Deck 20: Cancer
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Deck 20: Cancer
1
A tumor is
A) a malignant growth.
B) any abnormal growth of cells.
C) a benign growth.
D) a cancerous growth.
A) a malignant growth.
B) any abnormal growth of cells.
C) a benign growth.
D) a cancerous growth.
B
2
Cancer is usually caused by
A) a cancer virus.
B) an inherited oncogene.
C) the stepwise breakdown of normal cell regulatory processes.
D) X rays.
A) a cancer virus.
B) an inherited oncogene.
C) the stepwise breakdown of normal cell regulatory processes.
D) X rays.
C
3
Tumor initiation occurs in a
A) single protein molecule.
B) single cell.
C) few cells.
D) single tissue.
A) single protein molecule.
B) single cell.
C) few cells.
D) single tissue.
B
4
The form of cancer with the highest mortality rate in the United States is _______ cancer.
A) breast
B) prostate
C) lung
D) colon
A) breast
B) prostate
C) lung
D) colon
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5
The mechanism by which normal cells stop proliferating as a result of reduced availability of growth factors is called
A) density dependent inhibition.
B) contact inhibition.
C) differentiation.
D) senescence.
A) density dependent inhibition.
B) contact inhibition.
C) differentiation.
D) senescence.
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6
Which characteristic is commonly the same in both normal cells and cancer cells?
A) Density-dependent inhibition of proliferation
B) Contact inhibition of migration
C) Growth factor requirements
D) Dependence on oxygen and nutrients
A) Density-dependent inhibition of proliferation
B) Contact inhibition of migration
C) Growth factor requirements
D) Dependence on oxygen and nutrients
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7
Compared to their normal counterparts, leukemic cells
A) continue to differentiate.
B) fail to proliferate.
C) fail to undergo apoptosis.
D) induce widespread apoptosis.
A) continue to differentiate.
B) fail to proliferate.
C) fail to undergo apoptosis.
D) induce widespread apoptosis.
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8
In some cases, tumors support their unrestricted proliferation producing a growth factor that they also respond to. This mechanism is called _______ signaling.
A) endocrine
B) juxtacrine
C) autocrine
D) paracrine
A) endocrine
B) juxtacrine
C) autocrine
D) paracrine
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9
A tumor promoter is a type of carcinogen that
A) induces apoptosis of healthy cells.
B) decreases chromosomal stability.
C) increases cell proliferation.
D) immortalizes cancer cells.
A) induces apoptosis of healthy cells.
B) decreases chromosomal stability.
C) increases cell proliferation.
D) immortalizes cancer cells.
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10
Ultraviolet radiation increases the likelihood of a cell becoming malignant primarily because UV radiation
A) induces melanocytes to express more melanin.
B) breaks DNA into fragments.
C) makes RNA polymerase more error-prone.
D) causes DNA damage that leads to mutations.
A) induces melanocytes to express more melanin.
B) breaks DNA into fragments.
C) makes RNA polymerase more error-prone.
D) causes DNA damage that leads to mutations.
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11
Asbestos increases the risk of mesothelioma and lung cancer because it
A) inhibits differentiation.
B) causes DNA damage.
C) turns on the BRCA oncogenes.
D) acts as a tumor promoter by stimulating cell proliferation.
A) inhibits differentiation.
B) causes DNA damage.
C) turns on the BRCA oncogenes.
D) acts as a tumor promoter by stimulating cell proliferation.
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12
Which of the following behaviors most increases the likelihood of developing cancer?
A) Drinking a glass of wine a day
B) Smoking a pack of cigarettes a day
C) Kissing a person who has cancer
D) Breathing the sawdust from a crown gall tumor
A) Drinking a glass of wine a day
B) Smoking a pack of cigarettes a day
C) Kissing a person who has cancer
D) Breathing the sawdust from a crown gall tumor
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13
Oncogenes were first discovered in
A) a chicken retrovirus.
B) a human DNA virus.
C) mouse cancer cells.
D) human cancer cells.
A) a chicken retrovirus.
B) a human DNA virus.
C) mouse cancer cells.
D) human cancer cells.
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14
The RNA viruses that most commonly pick up cellular oncogenes are the
A) adenoviruses.
B) retroviruses.
C) papilloma viruses.
D) HIV viruses.
A) adenoviruses.
B) retroviruses.
