Genetics: From Genes to Genomes
6th Edition
ISBN: 9781259700903
Author: Leland Hartwell Dr., Michael L. Goldberg Professor Dr., Janice Fischer, Leroy Hood Dr.
Publisher: McGraw-Hill Education
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Textbook Question
Chapter 20, Problem 22P
Neurofibromatosis type 1 (NF1; also known as von Recklinghausen disease) is an inherited dominant disorder. The
a. | Is it likely that NF1 is a tumor-suppressor gene or an oncogene? | ||||||||||||||
b. | Are the NF1 neurofibromatosis-causing mutations that are inherited by affected children from affected parents likely to be loss-of-function or gain-of-function mutations? | ||||||||||||||
c. | Neurofibromin, the protein product of NF1, has been found to be associated with the Ras protein. Ras is involved in the transduction of extracellular signals from growth factors. The active form of Ras (the form initiating the signal transduction cascade causing proliferation) is complexed with GTP; the inactive form of Ras is complexed with GDP. Would the wild-type neurofibromin protein favor the formation of Ras–GTP or Ras–GDP? | ||||||||||||||
d. | Which of the following events in a normal cell from an individual inheriting a neurofibromatosis-causing allele could cause the descendants of that cell to grow into a neurofibroma?
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e. | A much rarer form of neurofibromatosis exists called segmental neurofibromatosis. In this form of the disease, neither parent of the patient has any clinical sign of the disease. The tumors in the patient are restricted to one part of the body, like the right leg. Suggest an explanation for the genesis of segmental neurofibromatosis that clarifies why it is restricted to one part of the body. |
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The level of carbon dioxide increases with the level of available oxygen.
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The TP53 gene provides instructions for making a protein called tumor protein p53. Known as the guardian of the genome,
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too fast or in an uncontrolled way. The p53 protein is located in the nucleus of cells throughout the body, where it attaches
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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.
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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…
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…
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.
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3) Define the role of Bcl-2 in normal cellular function and how this changed in Bcl-2 associated lymphoma.
Chapter 20 Solutions
Genetics: From Genes to Genomes
Ch. 20 - For each of the terms in the left column, choose...Ch. 20 - Characterize the differences between tumor cells...Ch. 20 - Prob. 3PCh. 20 - Prob. 4PCh. 20 - A carcinogenic compound is placed on the skin of...Ch. 20 - You have decided to study genetic factors...Ch. 20 - B cells are specialized blood cells that secrete...Ch. 20 - Molecules outside and inside the cell regulate the...Ch. 20 - Put the following steps in the correct ordered...Ch. 20 - a. Would you expect a cell to continue or to stop...
Ch. 20 - Two different protein complexes called SCF and APC...Ch. 20 - One of the hallmarks of mitotic anaphase is the...Ch. 20 - Concerning the Tools of Genetics Box Analysis of...Ch. 20 - Are genome and karyotype instabilities...Ch. 20 - Prob. 15PCh. 20 - Why dont all loss-of-function mutations that are...Ch. 20 - Chromothripsis is a rare phenomenon, first...Ch. 20 - The chromosome 9/22 translocation associated with...Ch. 20 - A female patient 19 years old, whose symptoms are...Ch. 20 - Prob. 20PCh. 20 - A generic signaling cascade is shown in the...Ch. 20 - Neurofibromatosis type 1 NF1; also known as von...Ch. 20 - Families with germ-line BRCA1 or BRCA2...Ch. 20 - The text explained that retroviruses can cause...Ch. 20 - Hepatocellular carcinoma is the most frequent form...Ch. 20 - Suppose that instead of microarrays, you analyzed...Ch. 20 - Prob. 27PCh. 20 - Glioblastoma multiforme GBM is the most common and...Ch. 20 - a. The legend to Fig. 20.29 identifies which of...Ch. 20 - The website CBioPortal http://www.cbioportal.org...
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- 1. a)Proteins that stimulate/promote progression through the cell cycle are encoded by (oncogenes or tumor suppressor genes). Boldface one. b)Proteins that inhibit progression through the cell cycle are encoded by (oncogenes or tumor suppressor genes). Boldface one. c)What is the difference between a proto-oncogene and an oncogene? d)To cause cancer, proto-oncogenes require (1 or 2)allele(s) to be mutated and therefore are considered (dominant or recessive). The mutation results in a (loss or gain) of function. For each underlined pair, boldface one. e)To cause cancer, tumor suppressor genes require (1 or 2)allele(s) to be mutated and therefore are considered (dominant or recessive). The mutation results in a (loss or gain) of function. For each underlined pair, boldface one.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_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
- 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.arrow_forwardDescribe the mutational event that produces the MYC oncogene in Burkitt’s lymphoma. Why does the particular mechanism for generating oncogenic MYC result in a lymphoma rather than another type of cancer? Describe another mechanism for generating oncogenic MYC.arrow_forwardIdentify two genetic mechanisms whereby proto-oncogenes can become overexpressed. Select the two mechanisms. Identify two genetic mechanisms whereby proto-oncogenes can become overexpressed.Select the two mechanisms. 1) alterations in chromatin structure 2) a gain-of-function alteration 3)modification of proto-oncogenes products 4)mutations that result in an abnormal protein product 5)mutations within gene-regulatory regionsarrow_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_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_forwardd)To cause cancer, proto-oncogenes require (1 or 2)allele(s) to be mutated and therefore are considered (dominant or recessive). The mutation results in a (loss or gain) of function. For each underlined pair, boldface one. e)To cause cancer, tumor suppressor genes require (1 or 2)allele(s) to be mutated and therefore are considered (dominant or recessive). The mutation results in a (loss or gain) of function. For each underlined pair, boldface one.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_forwardExplain why mutations in tumor suppressor genes are recessive (both copies of the gene must be defective for the regulation of cell division to be defective), whereas mutations in oncogenes are dominant.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
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