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 25ESP
Mutations in tumor-suppressor genes are associated with many types of cancers. In addition, epigenetic changes (such as DNA methylation) of tumor-suppressor genes are also associated with tumorigenesis [Otani et al (2013). Expert Rev Mol Diagn 13:445–455].
- (a) How might hypermethylation of the TP53 gene promoter influence tumorigenesis?
- (b) Knowing that tumors release free DNA into certain surrounding body fluids through necrosis and apoptosis Kloten et al. [(2013). Breast Cancer Res. 15(1):R4] outline an experimental protocol for using human blood as a biomarker for cancer and as a method for monitoring the progression of cancer in an individual.
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Describe 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?
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…
D)
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…
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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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
- Can restoring tumor suppressor function, such as mutant p53 or pRb, be used to cure cancer? If that's the case, how is it possible?arrow_forwardStudies suggest that the presence of oncogenic Ras is not sufficient to drive tumorigenesis. Instead, the activity of Ras needs to be amplified and sustained to induce pathological consequences. Recent studies have suggested a role for inflammatory stimuli on tumor development in the context of oncogenic Ras. Is the presence of oncogenic Ras necessary for transient inflammatory stimulation to induce chronic pathologies (such as cancer) OR is chronic inflammation essential for oncogenic Ras to induce tumorigenesis?arrow_forwardWhy is it important to model cancer through the generation of induced pluripotent stem cells ? Explain in detail the main findings.arrow_forward
- Acquired mutation in the p53 gene is the most common genetic alteration found in human cancer (> 50% of all cancers). A germline mutation in p53 is the causative lesion of Li- Fraumeni familial cancer syndrome. In many tumors, one p53 allele on chromosome 17p is deleted and the other is mutated. What type of protein is encoded by the p53 gene? (A) Caspase (B) DNA repair enzyme (C) Membrane cell adhesion molecule (D) Serine phosphatase (E) Telomerase (F) Transcription factor (G) Tyrosine kinasearrow_forwardDescribe how mutations in genome maintenance factors promote tumorigenesis. Why would inactivation of a mis- match repair gene cause colon cancer?arrow_forwardDistinguish 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_forward
- What would be the effect of a mutation that inactivates the p14ARF tumor suppressor upon p53 functions?arrow_forwardDescribe the molecular mechanisms involved in P53’s role as a tumor repressor proteinarrow_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_forward
- p53 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_forwardGenetic 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 mutationsarrow_forwarda. Why would a mutation in BRCA1 be considered a driver mutation? b. Based on what you’ve learned thus far, would ATM be considered a tumor suppressor? Explain your reasoning.arrow_forward
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