Life: The Science of Biology
11th Edition
ISBN: 9781319010164
Author: David E. Sadava, David M. Hillis, H. Craig Heller, Sally D. Hacker
Publisher: W. H. Freeman
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Chapter 13.4, Problem 2R
Summary Introduction
To review: The consequences of mismatch mutation in the formation of cancer.
Introduction:
There are many oncogenes and tumor suppressor genes that are involved in the formation of a single tumor. Two vital oncogenes that were identified were Myc and Ras and their expression regulates the cell cycle and avoids apoptosis process. Experiments reveal that it takes the expression of both the oncogenes to set the motion of the cell cycle in the cells of the mouse and then converts them into the tumor cells. The experiment is explained below:
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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.
Some cancers are consistently associated with the deletion of a particularpart of a chromosome. Does the deleted region contain an oncogene or atumor-suppressor gene? Explain.
Explain 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?
Chapter 13 Solutions
Life: The Science of Biology
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- What cell-cycle events will be affected in a cell that produces mutated (non-functional) cohesin protein?arrow_forwardDuring M phase of the cell cycle, how M-Cdk can trigger cohesin dissociation?arrow_forwardThe p53 protein regulates the expression of BAX and Bcl2 to keep division at normal rate. Explain how is this achieved?arrow_forward
- In cell cycle, under the control system, explain in details (including roles of related proteins): During M phase, how M-Cdk can trigger cohesin dissociation as well as Mad2 triggers mitotic checkpoint to delay metaphase to anaphase transition.arrow_forwardBriefly describe three ways that ATP-dependent chromatin-remodeling complexes may change chromatin structure.arrow_forwardDescribe the steps by which the TP53 gene responds to DNA damage and/or cellular stress to promote cell-cycle arrest and apoptosis. Given that TP53 is a recessive gene and is not located on the X chromosome, why would people who inherit just one mutant copy of a recessive tumor-suppressor gene be at higher risk of developing cancer than those without the recessive gene?arrow_forward
- Classify the following genes as proto-oncogenes or tumor-suppressor genes: p53, ras, Bcl-2, telomerase, jun, andarrow_forwardYou are working in a cell biology lab that investigates non-small cell lung cancer cells, which of these cellular features will be suggestive of senescence in the cells observed? Choose all that apply: Group of answer choices Large flattened morphology Reduced incorporation of 5-bromodeoxyuridine (in DNA replication) Increased p53 expression Decreased expression of p15INK4Barrow_forwardA second hit might also occur through loss of heterozygosity (LOH). An example of how LOH may occur by reciprocal crossing over during mitosis is diagrammed in the figure attached. Discuss and interpret this model. Write a brief explanation of (a) what LOH means and (b) how LOH by mitotic reciprocal crossing over can give rise to a cell lineage with functional loss of the wild-type copy of a tumor suppressor gene.arrow_forward
- Describe how Ras and p53 can alter the simplified genetic pathway controlling cell division shown below. For each of the two genes, would uncontrolled cell division result from a loss-of-function or a gain-of-function mutation? growth factors - receptors - cyclins - cyclin-dependent kinases - cell divisionarrow_forwardIn cell cycle, under the control system, explain in details (including roles of related proteins): a) How mitogens trigger transcription of genes for entry into S phase. b) During M phase, how M-Cdk can trigger cohesin dissociation as well as Mad2 triggers mitotic checkpoint to delay metaphase to anaphase transition.arrow_forwardBenign and cancerous tumors occur when the cell cycle control mechanisms no longer operate correctly. What types of genes may be involved in these cell cycle control mechanisms?arrow_forward
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