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Ch. 24 - Cancer Genetics

Chapter 23, Problem 26

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 do not develop CML.

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Hi everybody. Let's take a look at this practice problem together. Which of the following is directly related to the development of chronic myelogenous leukemia. Now this type of leukemia is abbreviated by CML. It is a rare blood cell cancer and is typically seen in older adults. What happens in CML is that there's overproduction of abnormal white blood cells that are produced in the bone marrow. So let's look at our options and figure out which one is directly related to the development of CML. We've got a radiation exposure. Now radiation exposure does cause some D. N. A. Damage and it increases the risk of developing cancers. In general. However, it's not directly related to the development of CML and so A. Is wrong. Now let's discuss c infectious diseases. There are no known infectious diseases that are related to CML development. So C is also incorrect. Now let's discuss be genetic factors. You should recall that there is the philadelphia chromosome that is associated with CML and the philadelphia chromosome is an abnormal short chromosome. 22. It's produced by reciprocal translocation. We're part of chromosome nine and 22 swap pieces of the DNA and it is directly related to CML because it is in 90% of cases of CML and so the correct answer therefore is be genetic factors. Alright everybody, I hope you found this helpful and I'll see you soon for the next practice problem
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].

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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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

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 develop 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, and (c) if the addition of a normal RB1 gene will change the cancer-causing potential of osteosarcoma cells?

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Textbook Question

What evidence indicates that mutations in human DNA mismatch repair genes are related to certain forms of cancer?

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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.

Predisposing Mutations in BRCA1
Kindred    Codon    Nucleotide     Coding Effect     Frequency in
                               Change                                    Control
                                                                                Chromosomes    
 1901          24           -11 bp          Frameshift           0/180
                                                       or splice
 2082        1313         C→T           Gln→Stop            0/170
 1910        1756         Extra C        Frameshift           0/162
 2099        1775         T→G            Met→Arg            0/120
 2035         NA*          ?                  Loss of                NA*
                                                       transcript                                      _
Source: (1994). Science 266:66–71. © AAAS.

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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