C) papilloma viruses.
D) HIV viruses.
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15
A proto-oncogene is
A) a normal gene from which an oncogene can arise.
B) one that has been picked up by an oncogenic virus.
C) evolving into an oncogene.
D) expressed normally in tumor cells.
A) a normal gene from which an oncogene can arise.
B) one that has been picked up by an oncogenic virus.
C) evolving into an oncogene.
D) expressed normally in tumor cells.
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16
The viral raf oncogene produces a constitutively active protein because the
A) gene is always on.
B) kinase domain is mutant and cannot be competitively inhibited.
C) regulatory domain has been replaced by viral sequences so the protein cannot be turned off.
D) GTPase activity is deficient and the protein is always in the GTP form.
A) gene is always on.
B) kinase domain is mutant and cannot be competitively inhibited.
C) regulatory domain has been replaced by viral sequences so the protein cannot be turned off.
D) GTPase activity is deficient and the protein is always in the GTP form.
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17
Which statement describes the first direct evidence for involvement of cellular oncogenes in human tumors?
A) Normal human cells could be transformed by the src-containing Rous sarcoma viruses.
B) DNA extracted from a human bladder carcinoma was able to transform recipient mouse cells in culture.
C) DNA extracted from a mouse carcinoma was able to transform recipient human cells in culture.
D) DNA extracted from a human carcinoma was able to transform recipient chicken cells in culture.
A) Normal human cells could be transformed by the src-containing Rous sarcoma viruses.
B) DNA extracted from a human bladder carcinoma was able to transform recipient mouse cells in culture.
C) DNA extracted from a mouse carcinoma was able to transform recipient human cells in culture.
D) DNA extracted from a human carcinoma was able to transform recipient chicken cells in culture.
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18
The most frequently encountered oncogene in human tumors is
A) fos.
B) myc.
C) ras.
D) src.
A) fos.
B) myc.
C) ras.
D) src.
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19
C-myc becomes an oncogene in Burkitt's lymphoma and several plasmacytomas by a
A) point mutation.
B) duplication.
C) translocation to the immunoglobulin heavy chain locus.
D) deletion of a regulatory sequence.
A) point mutation.
B) duplication.
C) translocation to the immunoglobulin heavy chain locus.
D) deletion of a regulatory sequence.
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20
The ras proto-oncogene can become an oncogene by a single point mutation that alters its protein product to have _______ activity.
A) more GTPase
B) constitutive Raf-activation
C) greater nucleotide exchange
D) less nucleotide exchange
A) more GTPase
B) constitutive Raf-activation
C) greater nucleotide exchange
D) less nucleotide exchange
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21
Translocation of a gene can produce a fusion product with uncontrolled protein kinase activity. An example of this type of fusion protein is
A) Tel/PDGFR.
B) Myc/Max.
C) Fos/Jun.
D) ErbB/Ras.
A) Tel/PDGFR.
B) Myc/Max.
C) Fos/Jun.
D) ErbB/Ras.
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22
What normal cellular process would be affected in a cell line in which Bcl-2 was mutated?
A) Cell cycle
B) Apoptosis
C) cAMP signaling
D) Terminal differentiation
A) Cell cycle
B) Apoptosis
C) cAMP signaling
D) Terminal differentiation
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23
Loss-of-function mutations can be oncogenic if the mutant gene codes for a
A) telomerase.
B) tumor suppressor protein.
C) cyclin-dependent kinase.
D) DNA synthesis enzyme.
A) telomerase.
B) tumor suppressor protein.
C) cyclin-dependent kinase.
D) DNA synthesis enzyme.
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24
Tumors would likely develop in _______ of the mice.
A) less than 1%
B) 25%
C) 50%
D) nearly 100%
A) less than 1%
B) 25%
C) 50%
D) nearly 100%
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25
What is the reason for the likely result of the experiment described?
A) Tumorigenicity is dominant.
B) 50% of the cells get a tumor suppressor gene.
C) Tumor suppressor genes are recessive.
D) Tumor suppressor genes are dominant.
A) Tumorigenicity is dominant.
B) 50% of the cells get a tumor suppressor gene.
C) Tumor suppressor genes are recessive.
D) Tumor suppressor genes are dominant.
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26
The first tumor suppressor gene was identified in studies of which human tumor?
