxyribonucleic acid), cell shrinkage, and engulfment by the phagocytes.
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Explain how p53 functions as a tumor suppressor gene. How can mutations in p53 lead to cancer, and how might gene therapy or other drug interventions inhibit the growth of a tumor?
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Chapter 16 Solutions
CAMPBELL BIOLOGY IN FOCUS-TEXT,AP ED.
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- How can a defect in p53 gene contribute to cancer development?arrow_forwardExplain the role of p53 protein in protecting normal cells against cancer. With respect to this protein and its function, explain how a normal cell turns cancerous.arrow_forwardThe p53 gene is a tumor-suppressor gene while Ras is a proto-oncogene. Mutation in either one can result in the transformation of a normal cell into a cancer cell. Explain the difference between the functions of the two proteins and how their mutation can lead to cancer development.arrow_forward
- What would be the effect of a mutation that inactivates the p14ARF tumor suppressor upon p53 functions?arrow_forwardDistinguish between proto-oncogenes and tumor-suppressor genes. To become cancer promoting, do proto-oncogenes and tumor-suppressor genes undergo gain-of-function or loss-of-function mutations? Classify the following genes as proto-oncogenes or tumor-suppressor genes: p53, ras, BCL-2, JUN, MDM2, and p16.arrow_forwardOverexpression of the Myc protein is a common feature of many types of cancer cells, contributing to their excessive cell growth and proliferation. By contrast, when Myc is overexpressed in most normal cells, the result is not excessive proliferation, but cell-cycle arrest or apoptosis.Which one of the following statements provides the most likely explanation for why overexpression of Myc can have such different outcomes in normal cells and in cancer cells? A. Normal cells contain checks and balances that prevent Myc-induced proliferation. B. In normal cells, Myc protein acts as a mediator in cell-cycle arrest and apoptosis. C. The target protein for Myc-induced proliferation is missing from most normal cells. D. In normal cells, when Myc is overexpressed, the excess Myc protein precipitates.arrow_forward
- Why is it important to model cancer through the generation of induced pluripotent stem cells ? Please list item by item. Explain in detail the main findings.arrow_forwardCancer is caused by many different types of gene mutations. Some mutations are in proto-oncogenes, which lead to overexpression of the genes, and other mutations are in tumor suppressor genes, which lead to under expression or no expression in these genes. Which kinds of gene mutations would RNA interference (RNAi) be better at treating? Explain.arrow_forwardThe p53 gene is a tumor-suppressor gene while p634 gene is an oncogene. Mutation in either one can result in the transformation of a normal cell into a cancer cell. Explain the difference between the functions of the two proteins and how their mutation can lead to cancer development.arrow_forward
- Can restoring tumor suppressor function, such as mutant p53 or pRb, be used to cure cancer? If that's the case, how is it possible?arrow_forwardp53 iš an important tumor suppressor gene that is activated in response to a variety of stress signals. Upon activation it induces a cell cycle arrest or cell death. Hence, loss-of-function mutations in the p53 gene are found in almost every type of cancer. How do you predict loss-of-function mutations in the DNA binding domain of the p53 protein affect its function? OIt no longer will act as activator of gene expression O It no longer will act as repressor of gene expression O It no longer will act as activator or repressor of gene expression O It no longer will act as coactivator or corepressorarrow_forwardCellular levels of tumor suppressor protein p53 is maintained by a ubiquitin ligase protein, called Mdm2. Over expression of Mdm2 destabilizes p53. Another protein p19ARF inhibits the activity of Mdm2, thus stabilizing p53. Loss of p19ARF function converts normal cells into cancer cells With the above information, which of the following statements are true? Mdm2 is a tumor suppressor gene but p19ARF is an oncogene Both Mdm2 & P19ARF are oncogenes Both Mdm2 & P19ARF are tumor suppressor genes O Mdm2 is an oncogene but p19ARF is a tumor suppressor genearrow_forward
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