Exam 2
In cells infected with simian sarcoma virus, the sis oncogene causes the cells to release increased amounts of Sis protein, which is recognized by PDGF-receptor on the same cells’ surface. This type of signaling loop is an example of _____
A. Endocrine signaling.
B. Paracrine signaling.
C. Autocrine signaling.
D. Trans-receptor signaling
C. Autocrine signaling.
Cell surface receptors that are able to create mechanical stability by tethering cells to the extracellular matrix (ECM) are known as _____
A. Adhesions.
B. Integrases.
C. Integrins.
D. Cytokines
C. Integrins.
Which of the following signaling pathways is in the correct order?
A. Receptor → Sos → Ras
B. Receptor → Ras → Sos
C. Ras → Sos → receptor
D. Sos → Ras → receptor
A. Receptor → Sos → Ras
11. If a normal cell and a cancer cell are fused and the resulting hybrids lose their ability to form tumors, it suggests that ______.
A. The cancer cell alleles are dominant over the normal cell alleles.
B. The cancer cell alleles are recessive to the normal cell alleles.
C. The normal and cancer cell alleles are co-dominant.
D. The original tumor formed as a result of infection by a tumor virus
B. The cancer cell alleles are recessive to the normal cell alleles.
9. Which of the following is NOT true of β-catenin?
A. It acts as the receptor for Wnt signaling molecules.
B. In the presence of Wnt signal, it translocates to the nucleus to drive transcription of target genes.
C. It is degraded when bound to active GSK-3β.
D. It is a downstream effector in the Wnt signaling pathway.
A. It acts as the receptor for Wnt signaling molecules.
16. Which of the following is NOT true of p53?
A. Most tumor-associated p53 mutations are the result of frameshift mutations.
B. p53 is mutated in over 30–50% of all cancers.
C. Normal p53 functions as a “tumor suppressor.”
D. Exposure to UV radiation results in increased expression of p53.
A. Most tumor-associated p53 mutations are the result of frameshift mutations.
17. Increased expression of MDM2 may result in _____.
A. Increased expression of p53.
B. Apoptosis.
C. Cell cycle arrest.
D. Degradation of p53.
D. Degradation of p53.
10. ________signaling is unique in that the downstream effector molecule can act as either a repressor or an activator.
A. GPCR
B. Notch
C. TGF-b
D. Hedgehog
D. Hedgehog
21. Transfection experiments show that you only need to transfect two oncogenes in mouse primary cells to transform cells whereas human primary cells require transfection of at least five oncogenes to lead to transformation. Why is this?