A) Burkitt's lymphoma
B) Retinoblastoma
C) Glioblastoma
D) Promyelocytic leukemia
A) Burkitt's lymphoma
B) Retinoblastoma
C) Glioblastoma
D) Promyelocytic leukemia
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27
Nonhereditary retinoblastoma develops only when
A) a somatic mutation inactivates the Rb gene.
B) a somatic mutation activates the Rb gene.
C) two somatic mutations inactivate two separate Rb genes.
D) one germ-line mutation and one somatic mutation inactivate Rb genes.
A) a somatic mutation inactivates the Rb gene.
B) a somatic mutation activates the Rb gene.
C) two somatic mutations inactivate two separate Rb genes.
D) one germ-line mutation and one somatic mutation inactivate Rb genes.
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28
The product of the human papillomavirus oncogene E7 promotes cancer by
A) inhibiting DNA damage repair pathways.
B) binding and preventing function of Rb protein.
C) ubiquitinating the tumor suppressor p53.
D) enhancing expression of telomerase.
A) inhibiting DNA damage repair pathways.
B) binding and preventing function of Rb protein.
C) ubiquitinating the tumor suppressor p53.
D) enhancing expression of telomerase.
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29
The tumor suppressor genes Smad2 and Smad4 encode
A) growth factor receptors.
B) GTP-binding signal molecules.
C) transcription factors.
D) inhibitors that bind to transcription factors.
A) growth factor receptors.
B) GTP-binding signal molecules.
C) transcription factors.
D) inhibitors that bind to transcription factors.
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30
The normal function of the tumor suppressor protein Rb is to
A) induce apoptosis.
B) inhibit Ras.
C) inhibit progression through the G1 restriction point.
D) inhibit Cdk4/cyclin B activity.
A) induce apoptosis.
B) inhibit Ras.
C) inhibit progression through the G1 restriction point.
D) inhibit Cdk4/cyclin B activity.
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31
An increase in p53 activity usually results after a cell receives
A) extracellular growth inhibition signals.
B) DNA damage.
C) heat shock.
D) extracellular growth stimulating signals.
A) extracellular growth inhibition signals.
B) DNA damage.
C) heat shock.
D) extracellular growth stimulating signals.
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32
p53 induces apoptosis by
A) inactivating a growth factor receptor.
B) activating transcription of a Bcl-2 family member.
C) activating transcription of a caspase.
D) directly activating a caspase.
A) inactivating a growth factor receptor.
B) activating transcription of a Bcl-2 family member.
C) activating transcription of a caspase.
D) directly activating a caspase.
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33
Apoptosis is induced by p53 when
A) a cell is programmed to die during development.
B) growth factor levels decline to zero.
C) any DNA damage is detected.
D) severe DNA damage is detected and cannot be repaired.
A) a cell is programmed to die during development.
B) growth factor levels decline to zero.
C) any DNA damage is detected.
D) severe DNA damage is detected and cannot be repaired.
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34
One function of the tumor suppressor protein p53 is to
A) activate synthesis of p21, a Cdk inhibitor.
B) inhibit phosphodiesterase.
C) stimulate cell cycle progression.
D) phosphorylate cyclin-dependent kinases on an inhibitory site.
A) activate synthesis of p21, a Cdk inhibitor.
B) inhibit phosphodiesterase.
C) stimulate cell cycle progression.
D) phosphorylate cyclin-dependent kinases on an inhibitory site.
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35
MicroRNAs can act as tumor suppressors by inhibiting expression of all of the following except
A) Cdk.
B) ras.
C) myc.
D) PTEN.
A) Cdk.
B) ras.
C) myc.
D) PTEN.
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36
Malignant colon cancers are usually the result of
A) inherited mutant oncogenes.
B) inherited mutant tumor suppressor genes.
C) somatic mutation of an oncogene or tumor suppressor gene.
D) multiple mutations activating oncogenes and inactivating tumor suppressor genes.
A) inherited mutant oncogenes.
B) inherited mutant tumor suppressor genes.
C) somatic mutation of an oncogene or tumor suppressor gene.
D) multiple mutations activating oncogenes and inactivating tumor suppressor genes.
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37
What is the cure rate for colon carcinomas that remain localized to their site of origin?
A) 90%
B) 75%
C) 50%
D) 25%
A) 90%
B) 75%
C) 50%
D) 25%
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38
Genetic testing for mutant oncogenes or tumor suppressor genes
A) helps identify high-risk individuals before a tumor develops.
