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Ch. 11 - Gene Mutation, DNA Repair, and Homologous Recombination
All textbooksSanders 3rd EditionCh. 11 - Gene Mutation, DNA Repair, and Homologous RecombinationProblem 4
Chapter 11, Problem 4

Explain the following processes involving chromosome mutations and cancer development. How the chromosome mutation producing Burkitt lymphoma generates the disease.

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1
Understand that Burkitt lymphoma is associated with a specific chromosomal translocation, typically between chromosome 8 and chromosome 14.
Recognize that this translocation involves the MYC oncogene on chromosome 8 being placed near the immunoglobulin heavy chain locus on chromosome 14.
Realize that the translocation leads to the deregulation of the MYC gene, causing it to be overexpressed due to the active promoter of the immunoglobulin gene.
Acknowledge that the overexpression of the MYC oncogene results in uncontrolled cell proliferation, a hallmark of cancer development.
Connect the dots by understanding that this chromosomal mutation and subsequent MYC overexpression drive the development of Burkitt lymphoma, a type of cancer.

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Key Concepts

Here are the essential concepts you must grasp in order to answer the question correctly.

Chromosome Mutations

Chromosome mutations refer to alterations in the structure or number of chromosomes, which can lead to genetic disorders or diseases. These mutations can occur through various mechanisms, such as deletions, duplications, inversions, or translocations. In the context of cancer, specific chromosome mutations can disrupt normal cell cycle regulation, leading to uncontrolled cell growth.
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Mutations and Phenotypes

Burkitt Lymphoma

Burkitt lymphoma is a type of non-Hodgkin lymphoma characterized by the rapid growth of tumors, often in the jaw or abdomen. It is associated with a specific chromosomal translocation, typically involving the MYC gene on chromosome 8 and immunoglobulin genes on chromosomes 14, 2, or 22. This translocation leads to the overexpression of the MYC oncogene, driving the proliferation of B-cells and contributing to cancer development.

Oncogenes and Tumor Suppressor Genes

Oncogenes are mutated forms of normal genes (proto-oncogenes) that promote cell division and survival, often leading to cancer when overactive. In contrast, tumor suppressor genes normally inhibit cell division or promote apoptosis, and their loss of function can also contribute to cancer. The interplay between oncogenes and tumor suppressor genes is crucial in understanding how chromosome mutations, like those seen in Burkitt lymphoma, can lead to malignant transformations.
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Related Practice
Textbook Question

For the retinal cancer retinoblastoma, the inheritance of one mutated copy of RB1 from one of the parents is often referred to as a mutation that produces a 'dominant predisposition to cancer.' This means that the first mutation does not produce cancer but makes it very likely that cancer will develop.

Explain why cancer is almost certain to develop with the inheritance of one mutated copy of RB1.

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Textbook Question

What are the differences between a synonymous mutation, a missense mutation, and a nonsense mutation?

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Textbook Question

Explain the following processes involving chromosome mutations and cancer development.

How the chromosome mutation producing the Philadelphia chromosome leads to CML.

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Textbook Question
In March 2011 an earthquake measuring approximately 9.0 on the Richter scale struck Fukushima, Japan. Several nuclear reactors at the Fukushima Daichii Nuclear Power Plant were damaged, and nuclear core meltdown occurred. A massive release of radiation accompanied damage to the plant, and 5 years later the incidence of thyroid cancer in children exposed to the radiation was determined to be well over 100 times more frequent than expected without radiation exposure. DNA damage and mutations resulting from radiation exposure are suspected of causing this increased cancer rate. What gene discussed in this chapter might be responsible for pausing the cell cycle of dividing cells long enough for radiation-induced damage to be repaired in cells?
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Textbook Question
In March 2011 an earthquake measuring approximately 9.0 on the Richter scale struck Fukushima, Japan. Several nuclear reactors at the Fukushima Daichii Nuclear Power Plant were damaged, and nuclear core meltdown occurred. A massive release of radiation accompanied damage to the plant, and 5 years later the incidence of thyroid cancer in children exposed to the radiation was determined to be well over 100 times more frequent than expected without radiation exposure. DNA damage and mutations resulting from radiation exposure are suspected of causing this increased cancer rate. Do you think it is possible that significant increases in the incidence of other types of cancer will occur in the future among people who were exposed to the Fukushima radiation? Why?
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Textbook Question

UV irradiation causes damage to bacterial DNA. What kind of damage is frequently caused and how does photolyase repair the damage?

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