Essentials of Genetics (9th Edition) - Standalone book
9th Edition
ISBN: 9780134047799
Author: William S. Klug, Michael R. Cummings, Charlotte A. Spencer, Michael A. Palladino
Publisher: PEARSON
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Chapter 16, Problem 1PDQ
HOW DO WE KNOW?
In this chapter, we focused on cancer as a genetic disease. In particular, we discussed the relationship between cancer, the cell cycle, and mutations in proto-oncogenes and tumor-suppressor genes. Based on your knowledge of these topics, answer several fundamental questions:
(a) How do we know that malignant tumors arise from a single cell that contains mutations?
(b) How do we know that cancer development requires more than one mutation?
(c) How do we know that cancer cells contain defects in DNA repair?
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Students have asked these similar questions
Genetic instability in the form of point mutations, chromosome rearrangements, and
epigenetic changes needs to be maximal to allow the development of cancer.
(a) With diagrams explain point mutations
Which 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 gene
A cell inherits a mutation in a gene that results in a transcription factor, called NF-kB, constantly being in its active conformation. When active, NF-kB stimulates the expression of cyclins that promote progression of the cell cycle, regardless of other conditions. As a result of this mutation, how would this cell's phenotype be affected by this mutation?
A) This cell would have a cancer phenotype
B) This cell would grow larger in size, but would never divide
C) This cell would likely undergo apoptosis
D) This cell would not duplicate its chromosomes
.
Chapter 16 Solutions
Essentials of Genetics (9th Edition) - Standalone book
Ch. 16 -
CASE STUDY | I thought it was safe
A middle-aged...Ch. 16 -
CASE STUDY | I thought it was safe
A middle-aged...Ch. 16 -
CASE STUDY | I thought it was safe
A middle-aged...Ch. 16 - HOW DO WE KNOW? In this chapter, we focused on...Ch. 16 -
2. Review the Chapter Concepts list on page 307....Ch. 16 - What is the relationship between signal...Ch. 16 - Where are the major regulatory points in the cell...Ch. 16 -
5. Describe kinases and cyclins. How do they...Ch. 16 - (a) How does pRB function to keep cells at the G1...Ch. 16 - What is the difference between saying that cancer...
Ch. 16 -
8. What is apoptosis, and under what...Ch. 16 - Define tumor-suppressor genes. Why is a mutation...Ch. 16 - A genetic variant of the retinoblastoma protein,...Ch. 16 -
11. Part of the Ras protein is associated with...Ch. 16 - If a cell suffers damage to its DNA while in S...Ch. 16 - Prob. 13PDQCh. 16 - Prob. 14PDQCh. 16 - Prob. 15PDQCh. 16 - Prob. 16PDQCh. 16 - Prob. 17PDQCh. 16 - How do normal cells protect themselves from...Ch. 16 - Prob. 19PDQCh. 16 - Explain how environmental agents such as chemicals...Ch. 16 - Radiotherapy (treatment with ionizing radiation)...Ch. 16 - Genetic tests that detect mutations in the BRCA1...Ch. 16 - Prob. 23PDQCh. 16 - Prob. 24PDQCh. 16 - Prob. 25PDQCh. 16 - Prob. 26PDQCh. 16 - Prob. 27PDQCh. 16 - Prob. 28PDQ
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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 p53 considered a tumor suppressor protein? Question 12 options: a) Because p53 normally detects breaks in DNA. b) Because p53 normally causes progression from G1 to S phase to halt until damaged DNA is fully repaired. c) Because p53 normally repairs breaks in DNA. d) Because p53 normally stimulates transcription of Repair Polymerase. e) Because p53 normally reduces the mutation rate of DNA polymerase.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_forwardWhich of the following statements about cancer is false? (a) oncogenes arise from mutations in proto-oncogenes (b) tumor suppressor genes normally interact with growthinhibiting factors to block cell division (c) more than 120cancer-driving genes have been discovered (d) oncogenes were first discovered in mouse models for cancer (e) the development of cancer is usually a multistep process involving both oncogenes and mutated tumor suppressor genesarrow_forward
- Discuss the complete cell cycle in a human cell, mitosis and meiosis, and the regulatory components (i.e. the proteins associated with cellular checkpoints) of the cell cycle. Tumor growth results when the cell cycle checkpoints are ignored. Give an example of how tumor growth could result from either a loss-of-function or a gain-of-function mutation.arrow_forwardDespite all that we know about cancer today, some types of cancers are still increasing in frequency. Lung cancer among nonsmoking women is one of these. What reason(s) might there be for this increasing problem?arrow_forwardWhat is the difference in an oncogene and tumor suppressor gene and how can each potentially lead to cancer?arrow_forward
- 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_forwardTumor suppressor proteins can assist in slowing down the cell cycle under appropriate conditions. In humans, the TP53 gene encodes a tumor suppressor called p53. Most mutations in the TP53 gene result in a mutant form of p53 that can no longer function to slow down the cell cycle, which can lead to a cell becoming cancerous. However, some mutant forms of p53 actually possess the ability to increase a cell's resistance to anticancer treatments. Which of the following BEST describes the latter type of mutation? loss-of-function mutation gain-of-function mutation suppressor mutation reverse mutationarrow_forwardWhat is the difference between a proto-oncogene and a tumor suppressor gene? How can mutations in these genes lead to cancer?arrow_forward
- What is cancer? What defects are commonly found in cancer cells? Do all cancer cells have mutations in the same genes? Explain.arrow_forwardDescribe the steps by which the TP53 gene responds to DNA damage and/or cellular stress to promote cell-cycle arrest and apoptosis. Given that TP53 is a recessive gene and is not located on the X chromosome, why would people who inherit just one mutant copy of a recessive tumor-suppressor gene be at higher risk of developing cancer than those without the recessive gene?arrow_forwardhow are the hallmarks resisting cell death and enabling replicative immortality essential for cancer development. explain each in 3-5 sentences.arrow_forward
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