Concepts of Genetics (12th Edition)
12th Edition
ISBN: 9780134604718
Author: William S. Klug, Michael R. Cummings, Charlotte A. Spencer, Michael A. Palladino, Darrell Killian
Publisher: PEARSON
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Chapter 17, Problem 21ESP
Summary Introduction
To determine: The reasons that in case of either hypomethylation or hypermethylation therapies, the different types of cancer respond differently.
Introduction: Cancer is an abnormal growth of normal cells and mainly occur due to mutation in normal genes. Various epigenetic changes in the cell may also lead to cancer development.
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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?
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Chapter 17 Solutions
Concepts of Genetics (12th Edition)
Ch. 17 - Cancer cells often have abnormal patterns of...Ch. 17 - The hormone estrogen converts the estrogen...Ch. 17 - Each year in the United States, there are over...Ch. 17 - Prob. 2CSCh. 17 - Each year in the United States, there are over...Ch. 17 - HOW DO WE KNOW? In this chapter, we focused on how...Ch. 17 - CONCEPT QUESTION Review the Chapter Concepts list...Ch. 17 - What features of eukaryotes provide additional...Ch. 17 - Provide a definition of chromatin remodeling, and...Ch. 17 - Describe the organization of the interphase...
Ch. 17 - A number of experiments have demonstrated that...Ch. 17 - Provide a brief description of two different types...Ch. 17 - Present an overview of the manner in which...Ch. 17 - Prob. 9PDQCh. 17 - Explain how the addition of acetyl groups to...Ch. 17 - Distinguish between the cis-acting regulatory...Ch. 17 - Prob. 12PDQCh. 17 - Describe the manner in which activators and...Ch. 17 - Compare the control of gene regulation in...Ch. 17 - Many promoter regions contain CAAT boxes...Ch. 17 - Prob. 16PDQCh. 17 - Prob. 17PDQCh. 17 - Many transcriptional activators are proteins with...Ch. 17 - Prob. 19PDQCh. 17 - DNA supercoiling, which occurs when coiling...Ch. 17 - Prob. 21ESPCh. 17 - Prob. 22ESPCh. 17 - Because the degree of DNA methylation appears to...Ch. 17 - A particular type of anemia in humans, called...Ch. 17 - Regulation of the lac operon in E. coli (see...Ch. 17 - DNA methylation is commonly associated with a...Ch. 17 - During an examination of the genomic sequences...Ch. 17 - Prob. 28ESPCh. 17 - Although a single activator may bind many...Ch. 17 - Hereditary spherocytosis (HS) is a disorder...Ch. 17 - Transcription factors play key roles in the...
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- Describe error prone polymerases and the process of translesion synthesis (TLS). In regards to tumor biology, what is the mutator phenotype hypothesis? What are some ways in which error-prone polymerases could be targeted for potential anti-cancer treatments?arrow_forwardDescribe how mutations in genome maintenance factors promote tumorigenesis. Why would inactivation of a mis- match repair gene cause colon cancer?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_forward
- Describe the general process of cell signalling pathways: what events take place for a signal to cause cellular changes? Provide examples and how perturbation of these events can result in “cancer pathways”. In addition, describe in detail a typical cancer pathway and its strategy to activate gene expression. What is the origin of many cancer pathways, i.e., during which stage of an organism’s live process(es) are they physiologically activated? Why is this important for cancer development?arrow_forwardWhy is it important to model cancer through the generation of induced pluripotent stem cells ? Explain in detail the main findings. Please sort as a list.arrow_forwardWhy is it important to model cancer through the generation of induced pluripotent stem cells ? Please list item by item. Explain in detail the main findings.arrow_forward
- Cellular levels of tumor suppressor protein p53 is maintained by a ubiquitin ligase protein, called Mdm2. Over expression of Mdm2 destabilizes p53. Another protein p19ARF inhibits the activity of Mdm2, thus stabilizing p53. Loss of p19ARF function converts normal cells into cancer cells With the above information, which of the following statements are true? Mdm2 is a tumor suppressor gene but p19ARF is an oncogene Both Mdm2 & P19ARF are oncogenes Both Mdm2 & P19ARF are tumor suppressor genes O Mdm2 is an oncogene but p19ARF is a tumor suppressor genearrow_forwardWhy is it important to model cancer through the generation of induced pluripotent stem cells ? Explain in detail the main findings.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
- Tumor suppressor genes and oncogenes are implicated in carcinogenesis. However, one can predict whether a gene potentially encodes for a protein that influences carcinogenesis by examining their mutational profile. You sequence the genome of 4 cancers and identify 3 genes of interest. Which of the following genes has the best potential to an oncogene? Tumor 1 Tumor 2 Tumor 3 Tumor 4 Gene A S24F, N465T R33T T345S, G366R P367E, P368Y Gene B S34R, F360I S34R V254I S34E, T67Y Gene C S24F, I322E C255I, E344D S34E, P367Earrow_forwardRelatively 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_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_forward
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