B) offers a definitive indication of which individuals will develop tumors.
C) aids the discovery of other mutations that lead to cancer.
D) is not significantly useful as a healthcare practice.
A) helps identify high-risk individuals before a tumor develops.
B) offers a definitive indication of which individuals will develop tumors.
C) aids the discovery of other mutations that lead to cancer.
D) is not significantly useful as a healthcare practice.
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39
Traditional drugs used to treat cancer patients
A) target oncogene function.
B) kill cancer cells specifically.
C) damage DNA or inhibit DNA replication.
D) target tumor suppressor protein function.
A) target oncogene function.
B) kill cancer cells specifically.
C) damage DNA or inhibit DNA replication.
D) target tumor suppressor protein function.
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40
Drugs that inhibit general expression or function of an oncogene will
A) inhibit division of tumor cells only.
B) kill tumor cells only.
C) kill tumor cells as well as normal cells.
D) inhibit cell division of tumor cells and normal cells.
A) inhibit division of tumor cells only.
B) kill tumor cells only.
C) kill tumor cells as well as normal cells.
D) inhibit cell division of tumor cells and normal cells.
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41
The therapeutic use of monoclonal antibodies against oncogene proteins is limited to
A) secreted targets, such as growth factors.
B) extracellular targets, such as cell surface receptors.
C) extracellular and cytosolic targets.
D) protein targets.
A) secreted targets, such as growth factors.
B) extracellular targets, such as cell surface receptors.
C) extracellular and cytosolic targets.
D) protein targets.
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42
Herceptin is a monoclonal antibody against the oncogene protein
A) EGF.
B) Bcr/Abl.
C) ErbB-2.
D) Sis.
A) EGF.
B) Bcr/Abl.
C) ErbB-2.
D) Sis.
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43
Imatinib (Gleevec) blocks proliferation of chronic myeloid leukemia cells by inhibiting the protein kinase
A) Bcr/Abl.
B) Cdk/cyclin.
C) MAP kinase.
D) ErbB.
A) Bcr/Abl.
B) Cdk/cyclin.
C) MAP kinase.
D) ErbB.
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44
The process by which tumor cells whose mutations give them a selective advantage grow preferentially is called _______.
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45
Cancer cells can acquire the capacity for unlimited growth by turning on the gene for _______.
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46
SV40, papillomaviruses, and adenoviruses are _______ tumor viruses.
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47
Herpes viruses (HSV) can induce _______ sarcoma.
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48
Common human cancers caused by viruses include cervical carcinoma and _______ cancer.
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49
Xeroderma pigmentosum is caused by mutations in _______ genes.
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50
Many cases of breast cancer can be traced to the _______ and _______ genes.
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51
_______ treatment of promyelocytic leukemia induces terminal differentiation, forcing the cancer cells to withdraw from the cell cycle.
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52
Transformation can be assayed in cell culture.
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53
Leukemias arise from cells of the immune system.
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54
Viruses do not induce tumors in humans.
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55
SV40, papillomaviruses, and adenoviruses induce transformation by producing proteins that interact with the tumor suppressor proteins p53 and Rb.
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56
Oncogenic mutations in ras promote accumulation of the GDP bound form of the protein.
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57
Several oncogenes encode antiapoptotic proteins that promote cell survival.
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58
BRCA1 and BRCA2 prevent breast cancer by maintaining the integrity of the genome.
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59
The cure rate for carcinomas detected early, when they have not spread from their site of origin, is 50%.
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60
Acute promyelocytic leukemia results from a mutated retinoic acid receptor, effectively blocking cell differentiation and allowing leukemic cells to continue proliferation.
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61
Cancer patients with mutant p53 can be treated effectively with radiation therapy.
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62
The sensitivity of tumors to inhibition of activated oncogenes is called oncogene addiction.
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63
The first drug developed against a specific oncogene and approved for clinical use was a monoclonal antibody against ErbB-2.
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64
How do cancer cells become able to proliferate indefinitely, while normal cells become senescent after a limited number of cell divisions?
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65
When does autocrine induction of cell proliferation occur?
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66
List three ways in which a proto-oncogene can be activated to become an oncogene.
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67
Explain the conditions in which the following oncogene protein products may be oncogenic.
