Deck 23: Cancer
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Deck 23: Cancer
1
Describe the differences between direct-acting and indirect-acting carcinogens.
Direct-acting carcinogens have reactive electrophiles that react with nitrogen and oxygen atoms in DNA.These modified nucleotides distort the normal pattern of base pairing.Indirect-acting carcinogens are generally unreactive,water-insoluble compounds.These compounds must first be converted to ultimate carcinogens by the introduction of electrophilic centers,usually by cytochrome P-450 enzymes in the liver.
2
Direct-acting carcinogens are those that:
A)chemically react with nitrogen and phosphorous atoms in DNA.
B)work in conjunction with cytochrome P-450 in the endoplasmic reticulum.
C)are mainly reactive electrophiles.
D)all of the above
A)chemically react with nitrogen and phosphorous atoms in DNA.
B)work in conjunction with cytochrome P-450 in the endoplasmic reticulum.
C)are mainly reactive electrophiles.
D)all of the above
C
3
Describe the Warburg effect and how it applies to cancer cells.
Otto Warburg described how cancer cells,regardless of the level of oxygen in their environment,produce large amounts of lactate as a result of using aerobic glycolysis to produce energy.
4
Which of the following is NOT a role for the tumor microenvironment?
A)tumor cells contain mutations
B)interaction with immune cells
C)neighboring cells relay information to cancer cells
D)HCV-mediated inflammation
A)tumor cells contain mutations
B)interaction with immune cells
C)neighboring cells relay information to cancer cells
D)HCV-mediated inflammation
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5
Which of the following is NOT a microscopic characteristic of tumor cells?
A)high nuclear to cytoplasmic ratio
B)greater percentage of mitotic cells
C)larger size
D)few specialized structures
A)high nuclear to cytoplasmic ratio
B)greater percentage of mitotic cells
C)larger size
D)few specialized structures
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6
Gain-of-function mutations in which of the following genes typify colorectal carcinomas?
A)APC
B)p53
C)K-ras
D)all of the above
A)APC
B)p53
C)K-ras
D)all of the above
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7
Which of the following promotes angiogenesis?
A)EGF
B)PDGF
C)TGFβ
D)VEGF
A)EGF
B)PDGF
C)TGFβ
D)VEGF
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8
What is the multi-hit model of cancer? What data support this model?
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9
Which of the following proteins involved in angiogenesis is paired correctly with its function?
A)HIF - tyrosine kinase
B)VEGF - receives a secreted signal to induce blood vessel growth
C)oxygen sensor - transcription factor
D)VEGF receptor - tyrosine kinase
A)HIF - tyrosine kinase
B)VEGF - receives a secreted signal to induce blood vessel growth
C)oxygen sensor - transcription factor
D)VEGF receptor - tyrosine kinase
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10
Name the six fundamental properties of malignant tumors.Which of these properties are amenable to study in a cell culture model of cancer?
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11
In females,all the cells in a tumor have the same inactive X chromosome.The reason for this is that:
A)all of the cells in a tumor are derived from a single progenitor cell.
B)all late-stage tumors have chromosome abnormalities.
C)multiple mutations are required for tumor induction.
D)many tumor-suppressor genes are on the X chromosome.
A)all of the cells in a tumor are derived from a single progenitor cell.
B)all late-stage tumors have chromosome abnormalities.
C)multiple mutations are required for tumor induction.
D)many tumor-suppressor genes are on the X chromosome.
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12
The first line of defense against point mutations is:
A)BRCA1.
B)cytochrome P-450.
C)DNA polymerase.
D)MSH2.
A)BRCA1.
B)cytochrome P-450.
C)DNA polymerase.
D)MSH2.
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13
Exposure to benzo(a)pyrene is most frequently associated with which type of cancer?
A)lung cancer
B)Burkitt's lymphoma
C)colorectal cancer
D)breast cancer
A)lung cancer
B)Burkitt's lymphoma
C)colorectal cancer
D)breast cancer
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14
Which of the following interventions would NOT be likely to prevent tumor cells from metastasizing?
