Campbell Biology (11th Edition)
11th Edition
ISBN: 9780134093413
Author: Lisa A. Urry, Michael L. Cain, Steven A. Wasserman, Peter V. Minorsky, Jane B. Reece
Publisher: PEARSON
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Chapter 18.5, Problem 1CC
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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Chapter 18 Solutions
Campbell Biology (11th 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 - MAKE CONNECTIONS Speculate about whether the same...Ch. 18.2 - Compare the roles of general and specific...Ch. 18.2 - Once mRNA encoding a particular protein reaches...Ch. 18.2 - WHAT IF? Suppose you compared the nucleotide...Ch. 18.3 - Compare miRNAs and siRNAs, including their...Ch. 18.3 - WH AT IF? Suppose the mRNA being degraded in...
Ch. 18.3 - MAKE CONNECTIONS Inactivation of one of the X...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 - Prob. 1CCCh. 18.5 - Under what circumstances is cancer considered to...Ch. 18.5 - MAKE CONNECTIONS The p53 protein can activate...Ch. 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 - draw it The diagram below shows five genes,...Ch. 18 - Prob. 12TYUCh. 18 - Prob. 13TYUCh. 18 - SCIENCE. TECHNOLOGY, AND SOCIETY Trace amounts of...Ch. 18 - WRITE ABOUT A THEME: INTERACTIONS In a Short essay...Ch. 18 - SYNTHESIZE YOUR KNOWLEDGE The flashlight fish has...
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- Studies suggest that the presence of oncogenic Ras is not sufficient to drive tumorigenesis. Instead, the activity of Ras needs to be amplified and sustained to induce pathological consequences. Recent studies have suggested a role for inflammatory stimuli on tumor development in the context of oncogenic Ras. Is the presence of oncogenic Ras necessary for transient inflammatory stimulation to induce chronic pathologies (such as cancer) OR is chronic inflammation essential for oncogenic Ras to induce tumorigenesis?arrow_forwardHow can the role of epigenetics in cancer be reconciled with the idea that cancer is caused by the accumulation of genetic mutations in tumor-suppressor genes and proto-oncogenes?arrow_forwardCompare and contrast oncogenes versus tumor-suppressorgenes.arrow_forward
- 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.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_forwardExplain why in cells that are genetically NF1–/–, basal levels of GTP-bound activated Ras are higher than normal and respond to growth factor stimulation by increasing rapidly to far higher levels.arrow_forward
- Why does a single mutation in a proto-oncogene, turning it into an oncogene potentially lead to a cancerous phenotype, while it takes two mutations in tumor suppressor genes to lead to a cancerous phenotype?arrow_forwardWould the function of KRAS gene be lost or gained in MDA-MB-231 breast cancer derived cells? Please explain why.arrow_forwardIdentify the two general functions of the proteins encoded bytumor-suppressor genes.arrow_forward
- Please answer all questions if possible. -B-Raf is not overexpressed in cancer though shows altered structure, why? -What is the specific structural change in B-Raf that causes oncogenic activation of this proto oncogene.arrow_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"In the cellular regulatory pathways that control cell growth and proliferation, the products of oncogenes are stimulatory components and the products of tumor suppressor genes are inhibitory components" is true or false.arrow_forward
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