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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Chapter 24, Problem 1PDQ
HOW DO WE KNOW? In this chapter, we focused on cancer as a genetic disease, with an emphasis on the relationship between cancer, the cell cycle, and DNA damage, as well as on the multiple steps that lead to cancer. At the same time, we found many opportunities to consider the methods and reasoning by which much of this information was acquired. From the explanations given in the chapter,
- (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
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.
3) Examine the graph showing the relative percentage normal and cancer cells spend in various stages of the cell cycle. Based on the information in the graphs, infer how cancer cells differ from typical, noncancerous cells. Select ALL that apply.
A) Cancer cells do not replicate their DNA.
B) Cancer cells replicate their DNA too quickly.
C) Cancer cells do not go through interphase during their cell cycle.
D) Cancer cells spend more time dividing compared to typical cells.
E) Cancer cells do not always grow to the same size as typical cells.
more than 1 answer. not graded
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
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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- 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_forwardWhy is it important to model cancer through the generation of induced pluripotent stem cells ? Please list item by item. Explain in detail the main findings.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
- How do we know that malignant tumors arise from a single cell that contains mutations?arrow_forwardone question with multiple parts! 1A) If you were a cancer biologist interested in developing new drugs that will slow down cancer cell metastasis, which of the following strategies would be most effective? a)Develop an activator of mitosis b)Make Her2 protein that is more active on the surface of the cancer cells c) Develop a molecule that increases telomerase activity d) Gene therapy to add a mutated p53 gene to the cancer cells 1B) You are a genetic counsellor, and a couple comes to you with concerns that if they have a child together the child could have the X-linked recessive disease Duchene muscular dystrophy. The man has the disease whereas the woman is a carrier. Which of the following would be a true statement to tell them? a) 100% of their male offspring will likely be carriers of the recessive allele that causes the disease b) 75% of their female offspring will likely be carriers of the recessive allele that causes the disease c) 100% of their male offspring will likely…arrow_forwardA 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 .arrow_forward
- What separates cancer cells from normal cells? Describe one form of mutation that can increase the risk of a normal cell being cancerous.arrow_forwardWhy 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.arrow_forwardWhich of the following mutations is MOST likely to cause cancer? A) a mutation that causes a cyclin gene to be expressed at all times during the cell cycle B) a mutation that causes an oncogene to be turned off so that no protein is made C) a mutation that causes a Cdk gene to be turned off so that no protein is made D) a mutation that causes a tumor suppressor gene to be over-expressedarrow_forward
- Why is it important to model cancer through the generation of induced pluripotent stem cells ? Explain in detail the main findings.arrow_forwardDr. Serena Velazquez lands a coveted post-doc position at Johns Hopkins following completion of her MD/PhD in cancer therapeutics to treat late-stage pancreatic cancer using a mouse model. Her post-doc will be devoted to targeted mutagenesis of replicative enzymes to halt cell division in cancerous cells. She reviews mitosis and meiosis before reporting for her first day of work. 1) If Dr. Velazquez was asked to review an article on the possibility of targeted mutagenesis of the gene for DNA pol III in a human fetus to make it immune to cancer, what do you think her response would be? a) LMAO! No human would survive without pol III since we need it to help resolve the issue with Okazaki fragments! b) LOL! Humans aren’t bacteria so WT* are the researchers even thinking?! c) LMAO! DNA pol I is the main replicative DNA polymerase. d) Hmmm! Why didn’t I think of that?!!arrow_forwardWhy would the failure of the p53 tumor supressor gene be more likely to cause cancer in a seventy year old person compared to a ten year old person? Group of answer choices A) The seventy year old is more likely to have pre-existing failures in cell cycle control B) cells divide more rapidly as people get older C) there are fewer mutations in genes controlling the cell cycle in older people D)the p53 gene never works well in old peoplearrow_forward
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