A. Mouse cells take up DNA easier.
B. Larger animals are more resistant to transformation since they have more cells that need to get mutated.
C. Mice are not exposed to carcinogens in the wild so they are less resistant to transformation.
D. Larger animals have evolved to be more resistant to transformation since they undergo more mitoses.
D. Larger animals have evolved to be more resistant to transformation since they undergo more mitoses.
20. Apoptotic cell death can be induced by _______.
A. p53 signaling.
B. Signaling from surface cell death receptors.
C. Extracellular stresses.
D. All of the above
D. All of the above
22. A tumor promoter_____
A. Induces mutations in DNA
B. Can cause cancer on its own
C. Enhances tumorigenesis through nongenetic mechanisms
D. Induces eipigenetic changes on DNA
C. Enhances tumorigenesis through nongenetic mechanisms
13. Which of the following is NOT an example of how tumor suppressor genes can become inactivated?
A. Somatic mutation.
B. Promoter demethylation.
C. Loss of heterozygosity.
D. Promoter hypermethylation.
B. Promoter demethylation.
18. Which of the following types of p53 mutations would be MOST beneficial to a tumor cell?
A. Premature stop codon.
B. Silent mutation.
C. Frameshift.
D. Missense mutation.
D. Missense mutation.
3. Which of the following statements is FALSE concerning nuclear receptors?
A. Their activation is dependent on small hydrophobic ligands
B. They usually reside within the plasma membrane
C. They often activate transcription by binding to DNA
D. They usually are often involved in hormonal signaling
B. They usually reside within the plasma membrane
15. Which of the following statements about familial cancers is TRUE?
A. DNA maintenance genes are inherited which function as the gatekeepers of the cell.
B. Tumor suppressor genes are inherited which function as the caretakers of the cell.
C. DNA maintenance genes are inherited which function as the caretakers of the cell.
D. Mutant genes are not inherited in familial cancers.
C. DNA maintenance genes are inherited which function as the caretakers of the cell.
8. Which of the following molecules is NOT a downstream effector of Ras?
A. Gal-GEFs
B. PI3K
C. Grb2
D. Raf
C. Grb2
24. Which of the following types of cells have the ability to form a tumor?
A. Any cell that acquired mutations in oncogenes or tumor suppressor genes
B. Cells that acquired mutations in oncogenes or tumor suppressor genes and are in a stem cell like state
C. Cells that acquired mutations in oncogenes or tumor suppressor genes and are in a terminally differentiated state
D. Any cell that is in a stem cell like state
B. Cells that acquired mutations in oncogenes or tumor suppressor genes and are in a stem cell like state
4. Which of the following is NOT a reason for deregulated firing of tyrosine kinase receptors in cancer?
A. Fusion events that prevent dimerization.
B. Mutations resulting in truncation of the receptor extracellular domain.
C. Overexpression of the receptor.
D. Translocations that fuse a dimerization domain to the receptor
A. Fusion events that prevent dimerization.
19. Which of the following is an anti-apoptotic strategy used by cancer cells?
A. Loss of expression of Mdm2
B. Activation of the p53 pathway
C. Inactivation of Bax
D. Activation of death receptors
C. Inactivation of Bax
5. Which of the following statements is FALSE regarding Ras mutations in cancer patients?
A. Mutations often occur at codons 12, 13, or 61.
B. Oncogenic mutations usually result in higher levels of GDP-bound Ras.
C. Oncogenic mutations usually result in higher levels of GTP-bound Ras.
D. Ras mutations lead to pleiotropic phenotypic effects.
B. Oncogenic mutations usually result in higher levels of GDP-bound Ras.
What is the function of SH-2-domain containing proteins?
A. To activate the tyrosine kinase by phosphorylating its cytoplasmic tail.
B. They act as guanine nucleotide exchange factors to activate downstream effectors in tyrosine kinase signaling cascades.
C. They are GTPase-activating proteins and function to deactivate downstream effectors in tyrosine kinase signaling cascades.
D. They recognize and bind to phospho-tyrosine residues on tyrosine kinase receptors to interact with and activate membrane tethered molecules
D. They recognize and bind to phospho-tyrosine residues on tyrosine kinase receptors to interact with and activate membrane tethered molecules
25. Which of the following is true regarding multi-step tumorigenesis?
A. Tumors from the same tissue all acquire mutations affecting the same pathways at progressive stages of tumorigenesis.
B. Tumors from the same tissue all acquire identical mutations at progressive stages of tumorigenesis.
C. Tumors from the same tissue all acquire an identical set of mutations before tumorigenesis gets initiated.
D. Tumors from the same tissue all acquire mutations affecting the same pathways before tumorigenesis gets initiated.
A. Tumors from the same tissue all acquire mutations affecting the same pathways at progressive stages of tumorigenesis.
23. The rate at which mutations occur in the cells within a tumor is most likely ____.
A. The same as in normal cells of that tissue type.
B. Less frequent than in normal cells of that tissue type.
C. More frequent than in normal cells of that tissue type during all stages of tumor progression.
D. More frequent that in normal cells of that tissue type only at advanced stages when genomic instability occurs.
D. More frequent that in normal cells of that tissue type only at advanced stages when genomic instability occurs.
12. You are studying a cell line in which the loss of just one copy of a tumor suppressor gene provides a growth advantage for the cells (the other copy is fully wildtype). This would be an example of _____.
A. Co-dominance.
B. A dominant negative effect.
C. A synergistic effect.
D. Loss of heterozygosity.
B. A dominant negative effect
14. You are studying cancer cells and hypothesize that you have found a previously unidentified tumor suppressor gene. Which of the following results would support your hypothesis?
A. You have found several gain-of-function mutations in this gene in a wide variety of cancers.
B. You have identified a gain-of-function mutation in this gene that results in the transformation of normal cells.
C. Functional analysis has revealed that the wild-type form of the gene that you have identified serves to drive proliferation.
D. You have found loss of heterozygosity in the locus containing your gene in a number of human lung cancer samples.
D. You have found loss of heterozygosity in the locus containing your gene in a number of human lung cancer samples.