-The growth factor EGF
-The growth factor EGF
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68
Explain the conditions in which the following oncogene protein products may be oncogenic.
-The transcription factors Myc, Fos, or Jun
-The transcription factors Myc, Fos, or Jun
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69
Explain the conditions in which the following oncogene protein products may be oncogenic.
-The growth factor receptor PDGFR
-The growth factor receptor PDGFR
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70
Explain the conditions in which the following oncogene protein products may be oncogenic.
-The intracellular signal transducing molecule Ras
-The intracellular signal transducing molecule Ras
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71
Explain the conditions in which the following oncogene protein products may be oncogenic.
-The Cdk-activating protein cyclin D
-The Cdk-activating protein cyclin D
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72
Explain the conditions in which the following oncogene protein products may be oncogenic.
-The cell-differentiation-inducing receptor ErbA (thyroid hormone receptor) or PML/RAR? (retinoic acid receptor)
-The cell-differentiation-inducing receptor ErbA (thyroid hormone receptor) or PML/RAR? (retinoic acid receptor)
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73
Explain the conditions in which the following oncogene protein products may be oncogenic.
-The tumor suppressor protein p53 or Rb
-The tumor suppressor protein p53 or Rb
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74
Name three tumor suppressor genes.
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75
What is the difference between a benign tumor and a malignant tumor?
A) A malignant tumor is painful, and a benign tumor is not.
B) A malignant tumor has the ability to spread to other tissues and to initiate tumors at secondary sites, whereas a benign tumor does not spread.
C) A benign tumor will cause a less severe form of cancer than a malignant tumor.
D) A malignant tumor is caused by a virus, whereas a benign tumor arises spontaneously.
A) A malignant tumor is painful, and a benign tumor is not.
B) A malignant tumor has the ability to spread to other tissues and to initiate tumors at secondary sites, whereas a benign tumor does not spread.
C) A benign tumor will cause a less severe form of cancer than a malignant tumor.
D) A malignant tumor is caused by a virus, whereas a benign tumor arises spontaneously.
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76
Which statement about cancers is false?
A) Carcinomas are malignancies of epithelial cells.
B) Leukemias are malignancies that arise from blood-forming cells.
C) Lymphomas are malignancies from colon tissue.
D) Sarcomas are malignancies of connective tissue like muscle and bone.
A) Carcinomas are malignancies of epithelial cells.
B) Leukemias are malignancies that arise from blood-forming cells.
C) Lymphomas are malignancies from colon tissue.
D) Sarcomas are malignancies of connective tissue like muscle and bone.
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77
The type of cancer with highest mortality in the United States is cancer of the
A) prostate.
B) colon/rectum.
C) breast.
D) lung.
A) prostate.
B) colon/rectum.
C) breast.
D) lung.
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78
Which statement concerning the difference between cancer cells and normal cells is false?
A) Normal cells display density-dependent inhibition of cell proliferation.
B) Cancer cells have reduced requirements for extracellular growth factors.
C) Malignant cells generally secrete proteases that digest extracellular matrix components.
D) Cancer cells undergo normal differentiation, but excessive proliferation.
A) Normal cells display density-dependent inhibition of cell proliferation.
B) Cancer cells have reduced requirements for extracellular growth factors.
C) Malignant cells generally secrete proteases that digest extracellular matrix components.
D) Cancer cells undergo normal differentiation, but excessive proliferation.
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79
Angiogenesis contributes to cancer development by
A) providing nutrients and oxygen to tumors and by facilitating metastasis.
B) initiating a mutation in a gene that causes uncontrolled cell growth.
C) inhibiting apoptosis (programmed cell death).
D) preventing the normal inhibition of growth that occurs when cells make contact.
A) providing nutrients and oxygen to tumors and by facilitating metastasis.
B) initiating a mutation in a gene that causes uncontrolled cell growth.
C) inhibiting apoptosis (programmed cell death).
D) preventing the normal inhibition of growth that occurs when cells make contact.
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80
Infection with which of the following viruses is associated with development of liver cancer in humans?
A) Simian virus 40 (SV40)
B) Hepatitis B viruses
C) Epstein-Barr virus
D) Papillomaviruses
A) Simian virus 40 (SV40)
B) Hepatitis B viruses
C) Epstein-Barr virus
D) Papillomaviruses
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