Textbook Question
Explain the apparent paradox that both hypermethylation and hypomethylation of DNA are often found in the same cancer cell.
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Ch. 24 - Cancer Genetics
Klug12th EditionConcepts of Genetics ISBN: 9780135564776
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Table of contents
- Ch. 1 - Introduction to Genetics17
- Ch. 2 - Mitosis and Meiosis36
- Ch. 3 - Mendelian Genetics51
- Ch. 4 - Extensions of Mendelian Genetics74
- Ch. 5 - Chromosome Mapping in Eukaryotes51
- Ch. 6 - Genetic Analysis and Mapping in Bacteria and Bacteriophages46
- Ch. 7 - Sex Determination and Sex Chromosomes33
- Ch. 8 - Chromosome Mutations: Variation in Number and Arrangement40
- Ch. 9 - Extranuclear Inheritance31
- Ch. 10 - DNA Structure and Analysis43
- Ch. 11 - DNA Replication and Recombination44
- Ch. 12 - DNA Organization in Chromosomes30
- Ch. 13 - The Genetic Code and Transcription54
- Ch. 14 - Translation and Proteins47
- Ch. 15 - Gene Mutation, DNA Repair, and Transposition41
- Ch. 16 - Regulation of Gene Expression in Bacteria29
- Ch. 17 - Transcriptional Regulation in Eukaryotes41
- Ch. 18 - Post-transcriptional Regulation in Eukaryotes33
- Ch. 19 - Epigenetics33
- Ch. 20 - Recombinant DNA Technology44
- Ch. 21 - Genomic Analysis36
- Ch. 22 - Applications of Genetic Engineering and Biotechnology36
- Ch. 23 - Developmental Genetics37
- Ch. 24 - Cancer Genetics34
- Ch. 25 - Quantitative Genetics and Multifactorial Traits54
- Ch. 26 - Population and Evolutionary Genetics45
Chapter 24, Problem 25b
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].
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] outlines 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.
Verified step by step guidance1
Understand the role of tumor-suppressor genes: Tumor-suppressor genes are responsible for regulating cell growth and preventing uncontrolled cell division. Mutations or epigenetic changes (e.g., DNA methylation) in these genes can lead to tumorigenesis, which is the formation of tumors.
Learn about DNA methylation: DNA methylation is an epigenetic modification where methyl groups are added to cytosine bases in DNA, often at CpG sites. This can silence gene expression, including tumor-suppressor genes, contributing to cancer development.
Explore the concept of free DNA release: Tumors release free DNA into surrounding body fluids (e.g., blood) through processes like necrosis (cell death due to injury) and apoptosis (programmed cell death). This free DNA can serve as a biomarker for detecting and monitoring cancer.
Review the experimental protocol: The study by Kloten et al. (2013) outlines a method for using human blood to detect free DNA from tumors. This involves isolating circulating tumor DNA (ctDNA) from blood samples and analyzing it for mutations or epigenetic changes in tumor-suppressor genes.
Consider applications in cancer monitoring: The detection of ctDNA in blood can be used to monitor cancer progression, assess treatment efficacy, and potentially identify early signs of recurrence. This approach provides a non-invasive method for tracking cancer in patients.
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Key Concepts
Here are the essential concepts you must grasp in order to answer the question correctly.
Tumor-Suppressor Genes
Tumor-suppressor genes are critical components of the cellular machinery that regulate cell growth and division. When these genes are mutated or inactivated, they can no longer perform their function of preventing uncontrolled cell proliferation, leading to tumorigenesis. Examples include the TP53 and BRCA1 genes, which are often implicated in various cancers.
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Mapping Genes
Epigenetic Changes
Epigenetic changes refer to modifications that affect gene expression without altering the underlying DNA sequence. One common form is DNA methylation, where methyl groups are added to DNA, often silencing gene expression. In the context of tumor-suppressor genes, abnormal methylation patterns can contribute to cancer development by turning off genes that normally prevent tumor growth.
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Circulating Free DNA (cfDNA)
Circulating free DNA (cfDNA) is DNA that is released into the bloodstream from cells undergoing necrosis or apoptosis. In cancer patients, cfDNA can contain genetic material from tumor cells, making it a valuable biomarker for cancer detection and monitoring. Analyzing cfDNA can provide insights into tumor characteristics and treatment responses, facilitating personalized medicine approaches.
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Related Practice
Textbook Question
As part of a cancer research project, you have discovered a gene that is mutated in many metastatic tumors. After determining the DNA sequence of this gene, you compare the sequence with those of other genes in the human genome sequence database. Your gene appears to code for an amino acid sequence that resembles sequences found in some serine proteases. Conjecture how your new gene might contribute to the development of highly invasive cancers.
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Textbook Question
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].
How might hypermethylation of the TP53 gene promoter influence tumorigenesis?
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Textbook Question
A study by Bose and colleagues (1998). Blood 92:3362-3367] and a previous study by Biernaux and others (1996). Bone Marrow Transplant 17:(Suppl. 3) S45–S47] showed that BCR-ABL fusion gene transcripts can be detected in 25 to 30 percent of healthy adults who do not develop chronic myelogenous leukemia (CML). Explain how these individuals can carry a fusion gene that is transcriptionally active and yet does not develop CML.
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Textbook Question
Those who inherit a mutant allele of the RB1 tumor-suppressor gene are at risk for developing a bone cancer called osteosarcoma. You suspect that in these cases, osteosarcoma requires a mutation in the second RB1 allele, and you have cultured some osteosarcoma cells and obtained a cDNA clone of a normal human RB1 gene. A colleague sends you a research paper revealing that a strain of cancer-prone mice develops malignant tumors when injected with osteosarcoma cells, and you obtain these mice. Using these three resources, what experiments would you perform to determine:
(a) Whether osteosarcoma cells carry two RB1 mutations
(b) Whether osteosarcoma cells produce any pRB protein
(c) If the addition of a normal RB1 gene will change the cancer-causing potential of osteosarcoma cells?
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Textbook Question
The table in this problem summarizes some of the data that have been collected on mutations in the BRCA1 tumor-suppressor gene in families with a high incidence of both early-onset breast cancer and ovarian cancer.
Note the coding effect of the mutation found in kindred group 2082. This results from a single base-pair substitution. Draw the normal double-stranded DNA sequence for this codon (with the 5' and 3' ends labeled), and show the sequence of events that generated this mutation, assuming that it resulted from an uncorrected mismatch event during DNA replication.
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