Deck 4: Cellular Oncogenes

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?

A)A reciprocal chromosomal translocation
B)A nonreciprocal chromosomal translocation
C)A frameshift mutation
D)A chromosomal deletion
E)None of the above

Answer 1

A reciprocal chromosomal translocation

Question 2

Which of the following types of genetic alterations would be associated with an increased aggressiveness of cancer cells?

A)Amplification of ErbB2
B)Amplification of Myc
C)Decreased expression of ErbB2
D)Lower expression of Myc
E)A and B

Answer 2

A and B

Question 3

Which of the following consequences of mutations would be LEAST likely to be associated with an increased cancer risk?

A)Truncation of the EGF receptor
B)Amplification of myc
C)Amplification of ErbB2
D)Truncation of H-Ras due to a premature stop codon.
E)Constitutive activation of K-Ras

Answer 3

Truncation of H-Ras due to a premature stop codon.

Question 4

Gene amplification can be detected by

A)Observation of homogeneously staining regions using microscopy.
B)Deletion of the arm of a chromosome.
C)Observation of extrachromosomal "double minutes."
D)A and C.
E)None of the above.

Question 5

Which of the following statements is TRUE?

A)All types of cancer are associated with a transforming retrovirus.
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.
C)Retrovirus-associated oncogenes are often related to the oncogenes found in increased copy numbers in non-virally induced tumor cells.
D)Patients with bladder cancer often have reduced levels of H-Ras expression.
E)None of the above.

Question 6

Oncogenic mutations in H-Ras are most often the result of

A)Point mutations resulting in a premature stop codon.
B)Point mutations that change the protein's structure and result in its constitutive activation.
C)Insertion of extra bases in exon 1 of the gene.
D)Frameshift mutations.
E)None of the above.

Question 7

Approximately what percentage of human tumors are associated with infectious agents?

A)5%
B)10%
C)20%
D)40%
E)60%

Question 8

Which of the following mechanisms may contribute to tumorigenesis driven by the myc oncogene?

A)Increased myc copy number
B)Constitutive activation of myc under the transcriptional control of viral promoters
C)Chromosomal translocations
D)A,B,and C
E)None of the above

Question 9

Which of the following factors are associated with Burkitt's lymphoma formation?

A)Malarial infection
B)Infection with Epstein-Barr virus EBV)
C)Mutation in c-myc
D)Mutation in ErbB2
E)A,B,and C

Question 10

Normal proto-oncogenes found in the human genome can be activated to become oncogenes by

A)Somatic mutations that result in higher levels of expression of the gene.
B)Deregulation by retroviral elements.
C)Mutations resulting in structural changes in the protein product of the gene.
D)A,B,and C.
E)None 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?

A)The SH1 domain
B)The SH2 domain
C)The SH3 domain
D)The DNA binding domain
E)None of the above

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.