Biological Science (6th Edition)
6th Edition
ISBN: 9780321976499
Author: Scott Freeman, Kim Quillin, Lizabeth Allison, Michael Black, Emily Taylor, Greg Podgorski, Jeff Carmichael
Publisher: PEARSON
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Chapter 12, Problem 16PIAT
Inhibiting expression of the stathmin gene arrests cells in M phase and is being investigated as an alternative therapy for treating cancer. What additional genes could be therapeutic targets that, when inactivated, would arrest cancerous cells in G1 phase?
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Chapter 12 Solutions
Biological Science (6th Edition)
Ch. 12 - 1. Which statement about the daughter cells...Ch. 12 - After S phase, what comprises a single chromosome?...Ch. 12 - Progression through the cell cycle is regulated by...Ch. 12 - 4. What major events occur during anaphase of...Ch. 12 - 5. Identify at least two events in the cell cycle...Ch. 12 - 6. What evidence suggests that during anaphase,...Ch. 12 - 7. Evaluate each of the following defects. Which...Ch. 12 - Prob. 8TYUCh. 12 - Prob. 9TYPSSCh. 12 - Prob. 10TYPSS
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- Describe the effects of the mutation causing the p21 promoter to no longer bind p53 on cell signaling pathways and metabolism or cell cycle control.arrow_forwardIn your own words: Describe the molecular mechanisms involved in P53’s role as a tumor repressor protein.arrow_forwardWhich of the following statements are correct about cytoplasmic signaling in cancer cells? Multiple answers. A. Only minor modifications of cell control machinery are required for normal cells to become highly proliferating cancer cells B. Immediate early genes are induced in the presence of protein synthesis inhibitors C. Many immediate -early genes are oncogenes D. Delayed early genes are highly expressed in the presence of protein synthesis inhibitors E. Delayed early genes are highly expressed in normal cells in the absence of growth factorsarrow_forward
- Describe the molecular mechanisms involved in P53’s role as a tumor repressor proteinarrow_forwardCancer-promoting mutations are likely to have different effects on the activity of proteins encoded byproto-oncogenes than they do on proteins encodedby tumor-suppressor genes. Explain.arrow_forwardDiscuss 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.arrow_forward
- The p53 gene was discovered in 1979, but it was not clear whether the gene functioned as an oncogene or a tumor-suppressor gene. Several years later, researchers showed that both p53 alleles are inactivated in some mouse cancers. This evidence suggests A. the p53 gene is an oncogene because inactivated alleles would produce mutated signal transduction proteins that would result in stimulating cell division. B. the p53 gene is an oncogene because the cell would overproduce transcription factors to compensate for the inactive alleles, resulting in increased cell division. C. the p53 gene is a tumor-suppressor gene because inactivated alleles indicate a loss of protein function which allowed the cancer to develop D. the p53 gene is a tumor-suppressor gene because the cell would produce too few transcription factors for gene activation, resulting in decreased cell division.arrow_forwardRole of Myc activation is the follows a. It directly inhibits Rb protein through phosphorylation b. It stimulates assembly of S-phase Cdk-cyclin complex c. It stimulates transcription of delayed response genes d. It increases the expression of early response genes Role of Myc activation is the follows a. It directly inhibits Rb protein through phosphorylation b. It stimulates assembly of S-phase Cdk-cyclin complex c. It stimulates transcription of delayed response genes d. It increases the expression of early response genesarrow_forwardYou are looking at the results of a western blot from the lysates of cells harvested from a suspected breast cancer tumor and you see that there is an increased expression of INK4-p16, you suspect that this will______________? Group of answer choices Increase S to G2 phase transition Initiate a cell cycle arrest in G1 Block M to G1 phase transition Promote tumorigenesisarrow_forward
- Distinguish 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_forwardPersonalized cancer treatments involve identifying specific pathways in an individual tumor and selecting drugs that are effective for the modified pathways. One way to do this is to take culture cells from a biopsy of a specific paient and test the effects of a battery of drugs on the patiets cells in culture. How might heterotypic interactions complicate this strategy? How might cells be cultured differently to minimize these complications (limit 5-6 sentences)?arrow_forwardIn other words, the master regulator initiates a program of gene expression that narrow the potential fates of the precursor's cells’ descendants to the type of cells that participate in the organ’s function. Question: Once a master regulator gene is turned on in some cells and not in others, how do cells “remember” that pattern through all the cell division that occur to form a specific organ?arrow_forward
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