Campbell Biology, Books a la Carte Plus Mastering Biology with eText -- Access Card Package (10th Edition)
10th Edition
ISBN: 9780133922851
Author: Jane B. Reece, Lisa A. Urry, Michael L. Cain, Steven A. Wasserman, Peter V. Minorsky, Robert B. Jackson
Publisher: PEARSON
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Chapter 18.5, Problem 3CC
Summary Introduction
To explain: Effect of cancer-promoting mutations on activity of proteins encoded by proto-oncogenes and tumor-suppressor genes.
Concept introduction:
Spontaneous or induced damage to cells causes mutations. The mutations in genes that regulate cell growth either inhibiting or promoting, result in abnormal uncontrolled growth. The accumulation of these mutations leads to cancer. On the basis of regulation, the genes are categorized as proto-oncogenes and tumor-suppressor genes. Proto-oncogenes are normal growth promoting genes and their mutated forms causing tumor are oncogenes. Tumor-suppressor genes normally inhibit cell proliferation and tumor formation.
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Relatively few inherited forms of cancer involve the inheritance of mutant oncogenes. Instead, most inherited forms of cancer are defects in tumor-suppressor genes. Give two or more reasons why inherited forms of cancer seldom involve activated oncogenes.
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Chapter 18 Solutions
Campbell Biology, Books a la Carte Plus Mastering Biology with eText -- Access Card Package (10th Edition)
Ch. 18.1 - How does binding of the trp corepressor to the trp...Ch. 18.1 - Describe the binding of RNA Polymerase,...Ch. 18.1 - WHAT IF? A certain mutation in E. coli changes...Ch. 18.2 - In general, what are the effects of histone...Ch. 18.2 - Compare the roles of general and specific...Ch. 18.2 - WHAT IF? Suppose you compared the nucleotide...Ch. 18.2 - Once mRNA encoding a particular protein reaches...Ch. 18.3 - Compare miRNAs and siRNAs, including their...Ch. 18.3 - WH AT IF? Suppose the mRNA being degraded in...Ch. 18.4 - MAKE CONNECTIONS As you learned in Chapter 12,...
Ch. 18.4 - MAKE CONNECTIONS Explain how the signaling...Ch. 18.4 - How do fruit fly maternal effect genes determine...Ch. 18.4 - Prob. 4CCCh. 18.5 - MAKE CONNECTIONS The p53 protein can activate...Ch. 18.5 - Under what circumstances is cancer considered to...Ch. 18.5 - Prob. 3CCCh. 18 - Compare and contrast the roles of a corepressor...Ch. 18 - Describe what must happen in a cell for a gene...Ch. 18 - Why are miRNAs called noncoding RNAs? Explsin how...Ch. 18 - Describe the two main processes that cause...Ch. 18 - Compare the usual functions of proteins encoded by...Ch. 18 - If a particular operon encodes enzymes for making...Ch. 18 - Muscle cells differ from nerve cells mainly...Ch. 18 - The functioning of enhancers is an example of (A)...Ch. 18 - Cell differentiation always involves (A)...Ch. 18 - Which of the following is an example of...Ch. 18 - What would occur if the repressor of an inducible...Ch. 18 - Absence of bicoid in mRNA from a Drosophila egg...Ch. 18 - Which of the following statements about the DNA in...Ch. 18 - Within a cell, the amount of protein made using a...Ch. 18 - Prob. 10TYUCh. 18 - Prob. 11TYUCh. 18 - Prob. 12TYUCh. 18 - Prob. 13TYUCh. 18 - Prob. 14TYUCh. 18 - WRITE ABOUT A THEME: INTERACTIONS In a Short essay...Ch. 18 - SYNTHESIZE YOUR KNOWLEDGE The flashlight fish has...
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- Explain why mutations in tumor suppressor genes are recessive (both copies of the gene must be defective for the regulation of cell division to be defective), whereas mutations in oncogenes are dominant.arrow_forwardDescribe the effects of the over-expression of mdm2 on cell proliferation and apoptosis on cell signaling pathways and metabolism or cell cycle control. Briefly explain the normal role of each component in the context of the pathway and why its loss or modification would have the expected effect.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_forward
- What would be the effect of a mutation that inactivates the p14ARF tumor suppressor upon p53 functions?arrow_forwardIdentify two genetic mechanisms whereby proto-oncogenes can become overexpressed. Select the two mechanisms. Identify two genetic mechanisms whereby proto-oncogenes can become overexpressed.Select the two mechanisms. 1) alterations in chromatin structure 2) a gain-of-function alteration 3)modification of proto-oncogenes products 4)mutations that result in an abnormal protein product 5)mutations within gene-regulatory regionsarrow_forwardDescribe the common signal transduction event that is perturbed by cancer-promoting mutations in the genes encoding RAS and NF-1. Why are mutations in RAS more commonly found in cancers than mutations in NF-1?arrow_forward
- The Human papillomavirus (HPV) has been linked to an increased risk of cervical cancer. The HPV E6 and E7 proteins govern the cell via altering cellular proteins. The E6 protein interacts with the tumor suppressor protein p53 and directs its ubiquitin-mediated destruction. Can you elaborate about the P63 gene: its function and if it can be altered/mutated by HPV? If it does, what is the relationship between P53 and P63? Thank you!arrow_forwardSome 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.arrow_forwardThe Bcl-2 protein was initially discovered via its ability to contribute to progression of B-cells to a cancerous "lymphoma" phenotype. 1) Define the mutation that was associated with the change in Bcl-2 in these cells. 2) Is Bcl-2 an oncogene or a tumor suppressor gene? 3) Define the role of Bcl-2 in normal cellular function and how this changed in Bcl-2 associated lymphoma.arrow_forward
- D) The level of carbon dioxide increases with the level of available oxygen. 60) The TPS3 gene provides instructions for making a protein called tumor protein p53. Known as the guardlan of the genome, this protein acts as a tumor suppressor, which means that it regulates cell division by keeping cells from growing and dividing t0o fast or in an uncontrolled way. The p53 protein is located in the nucleus of cells throughout the body, where it attaches directly to DNA and plays a critical role in determining whether the DNA will be repaired or the damaged cell will self- destruct (undergo apoptosis). If the DNA can be repaired, p53 activates other genes to fix the damage. If the DNA cannot be repaired, this protein prevents the cell from dividing and signals it to undergo apoptosis. Suppose chromosomes in a skin cell are damaged by ultraviolet radiation. If the damaged genes do not affect p53, which choice correctly predict if the cell will become cancerous and why? No, the cell will not…arrow_forwardResearchers have identified some tumors that have no recurrent mutations or deletions in known oncogenes or tumor-suppressor genes and no detectable epigenetic alterations. However, these tumors often have large chromosomal deletions. What are some possible explanations that could account for the genetic causes behind these tumors?arrow_forwardGiven the following scenario, indicate if this will ‘promote’ or ‘prevent’ cancer development: An over-expression of Bcl-2arrow_forward
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