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Ch. 24 - Cancer Genetics

Chapter 23, Problem 25

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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Hello everyone and welcome to today's video. So the silencing of the gene caused by hyper methylation of the TP 53 gene promoter can result in which of the following consequences. Well, remember that methylation is a process that can either enhance or repress gene expression here. In the question we're saying that is silencing the gene expression of this T P 53 gene. Now, what is this going to result in before we jump into that? Let's remember that the TP 53 gene is a two more suppressor. So if it is repressed or if it is silent, it's two more suppressed. Your ability is going to be compromised. Well, knowing that let's jump over into our answer choices beginning by answer choice. The loss of its tumor suppressor function. Again, if its size system or suppressor function will definitely be compromised. This is a correct answer choice. So we're not going to cancel this out and increased risk of tumor genesis. While these two more genesis refers to the creation or the formation of tumors. If a tumor suppressor is affected, then the formation of tumors may be more observed. It may be more common because of this. It is actually a correct answer choices. But also we're not going to cancel it out. Then we have sea uncontrolled cell proliferation and the formation of tumors. This is more or less the same as answer choice B And it is a consequence as well of the silencing of this gene. So we're not going to cancel this out. And then we have the all of the above. Since we're not able to cancel out any of the answer choices, we're going to select answer choice. All of the above are correct. I really hope this video helped you, and I hope to see you on the next one.
Related Practice
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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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

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

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