Genetics: Analysis and Principles
6th Edition
ISBN: 9781259616020
Author: Robert J. Brooker Professor Dr.
Publisher: McGraw-Hill Education
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Chapter 20, Problem 4EQ
Summary Introduction
To review:
Use of transposon tagging to identify the tumor-suppressor genes.
Introduction:
A gene which, prevents a normal cell to undergo the path of a malignant cell, is known as a tumor-suppressor gene. The absence or mutation of these genes lead to abnormal growth of the cell which, results in the production of cancer in an organism. These genes suppress the activation of the cell cycle which, initiates the growth of the cell cycle.
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Why 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.
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 gene
The best strategy for treating a specific type of human tumor can depend on identifying the type of cell that became cancerous to give rise to the tumor. For some tumors that have colonized a distant location (metastasized), identifying the parental cell type can be difficult. Because the type of IF protein expressed is cell-type-specific, using monoclonal antibodies that react with only one type of IF protein can help in this identification. What IF proteins would you produce monoclonal antibodies against to identify (a) a sarcoma of muscle cell origin, (b) an epithelial cell carcinoma, and (c) an astrocytoma (glial cell tumor)?
Chapter 20 Solutions
Genetics: Analysis and Principles
Ch. 20.1 - 1. Homologous recombination refers to the exchange...Ch. 20.1 - During the molecular process of homologous...Ch. 20.1 - 3. A key difference between the original Holliday...Ch. 20.1 - Which of the following mechanisms can cause gene...Ch. 20.2 - 1. During site-specific recombination that occurs...Ch. 20.2 - Prob. 2COMQCh. 20.3 - Which of the following types of transposable...Ch. 20.3 - Prob. 2COMQCh. 20.3 - Prob. 3COMQCh. 20 - 1. Describe the similarities and differences...
Ch. 20 - Prob. 2CONQCh. 20 - 3. Which steps in the double-strand break model...Ch. 20 - Prob. 4CONQCh. 20 - Prob. 5CONQCh. 20 - Prob. 6CONQCh. 20 - Prob. 7CONQCh. 20 - 8. What is gene conversion?
Ch. 20 - Make a list of the differences between the...Ch. 20 - Prob. 10CONQCh. 20 - Prob. 11CONQCh. 20 - 12. According to the double-strand break model,...Ch. 20 - What type of DNA structure is recognized by RecG...Ch. 20 - Briefly describe three ways that antibody...Ch. 20 - 15. Describe the functions of the RAG1 and RAG2...Ch. 20 - According to the scenario shown in Figure 20.7,...Ch. 20 - Prob. 17CONQCh. 20 - Prob. 18CONQCh. 20 - 19. Why does transposition always produce direct...Ch. 20 - 20. Which types of TEs have the greatest potential...Ch. 20 - Prob. 21CONQCh. 20 - 22. Let’s suppose that a species of mosquito has...Ch. 20 - This chapter describes different types of TEs,...Ch. 20 - Prob. 24CONQCh. 20 - Prob. 25CONQCh. 20 - 26. What is the difference between an autonomous...Ch. 20 - 1. Briefly explain how McClintock determined that...Ch. 20 - The work of McClintock showed that the presence of...Ch. 20 - 3. In your own words, explain the term transposon...Ch. 20 - Prob. 4EQCh. 20 - 5. Gerald Rubin and Allan Spradling devised a...Ch. 20 - Make a list of the similarities and differences...Ch. 20 - Prob. 2QSDCCh. 20 - Prob. 3QSDC
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- 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_forwardD) The level of carbon dioxide increases with the level of available oxygen. 60) The TP53 gene provides instructions for making a protein called tumor protein p53. Known as the guardian of the genome, this protein acts as a tumor suppressor, which means that it regulates cell division by keeping cells from growing and dividing too 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. eg 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…arrow_forwardLoss of p53 function occurs in the majority of human tumors. Name two ways in which loss of p53 function contributes to a malignant phenotype. Explain how benzo(a) pyrene can cause loss of p53 function.arrow_forward
- The MET oncogene is a growth factor receptor that is altered in many forms of cancer including lung and colon carcinomas as well as several forms of melanoma. One assay for characterizing the gene composition of tumor cells is Fluorescence in situ Hybridization (FISH) in which a fluorescently labeled DNA is used to show the presence of and level (i.e. number copies) of a gene inside cells. The experiment below is a FISH assay of two different tumor samples (Patient D and Patient E) using a MET gene probe labeled with a green fluorescent probe. The figure on the right presents the survival data from diagnosis of cancer patients with FISH data similar to Patient D or E. Based on this data, what has happened to the MET gene in Patient D population that has made their cancer more severe and reduced survival time (Limit 4-5 sentences). D Survival rate (%) 100 0 0 100 200 Time (days) 300 Earrow_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_forwardp53 is a tumor suppressor gene in human cells. Transcription of this gene leads to the production of the p53 protein in cells which modulates many signal pathways that lead to anti-tumor effects. The strength of anti-tumor effects is directly porportional to the accumulation of the protein within the cells of the person. Suppose a pediatric patient was recently admitted for a rare lung cancer related to p53 deficiencies (although the p53 itself is not mutated). what are some potential reasons for the deficiency in p53 levels and how can you restore them if the reason you assumed for the deficiency is not directly reparable (i.e if you assume that protein degradation is too fast, you cannot directly repair protein degradation but you may want to increase transcription & translation rates to compensate)? Will your hypothesized repair(s) cause negative impacts to the cell? Why?arrow_forward
- 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?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_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_forward
- The Bcl-2 protein was initially discovered via its ability to contribute to progression of B-cells to a cancerous "lymphoma" phenotype. 1) Define the mutation that was associated with the change in Bcl-2 in these cells. 2) Is Bcl-2 an oncogene or a tumor suppressor gene? 3) Define the role of Bcl-2 in normal cellular function and how this changed in Bcl-2 associated lymphoma.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_forwardDescribe 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_forward
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