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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Textbook Question
Chapter 24, Problem 2NST
People with a genetic condition known as Li-Fraumeni syndrome inherit one mutant copy of the TP53 gene. These people have a high risk of developing a number of different cancers, such as breast cancer, leukemia, bone cancer, adrenocortical tumors, and brain tumors. Explain how mutations in one cancer-related gene can give rise to such a diverse range of tumors.
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There are three broad categories of cancer-related genes: proto-oncogenes, tumor suppressor genes, and DNA stability/repair genes. Define each of these categories and indicate which one you think the RB1 gene belongs to and why.
The 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!
Loss 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.
Chapter 24 Solutions
Concepts of Genetics (12th Edition)
Ch. 24 - Prob. 1NSTCh. 24 - People with a genetic condition known as...Ch. 24 - Prob. 3NSTCh. 24 - Cancer can arise spontaneously, but it can also be...Ch. 24 - Prob. 1CSCh. 24 - Prob. 2CSCh. 24 - If you agree to participate and then learn that...Ch. 24 - HOW DO WE KNOW? In this chapter, we focused on...Ch. 24 - Prob. 2PDQCh. 24 - Where are the major regulatory points in the cell...
Ch. 24 - List the functions of kinases and cyclins, and...Ch. 24 - How can mutations in noncoding segments of DNA...Ch. 24 - What is the difference between saying that cancer...Ch. 24 - Prob. 7PDQCh. 24 - Prob. 8PDQCh. 24 - Define tumor-suppressor genes. Why is a mutated...Ch. 24 - Describe the steps by which the TP53 gene responds...Ch. 24 - Part of the Ras protein is associated with the...Ch. 24 - Prob. 12PDQCh. 24 - Distinguish between oncogenes and proto-oncogenes....Ch. 24 - Prob. 14PDQCh. 24 - How do translocations such as the Philadelphia...Ch. 24 - Explain why many oncogenic viruses contain genes...Ch. 24 - Prob. 17PDQCh. 24 - How do normal cells protect themselves from...Ch. 24 - Prob. 19PDQCh. 24 - Epigenetics is a relatively new area of genetics...Ch. 24 - Radiotherapy (treatment with ionizing radiation)...Ch. 24 - Genetic tests that detect mutations in the BRCA1...Ch. 24 - Explain the apparent paradox that both...Ch. 24 - As part of a cancer research project, you have...Ch. 24 - Mutations in tumor-suppressor genes are associated...Ch. 24 - Prob. 26ESPCh. 24 - Those who inherit a mutant allele of the RB1...Ch. 24 - The table in this problem summarizes some of the...Ch. 24 - Researchers have identified some tumors that have...Ch. 24 - Prob. 30ESP
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- Relatively 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_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_forwardWhich of the following effectively describes the situation of someone with an inherited predisposition to cancer such as familial adenomatous polyposis or BRCA-associated familial breast cancer? Choose all that apply a) If they get malignant cancer, somatic mutations will not have been a factor b) Their cancer will most likely arise in their germ cells, not their somatic cells c) None of the answers effectively describes the situation d) Every cell of their body contains a gain-of-function allele of an oncogene e) Most cells in their body contain multiple cancer-causing mutations f) Every cell of their body contains a defective, loss-of-function allele of a tumor suppressor genearrow_forward
- 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. Hint: Loss of p53 function occurs in the majority of human tumors.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_forwardWhat common mutation occurs in many human cancers? Explain how it can have this effect.arrow_forward
- 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_forwardIn Metastatic Breast Cancer [such as in Breast Invasive Ductal Carcinoma; Breast Invasive Carcinoma, NOS; Breast Invasive Cancer, NOS; Invasive Breast Carcinoma; Breast Invasive Lobular Carcinoma; Breast Mixed Ductal and Lobular Carcinoma] what role does the genes Tp53 and Tp63 have? Would one of them affect the other (i.e. mutation, etc) or there is not relationship among the two genes at all.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_forward
- 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_forwardThe C-myc gene is a proto-oncogene which is highly expressed in breast tissue and appears to cause proliferation of breast tissue and its elevated expression is associated with breast cancer. Based just on the ChIP data from the previous questions (also shown below), which of the three drugs (estrogen, tamoxifen and raloxifene) would you recommend for treating breast cancer? Justify your response and explain the potential side effects of each drug.arrow_forwardD) 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_forward
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