Question 1

How is the translocation between chromosomes 8 and 14 thought to cause Burkitt lymphoma?&#10;A) It puts a proto-oncogene downstream of a strong promoter&#10;B) It fuses a proto-oncogene with another protein and alters its activity&#10;C) It deletes its opposing tumor suppressor&#10;D) It deletes a regulatory region for the gene&#10;E) It removes its 3' UTR

Accepted Answer

The translocation between chromosomes 8 and 14 places a proto-oncogene (MYC) downstream of a strong promoter (IgH enhancer), leading to its overexpression and contributing to the development of Burkitt lymphoma.

Question 2

Loss of telomerase expression prevents cells from doing which of the following?&#10;A) Repairing mismatch mutations&#10;B) Regulating their cell cycle appropriately&#10;C) Dividing indefinitely&#10;D) Synthesizing the leading DNA strand during replication&#10;E) Becoming senescent

Accepted Answer

Telomerase is an enzyme that adds telomere repeats to the ends of chromosomes, which enables cells to divide indefinitely. Therefore, loss of telomerase expression would prevent cells from dividing indefinitely.

Question 3

Mismatch repair defects causing hereditary nonpolyposis colon cancer are associated with which molecular phenomenon,which can be helpful for diagnosis?&#10;A) DNA hypomethylation&#10;B) DNA hypermethylation&#10;C) DNA hypercondensation&#10;D) Microsatellite instability&#10;E) DNA breakage

Accepted Answer

Mismatch repair defects cause microsatellite instability, which refers to alterations in the lengths of short, tandemly repeated DNA sequences. This molecular phenomenon is helpful for the diagnosis of hereditary nonpolyposis colon cancer (HNPCC), also known as Lynch syndrome. As many as 90% of HNPCC cases are associated with microsatellite instability, which can be detected by analyzing tumor DNA using microsatellite markers.

Question 4

Which of the following classes of proteins are likely to be encoded by proto-oncogenes?&#10;A) Mismatch repair proteins&#10;B) Apoptosis inducing proteins&#10;C) Negative regulators of the cell cycle&#10;D) Growth factor receptors&#10;E) Proteins involved in homologous recombination

Accepted Answer

Proto-oncogenes encode proteins that promote cell growth and division. Growth factor receptors are key receptors that mediate cell proliferation and are commonly encoded by proto-oncogenes. The other choices are not typically encoded by proto-oncogenes. Mismatch repair proteins are involved in DNA repair, apoptosis inducing proteins promote cell death, negative regulators of the cell cycle slow down cell division, and proteins involved in homologous recombination are involved in DNA repair.

Question 5

In addition to mutations in the coding region and regulatory elements,oncogenes often arise by which mechanism?&#10;A) Gene amplification&#10;B) Loss of heterozygosity&#10;C) Splice mutations&#10;D) Interstitial deletions&#10;E) Nondisjunction

Accepted Answer

Oncogenes can arise through gene amplification, which results in an increased copy number of the oncogene. This can lead to high levels of expression and dysregulation of cellular processes. Loss of heterozygosity, splice mutations, interstitial deletions, and nondisjunction are also mechanisms that can contribute to the development of cancer, but they are not as commonly associated with the formation of oncogenes.

Question 6

How does the Philadelphia chromosome activate an oncogene?&#10;A) It puts a proto-oncogene downstream of a strong promoter&#10;B) It fuses a proto-oncogene with another protein and alters its activity&#10;C) It deletes its opposing tumor suppressor&#10;D) It deletes a regulatory region for the gene&#10;E) It removes its 3' UTR

Accepted Answer

The Philadelphia chromosome is a reciprocal translocation between chromosomes 9 and 22 that fuses the BCR (breakpoint cluster region) gene on chromosome 22 with the ABL (Abelson) gene on chromosome 9, creating a fusion gene called BCR-ABL. The ABL gene is a proto-oncogene that encodes a protein tyrosine kinase involved in cell signaling pathways. When it fuses with the BCR gene, which has a strong promoter, the resulting BCR-ABL fusion protein is constitutively active and promotes uncontrolled cell proliferation, leading to the development of chronic myelogenous leukemia (CML). Thus, the Philadelphia chromosome activates an oncogene (ABL) by fusing it with another protein (BCR) and altering its activity.

Question 7

Following a first mutation in a tumor suppressor gene,which of the following is commonly associated with the &#34;second hit&#34; in tumor generation?&#10;A) Loss of heterozygosity&#10;B) Fusion of two genes&#10;C) Insertional mutagenesis&#10;D) Gene duplication&#10;E) Any of the above

Accepted Answer

Loss of heterozygosity (LOH) is commonly associated with the second hit in tumor generation. LOH occurs when the second allele of the tumor suppressor gene is also lost or inactivated, leading to the complete loss of function of the gene. This is often the result of a chromosomal deletion or recombination event. While the other options can also contribute to tumor generation, they are not typically associated with the second hit in tumor suppressor genes.

Question 8

Which of the following epigenetic modifications is associated with cancer?&#10;A) DNA hypermethylation&#10;B) DNA hypomethylation&#10;C) Histone hypoacetylation&#10;D) All of the above&#10;E) None of the above

Accepted Answer

All three epigenetic modifications (DNA hypermethylation, DNA hypomethylation, and histone hypoacetylation) have been associated with cancer development and progression. DNA hypermethylation can silence tumor suppressor genes and lead to uncontrolled cell growth. DNA hypomethylation can activate oncogenes and cause genomic instability. Histone hypoacetylation can also silence tumor suppressor genes and alter gene expression patterns in cancer cells.

Deck 14: Cancer Genetics