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
expand_more
expand_more
format_list_bulleted
Concept explainers
Textbook Question
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?
Expert Solution & Answer
Want to see the full answer?
Check out a sample textbook solutionStudents have asked these similar questions
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?
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?
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?
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...
Knowledge Booster
Learn more about
Need a deep-dive on the concept behind this application? Look no further. Learn more about this topic, biology and related others by exploring similar questions and additional content below.Similar questions
- Why 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_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
- Imatinib is an anti-cancer drug that inhibits the function of CD117, a receptor protein coded for by the KIT gene. Mutations in the KIT gene are implicated in gastrointestinal cancers. Aimee, who has a gastrointestinal tumor asked her doctor if she could try Imatinib, but her doctor first required that she get a biopsy of her tumor. Hair loss is a well-known side effect of chemotherapy; why does this side effect occur? (1) Chemotherapy targets cells undergoing division. Hair stem cells are constantly replenishing (growing) just like cancer cells. They are then also targeted by chemotherapy, causing hair loss. (2) Chemotherapy targets all cells, whether dividing or not dividing, and hair cells are collateral in the fight against cancer (3) Chemotherapy targets proteins in our cells and hair cells have an abundance of proteinsarrow_forwardThe deregulation of several signal transduction pathways is integral to the onset of cancer. These pathways involve both tumor promoters (the "gas pedals") and tumor suppressors (the "brake pedals"). Which would be a more effective treatment for cancer: A small molecule inhibitor that targets a tumor suppressor or one that targets a tumor promoter? Briefly explain your choice. (THIS CAN BE DONE IN LESS THAN TWO SENTENCES, AND MINIMALLY IN ABOUT EIGHT WORDS.) Edit View. Insert Format Tools Table 12pt v Paragraph BI UAV 2VT² V| :arrow_forwardCancer-promoting mutations are likely to have different effects on the activity of proteins encoded byproto-oncogenes than they do on proteins encodedby tumor-suppressor genes. Explain.arrow_forward
- The rb gene encodes a protein that inhibits E2F, a transcriptionfactor that activates several genes involved in cell division.Mutations in rb are associated with certain forms of cancer,such as retinoblastoma. Under each of the following conditions,would you expect the cancer to occur?A. One copy of rb is defective; both copies of E2F are functional.B. Both copies of rb are defective; both copies of E2F arefunctional.C. Both copies of rb are defective; one copy of E2F is defective.D. Both copies of rb and E2F are defective.arrow_forwardWhat common mutation occurs in many human cancers? Explain how it can have this effect.arrow_forwardPlease distinguish driver and passenger mutations in cancer.arrow_forward
- Mutations in three broad classes of genes have been implicated in the onset of cancer. Can you explain how?arrow_forwardA research study indicated that an agent in cigarette smoke caused the silencing of a tumor suppressor gene called p53. However,upon sequencing, no mutation was found in the DNA sequence for this gene. Give two possible explanations for these results.arrow_forwardA. Which genes could be used to monitor the process of the disease? B.  If you worked for a drug company developing a treatment for the cancer, which genes would you target to turn on in cancer cells? C. Which genes would you target to turn off in cancer cells?arrow_forward
arrow_back_ios
SEE MORE QUESTIONS
arrow_forward_ios
Recommended textbooks for you
- Human Heredity: Principles and Issues (MindTap Co...BiologyISBN:9781305251052Author:Michael CummingsPublisher:Cengage Learning
Human Heredity: Principles and Issues (MindTap Co...
Biology
ISBN:9781305251052
Author:Michael Cummings
Publisher:Cengage Learning
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