A)inhibitors of adhesion molecules
B)inhibitors of enzymes that degrade the basement membrane
C)inhibitors of cell motility
D)inhibitors of EGF
A)inhibitors of adhesion molecules
B)inhibitors of enzymes that degrade the basement membrane
C)inhibitors of cell motility
D)inhibitors of EGF
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15
Leukemias are different from most other classes of cancers.Which of the fundamental properties of cancer cells are likely to be lacking in leukemias and why?
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16
Which of the following is a characteristic of malignant tumors?
A)localized to tissue of origin
B)metastatic
C)well differentiated
D)sense signals that restrict cell division
A)localized to tissue of origin
B)metastatic
C)well differentiated
D)sense signals that restrict cell division
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17
During metastasis,cells may undergo an epithelial-to-mesenchymal transition whereby there is a(n):
A)increase in cell polarity.
B)loss of cell-cell-adhesion.
C)down-regulation in the expression of the Snail and Twist transcription factors.
D)all of the above
A)increase in cell polarity.
B)loss of cell-cell-adhesion.
C)down-regulation in the expression of the Snail and Twist transcription factors.
D)all of the above
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18
Telomerase:
A)induces apoptosis.
B)contains reverse transcriptase.
C)is inactivated by Bcl-2.
D)is active in all normal adult cells.
A)induces apoptosis.
B)contains reverse transcriptase.
C)is inactivated by Bcl-2.
D)is active in all normal adult cells.
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19
A bone tumor sample appears to be heterozygous for a p53 mutation.The most likely explanation for this finding is:
A)Mutated p53 is an oncogene.
B)The p53 mutation is resulting in a dominant negative p53 protein.
C)The p53 mutation is resulting in a premature stop codon,and no functional protein is made from that allele.
D)There was a mistake in labeling the tissue sample-all tumors musts lack p53.
A)Mutated p53 is an oncogene.
B)The p53 mutation is resulting in a dominant negative p53 protein.
C)The p53 mutation is resulting in a premature stop codon,and no functional protein is made from that allele.
D)There was a mistake in labeling the tissue sample-all tumors musts lack p53.
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20
2-hydroxyglutarate is produced in cancer cells:
A)because cancer cells exhibit increased aerobic glycolysis.
B)that have mutations in isocitrate dehydrogenase.
C)to counteract all the lactate produced by aerobic glycolysis.
D)all of the above
A)because cancer cells exhibit increased aerobic glycolysis.
B)that have mutations in isocitrate dehydrogenase.
C)to counteract all the lactate produced by aerobic glycolysis.
D)all of the above
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21
Which of the following is NOT evidence that smoking causes lung cancer?
A)Epidemiological rates of lung cancer dramatically increased after more people started to smoke.
B)Exposure of lung cells to the active carcinogen found in cigarettes causes mutations in p53.
C)Mutations in p53 are found in the same codons in patients with lung cancer who smoke as in cultured cells treated with benzo(a)pyrene.
D)Epidemiological rates of lung cancer in women increased years after the rates in men increased.
A)Epidemiological rates of lung cancer dramatically increased after more people started to smoke.
B)Exposure of lung cells to the active carcinogen found in cigarettes causes mutations in p53.
C)Mutations in p53 are found in the same codons in patients with lung cancer who smoke as in cultured cells treated with benzo(a)pyrene.
D)Epidemiological rates of lung cancer in women increased years after the rates in men increased.
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22
What are the differences and similarities between the transforming genes of retroviruses and those of DNA tumor viruses?
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23
What renders erbB and her2 oncogenic? What are their normal proto-oncogene counterparts?
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24
Which of the following is a proto-oncogene?
A)APC
B)myc
C)ptc1
D)Rb
A)APC
B)myc
C)ptc1
D)Rb
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25
Ras is a:
A)growth factor.
B)kinase.
C)phosphatase.
D)none of the above
A)growth factor.
B)kinase.
C)phosphatase.
D)none of the above
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26
Burkitt's lymphoma results from the overproduction of:
A)Fos.
B)Myc.
C)Ras.
D)Src.
A)Fos.
B)Myc.
C)Ras.
D)Src.
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27
Describe gain-of-function and loss-of-function mutations with respect to cancer.
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28
Explain how the chemotherapeutic drug Gleevec works in the treatment of myelogenous leukemia.
