Human Anatomy & Physiology (11th Edition)
11th Edition
ISBN: 9780134580999
Author: Elaine N. Marieb, Katja N. Hoehn
Publisher: PEARSON
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Discuss the complete cell cycle in a human cell, mitosis and meiosis, and the regulatory components (i.e. the proteins associated with cellular checkpoints) of the cell cycle.
Tumor growth results when the cell cycle checkpoints are ignored. Give an example of how tumor growth could result from either a loss-of-function or a gain-of-function mutation.
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- Select the statements that accurately describe different ways that translocations could lead to cancer. A translocation breaks up the sequence of a gene for a protein that stimulates apoptosis. The resulting protein cannot function properly. A gene for a protein that stimulates apoptosis is placed next to a regulatory sequence that increases the expression of the gene. A translocation breaks up a gene that encodes a protein required to pass through mitotic checkpoints. The resulting protein cannot function normally. A gene for a protein that is involved in a mitotic checkpoint is placed next to the regulatory sequence of a different gene. The gene is now expressed at inappropriate times. A new sequence is added to a proto-oncogene. The modified gene now produces a new protein that increases the rate of cell division.arrow_forwardIdentify 2 proteins important for cell cycle regulation and explain why they play a critical role in cancerarrow_forwardExplain the molecular mechanisms of cancers caused by a P53 gene mutation.arrow_forward
- The 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_forwardProtein N, normally inactivates a tumor suppressor protein. Consider a cell with a mutation in one allele such that protein N is nonfunctional, while the other allele of gene N is wild-type. Which of the following is true for this cell? Gene N is a tumor suppressor gene, and the phenotype of the cell is not transformed. Gene N is a proto-oncogene, and the phenotype of the cell is transformed. Gene N is a tumor suppressor gene, and the phenotype of the cell is transformed. Gene N is a proto-oncogene, and the phenotype of the cell is not transformed.arrow_forwardExplain the concept of loss of heterozygosity (LOH). Why do most cancer cells exhibit LOH of one or more genes? How does failure of the spindle assembly checkpoint lead to loss of heterozygosity?arrow_forward
- Explain the difference between proto-oncogene and tumor suppressor mutations in terms of its potential to cause cancer.arrow_forwardWhich type of mutation would NOT be involved in the inactivation of a tumor suppressor gene? gain-of-function mutation in the tumar suppressor gene loss of a whole chromosome containing the tumor suppressor gene O silencing of the gene's activity by epigenetic changes chromosomal deletion of a region containing the tumor suppressor genearrow_forwardIdentify one way in which a specific cancer evades the controls of the cell cycle. Describe in a one paragraph.arrow_forward
- What might explain the association between malignant tumors and chromosomal abnormalities? What's the difference between cancer cells and normal cells? Consider cell cycle checkpoints, density dependency, anchorage-dependency, and growth hormones like PDGFarrow_forwardA. Name the two proteins that induce a negative feedback in this pathway and explain why both feedback mechanisms exist? B. Discuss how a mutation resulting in an aberrant protein could cause changes in the cell cycle leading to uncontrolled cell division. Explain what the effect of the mutation would be on the protein’s function and what the effect will be on downstream proteins leading to enhanced cell cycle progressionarrow_forwardCancer cells typically lose cell cycle entry control. Explain how the following mutations, which are found in some cancer cells, lead to a bypass of these controls: (a) overexpression of cyclin D, (b) loss of Rb function, (c) loss of p16 function, (d) hyperactive E2F.arrow_forward
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