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 17PDQ
Summary Introduction
To determine: The way scientists categorize the somatic mutations that are currently discovered in cancer cells.
Introduction: Currently, scientists are applying some of the advances in DNA (deoxyribonucleic acid) sequencing to identify all somatic mutations within the tumors.
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In the replica plate experiment, it shows that mutations are random. However, certain environmental stresses (such as high temperature, high salt, and low pH) can increase the mutation rate.
QUESTIONS:
Does this indicate that mutations are nonrandom, since they increase in response to cell stressors?
What are the biggest challenges that mutations pose to oncologists and cancer biologists who seek to find novel cures against cancers?
Gene mutations can be classified in two major ways:(1) hereditary or germline mutations that are inherited from a parent and are present throughout a person’s life in virtually every cell in the body.(2) acquired or somatic mutations that occur at some time during a person’s life and are present only in certain cells, not in every cell in the body.If there is no family history of a particular disease but a child has the disease then it may have arisen due to a(n) ________ mutation early during development.
A) acquired
B) inherited
C) silent
D) transition
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
- (a) How does the duplication of individual genes occur? (b) individual that inherit a genetic condition known as xeroderma pigmentosum exhibit an extreme sensitivity to sunlight exposure and often develop skin cancer by the age of 10. What repair pathway is most likely disrupted as a result of such mutation? Explain why?arrow_forwardWith age, somatic cells are thought to accumulate genomic "scars"as a result of the inaccurate repair of double-strand breaks by non homologous end-joining (NHEJ). Estimates based on the frequency of breaks in primary human fibroblasts suggest that by age 70 each human somatic cell may carry some 2000 NHEJ-induced mutations due to inaccurate repair. If these mutations were distributed randomly around the genome, how many genes would you expect to be affected? Would you expect cell function to be compromised? Why or why not? (Assume that 2% of the genome - 1.5% coding and 0.5% regulatory - is crucial information.)arrow_forwardCancer-causing mutations in genes can have different effects on the protein products expressed. a) What type of mutation would be dominant in the development of cancer? Why? b) What type of mutation would be expressed as a recessive trait in the development of cancer? Why? c) Based upon your answers to parts (a) and (b), how would you treat these situations using a gene therapy approach?arrow_forward
- Although it is well known that X-rays cause mutations, they are routinely used to diagnose medical problems, including potential tumors, broken bones, and dental cavities. Why is this done? What precautions need to be taken?arrow_forwardWhich of the following is an enabling characteristic for cancer that can increase the likelihood of both passenger and driver mutations? a) Increased angiogenesis O b) Tumor-promoting inflammation O c) Avoiding immune destruction O d) Genome instability acerarrow_forwardMany of the mutations in cancer samples are not necessarily driver mutations, but rather passenger mutations that are along for the ride. Just because the tumors with a strong environmental component possess a higher frequency of mutations does not mean more oncogenes or more failure of tumor suppressors is occurring. Hematologic childhood cancers have a lower frequency of mutations than tumors with a strong environmental component such as lung cancers and melanoma; WHY?arrow_forward
- Some initial studies looking at the carcinogenicity of tobacco products took extracts from those products and carried out various mutational assays on them. They rarely found any evidence that tobacco could cause cancer. Why would these experiments provide false negatives?arrow_forwardDNA repair systems are responsible for maintaining genomic fidelity in normal cells despite the high frequency with which mutational events occur. What type of DNA mutation is generated by (a) UV radiation and (b) ionizing radiation? Describe the system responsible for repairing each of these types of mutations in mammalian cells. Postulate why a loss of function in one or more DNA repair systems typifies many cancers.arrow_forwardHow can researchers pinpoint the particular driver mutations most responsible for the cancer phenotype?arrow_forward
- What common mutation occurs in many human cancers? Explain how it can have this effect.arrow_forwardDoes DNA alterations during DNA replication result in the formation of cancerous cells? And how does it occur? Is it possible to prevent genetic mutations before they emerge in any way? Is there a technology that can detect a change? asaparrow_forward1) A mutation is a change that occurs in our DNA sequence, either due to mistakes when the DNA is copied or as the result of environmental factors. All BUT ONE of the statements below correctly describes or explains genetic mutations. A) Mutation can disrupt normal cell activity and cause diseases, like cancer. B) Mutations in parents' cells are then passed down to offspring via reproduction. C) Our cells can recognise any potentially mutation-causing damage and repair it before it permanent. D) Mutations can occur as the result of exposure to environmental factors such as smoking, toxins and radiation.arrow_forward
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