Investigating Biology Laboratory Manual (9th Edition)
9th Edition
ISBN: 9780134473468
Author: Lisa A. Urry, Michael L. Cain, Steven A. Wasserman, Peter V. Minorsky, Jane B. Reece, Judith Giles Morgan, M. Eloise Brown Carter
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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Cancer is driven by alterations in the expression of critical genes, namely tumour suppressors,
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Chapter 18 Solutions
Investigating Biology Laboratory Manual (9th 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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- 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_forwardWhat 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_forward
- Describe 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_forwardDescribe how mutations in genome maintenance factors promote tumorigenesis. Why would inactivation of a mis- match repair gene cause colon cancer?arrow_forwardThe 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_forward
- 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.arrow_forwardDescribe the mutational event that produces the MYC oncogene in Burkitt’s lymphoma. Why does the particular mechanism for generating oncogenic MYC result in a lymphoma rather than another type of cancer? Describe another mechanism for generating oncogenic MYC.arrow_forwardThe p53 gene is a tumor-suppressor gene while Ras is a proto-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_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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