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 23ESP
Because the degree of DNA methylation appears to be a relatively reliable genetic marker for some forms of cancer, researchers have explored the possibility of altering DNA methylation as a form of cancer therapy. Initial studies indicate that while hypomethylation suppresses the formation of some tumors, other tumors thrive. Why would one expect different cancers to respond differently to either hypomethylation or hypermethylation therapies?
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Because the degree of DNA methylation appears to be a relatively reliable genetic marker for some forms of cancer, researchers have explored the possibility of altering DNA methylation as a form of cancer therapy. Initial studies indicate that while hypomethylation suppresses the formation of some tumors, other tumors thrive. Why would one expect different cancers to respond differently to either hypomethylation or hypermethylation therapies?
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?
Cancer often results from a multistage process involving an initiating event (mediated by a viral infection or a carcinogenic chemical), followed by exposure to tumor promoters. Tumor promoters, a group of molecules that stimulate cell proliferation, cannot induce tumor formation by themselves. The phorbol esters, found in croton oil (obtained from the seeds of the croton plant, Croton tiglium), are potent tumor promoters. (Other examples of tumor promoters include asbestos and several components of tobacco smoke.) In one of the tumor-promoting actions of the phorbol esters, these molecules mimic the actions of DAG. In contrast to DAG, the phorbol esters are not easily disposed of. Explain the possible biochemical consequences of phorbol esters in an “initiated” cell. What enzyme is activated by both DAG and phorbol esters?
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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- Researchers 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_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_forwardDescribe how mutations in genome maintenance factors promote tumorigenesis. Why would inactivation of a mis- match repair gene cause colon cancer?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_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_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_forward
- Why 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_forwardWhy is it important to model cancer through the generation of induced pluripotent stem cells ? Explain in detail the main findings.arrow_forwardCellular 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_forward
- The 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_forwardTumor 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_forward
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What is cancer? What causes cancer and how is it treated? *UPDATE*; Author: Cancer Treatment Centers of America - CTCA;https://www.youtube.com/watch?v=_N1Sk3aiSCE;License: Standard Youtube License