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29
How can DNA microarrays be used to detect gene amplifications in cancer cells?
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30
Cancer genome analysis has been utilized for all the following applications,except:
A)to identify which patients are good candidates for molecularly targeted drugs.
B)to identify cancerous cells in a biopsy based on morphological characteristics.
C)to identify driver mutations.
D)to identify the link between chromothripsis and aggressive neuroblastoma.
A)to identify which patients are good candidates for molecularly targeted drugs.
B)to identify cancerous cells in a biopsy based on morphological characteristics.
C)to identify driver mutations.
D)to identify the link between chromothripsis and aggressive neuroblastoma.
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31
Transgenic mice that express an activated oncogene like rasᴰ under the control of the TetOFF system are likely to undergo which of the following events when tetracycline is given?
A)growth of tumors
B)shrinkage of tumors
C)no effect on tumors
D)tumors become metastatic
A)growth of tumors
B)shrinkage of tumors
C)no effect on tumors
D)tumors become metastatic
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32
Nearly all malignant tumors possess a loss-of-function mutation in one or more cell cycle checkpoints.However,a loss of checkpoints is not a requisite characteristic of cancer cells per se.Explain this paradox.
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33
Which of the following proteins belong to the control system that regulates cells past a certain point in late G₁ (START)?
A)CDK4
B)cyclin B
C)Rb
D)CDK4 and Rb
A)CDK4
B)cyclin B
C)Rb
D)CDK4 and Rb
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34
A patient with B cell leukemia donates some cancer cells for analysis.The cells do not contain the usual chromosomal translocations associated with leukemia.Instead,a sporadic mutation seems to have arisen in a certain gene,followed by loss of heterozygosity in the second copy.This gene product is most likely:
A)Ras.
B)Rb.
C)VEGF.
D)telomerase.
A)Ras.
B)Rb.
C)VEGF.
D)telomerase.
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35
A loss-of-function mutation in _____ would have the same effect as a gain-of-function mutation in Ras.
A)Crk
B)Csk
C)Myc
D)NF1
A)Crk
B)Csk
C)Myc
D)NF1
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36
Hereditary cancers typically possess loss-of-heterozygosity in:
A)proto-oncogenes.
B)tumor-suppressor genes.
C)both proto-oncogenes and tumor-suppressor genes.
D)neither proto-oncogenes nor tumor-suppressor genes.
A)proto-oncogenes.
B)tumor-suppressor genes.
C)both proto-oncogenes and tumor-suppressor genes.
D)neither proto-oncogenes nor tumor-suppressor genes.
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37
Which of the following is(are)a tumor suppressor gene?
A)APC
B)ras
C)Rb
D)APC and Rb
A)APC
B)ras
C)Rb
D)APC and Rb
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38
If colon cancers could be prevented by intervening in the earliest molecular changes during multi-hit progression,the molecule you would target for intervention would be:
A)p53.
B)Ras.
C)APC.
D)VEGF.
A)p53.
B)Ras.
C)APC.
D)VEGF.
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39
Src is a:
A)growth factor.
B)kinase.
C)phosphatase.
D)transcription factor.
A)growth factor.
B)kinase.
C)phosphatase.
D)transcription factor.
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40
Germ-line mutations in which of the following has(have)been implicated in hereditary cancers?
A)HPV
B)BRCA1
C)Rb
D)BRCA1 and Rb
A)HPV
B)BRCA1
C)Rb
D)BRCA1 and Rb
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41
A gain-of-function mutation in _____ will bypass restriction point controls.
A)cyclin D
B)p16
C)Rb
D)cyclin D and p16
A)cyclin D
B)p16
C)Rb
D)cyclin D and p16
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42
The human papillomavirus E7 protein inhibits the function of:
A)p53.
B)Rb.
C)PDGF receptor.
D)all of the above
A)p53.
B)Rb.
C)PDGF receptor.
D)all of the above
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43
MicroRNAs are a new class of oncogenic factors because they function:
A)as tumor suppressors.
B)as oncogenes.
C)to induce errors during DNA replication.
D)as tumor suppressors and as oncogenes.
A)as tumor suppressors.
B)as oncogenes.
C)to induce errors during DNA replication.
D)as tumor suppressors and as oncogenes.
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