Question 1

Fusion of the reading frames of the bcr and abl genes,as is often observed in cases of chronic myelogenous leukemia CML),is an example of what type of genetic alteration?&#10;A)A reciprocal chromosomal translocation&#10;B)A nonreciprocal chromosomal translocation&#10;C)A frameshift mutation&#10;D)A chromosomal deletion&#10;E)None of the above

Accepted Answer

The fusion of the bcr and abl genes in chronic myelogenous leukemia (CML) is a result of a reciprocal chromosomal translocation, specifically the Philadelphia chromosome translocation (t(9;22)(q34;q11)). This translocation swaps portions of chromosomes 9 and 22, bringing the bcr and abl genes into close proximity, which leads to the formation of a hybrid gene that contributes to the development of CML.

Question 2

Which of the following types of genetic alterations would be associated with an increased aggressiveness of cancer cells?&#10;A)Amplification of ErbB2&#10;B)Amplification of Myc&#10;C)Decreased expression of ErbB2&#10;D)Lower expression of Myc&#10;E)A and B

Accepted Answer

Amplification of ErbB2 and Myc are frequently associated with increased aggressiveness of cancer cells. In contrast, decreased expression of ErbB2 and lower expression of Myc are not associated with increased aggressiveness.

Question 3

Which of the following consequences of mutations would be LEAST likely to be associated with an increased cancer risk?&#10;A)Truncation of the EGF receptor&#10;B)Amplification of myc&#10;C)Amplification of ErbB2&#10;D)Truncation of H-Ras due to a premature stop codon.&#10;E)Constitutive activation of K-Ras

Accepted Answer

Truncation of proteins like H-Ras due to a premature stop codon often results in a nonfunctional protein rather than one that promotes cell proliferation. In the context of cancer, mutations that lead to increased cell growth or survival (such as amplification of oncogenes like myc or ErbB2, or constitutive activation of proteins like K-Ras) are more likely to contribute to cancer risk. Truncation mutations can sometimes lead to loss of tumor suppressor function, but in the case of an oncogene like H-Ras, truncation is less likely to promote cancer compared to the other options listed.

Question 4

Gene amplification can be detected by&#10;A)Observation of homogeneously staining regions using microscopy.&#10;B)Deletion of the arm of a chromosome.&#10;C)Observation of extrachromosomal &#34;double minutes.&#34;&#10;D)A and C.&#10;E)None of the above.

Accepted Answer

Observation of homogeneously staining regions (HSRs) and extrachromosomal "double minutes" (DMs) are both indicative of gene amplification, with HSRs being localized amplification on a chromosome and DMs being extrachromosomal circles of DNA carrying amplified genes. Deletion of a chromosome arm is not indicative of gene amplification.

Question 5

Which of the following statements is TRUE?&#10;A)All types of cancer are associated with a transforming retrovirus.&#10;B)Breast cancer patients whose tumors express elevated levels of ErbB2 usually have a longer median survival after diagnosis than those with normal levels of this protein.&#10;C)Retrovirus-associated oncogenes are often related to the oncogenes found in increased copy numbers in non-virally induced tumor cells.&#10;D)Patients with bladder cancer often have reduced levels of H-Ras expression.&#10;E)None of the above.

Accepted Answer

Retrovirus-associated oncogenes often share similarity with cellular oncogenes, which can be found in increased copy numbers in tumor cells not caused by viruses. This reflects the common mechanisms of oncogene activation in cancer, whether virally induced or not.

Question 6

Oncogenic mutations in H-Ras are most often the result of&#10;A)Point mutations resulting in a premature stop codon.&#10;B)Point mutations that change the protein's structure and result in its constitutive activation.&#10;C)Insertion of extra bases in exon 1 of the gene.&#10;D)Frameshift mutations.&#10;E)None of the above.

Accepted Answer

Oncogenic mutations in H-Ras are most often point mutations in the gene that change the protein's structure and result in its constitutive activation. This means that the mutated H-Ras protein is always "on" and signaling to the cell to divide and grow, which can lead to the development of cancer.

Question 7

Approximately what percentage of human tumors are associated with infectious agents?&#10;A)5%&#10;B)10%&#10;C)20%&#10;D)40%&#10;E)60%

Accepted Answer

Approximately 20% of human tumors are associated with infectious agents, such as viruses or bacteria. This includes well-known examples such as HPV-associated cervical cancer and Helicobacter pylori-associated stomach cancer. However, it is important to note that not all infections lead to cancer and not all cancers are caused by infections.

Question 8

Which of the following mechanisms may contribute to tumorigenesis driven by the myc oncogene?&#10;A)Increased myc copy number&#10;B)Constitutive activation of myc under the transcriptional control of viral promoters&#10;C)Chromosomal translocations&#10;D)A,B,and C&#10;E)None of the above

Accepted Answer

Tumorigenesis driven by the myc oncogene can be caused by multiple mechanisms which includes increased myc copy number, constitutive activation of myc under the transcriptional control of viral promoters and chromosomal translocations. Therefore, option D is the correct choice.

Question 9

Which of the following factors are associated with Burkitt's lymphoma formation?&#10;A)Malarial infection&#10;B)Infection with Epstein-Barr virus EBV)&#10;C)Mutation in c-myc&#10;D)Mutation in ErbB2&#10;E)A,B,and C

Accepted Answer

Burkitt's lymphoma is associated with all three factors: Malarial infection, Epstein-Barr virus (EBV) infection, and mutation in c-myc. ErbB2 mutation is not specifically associated with Burkitt's lymphoma.

Question 10

Normal proto-oncogenes found in the human genome can be activated to become oncogenes by&#10;A)Somatic mutations that result in higher levels of expression of the gene.&#10;B)Deregulation by retroviral elements.&#10;C)Mutations resulting in structural changes in the protein product of the gene.&#10;D)A,B,and C.&#10;E)None of the above.

Accepted Answer

All three options (somatic mutations that result in higher levels of expression of the gene, deregulation by retroviral elements, mutations resulting in structural changes in the protein product of the gene) can activate proto-oncogenes to become oncogenes. Therefore, the correct answer is D, all of the above.

Question 11

The transforming abilities of the Bcr-Abl fusion protein are due primarily to the deregulated firing of its tyrosine kinase,which is equivalent to what domain of the normal Abl protein?&#10;A)The SH1 domain&#10;B)The SH2 domain&#10;C)The SH3 domain&#10;D)The DNA binding domain&#10;E)None of the above

Accepted Answer

The answer of The transforming abilities of the Bcr-Abl fusion...

Question 12

DNA from human lung tumor cells was used to transfect NIH 3T3 mouse embryo fibroblast)cells.After several weeks,some of these cells formed foci,or clusters of cells,on the plate.Cells isolated from these foci were able to grow in soft agar and formed tumors when injected subcutaneously into immunocompromised mice.These results suggest that

A)The oncogene present in the human lung tumor cells is also able to transform NIH 3T3 mouse cells.
B)The NIH 3T3 cells were most likely transformed by multiple oncogenes present in the donor cells.
C)The NIH 3T3 cells were most likely transformed by a single oncogene present in the donor cells.
D)A and C.
E)A,B,and C.

Accepted Answer

The answer of DNA from human lung tumor cells was...

Deck 4: Cellular Oncogenes