Deck 16: Cancer

Question 1

Hypoxic conditions ___________.

A)cause cancer cells to activate a transcription factor called Hif
B)can cause cancer cells to induce the formation of new blood vessels
C)can promote the migratory properties of cancer cells
D)can cause the spread of a tumor
E)All of these are correct.

Answer 1

E

Question 2

What does telomerase do?

A)It maintains centromeres at chromosome ends (telomeres),thus allowing cells to continue to divide.
B)It degrades centromeres at the telomeres of chromosomes,thus allowing cells to continue to divide.
C)It maintains telomeres at the ends of chromosomes,thus allowing cells to continue to divide.
D)It degrades telomeres at the ends of chromosomes,thus allowing cells to continue to divide.
E)It maintains telomeres at the ends of chromosomes,thus preventing cells from continuing to divide.

Answer 2

C

Question 3

Which statement below is a correct statement about the abilities of normal cells and cancer cells to grow and divide when cultured under conditions favorable for cell proliferation?

A)Malignant cells grow and divide at a somewhat faster rate than normal cells.
B)Normal cells grow and divide at a faster rate than malignant cells.
C)Malignant and normal cells grow and divide at similar rates.
D)Neither type of cell grows well in culture.
E)Normal cells do not grow at all,while malignant cells grow very rapidly.

Answer 3

C

Question 4

Retinoblastoma is inherited as a ____________.

A)dominant genetic trait
B)recessive genetic trait
C)sex-linked recessive treat
D)sex-linked dominant trait
E)codominant trait

Question 5

Why can cancer cells proliferate in the absence of serum?

A)Their nuclei depend on these serum growth factors to maintain their structure.
B)The serum inhibits their growth,while it is necessary for normal cells.
C)The cell cycle of cancer cells does not depend on signals transmitted from serum growth-factor receptors located at their surface.
D)The cell cycle of cancer cells depends on signals transmitted from serum growth-factor receptors located in their cytoplasm.
E)Their mitochondria depend on serum growth factors for their activity.

Question 6

Cancer results from the uncontrolled proliferation of a single wayward cell and is therefore considered to be _________.

A)polyclonal
B)biclonal
C)monoclonal
D)variant
E)obstreperous

Question 7

When telomerase appears in a cell,it is not because the coding sequences of the gene have been changed.Instead,the protein produced is essentially normal,but it is being produced at an abnormal time.A gene that is normally repressed has been activated for some reason.Such an alteration in cell behavior is referred to as a(n)_________ change.

A)androgenous
B)mutational
C)epigenetic
D)structural
E)ancillary

Question 8

Another word for malignant transformation is ________.

A)oncorariness
B)ontogenesis
C)cancerogenesis
D)tumorigenesis
E)oncogenation

Question 9

Mutant forms of tumor-suppressor genes act _____;both copies of the gene must be _______ before their protective function is lost.

A)as dominant Mendelian traits,mutated or deleted
B)as dominant Mendelian traits,preserved
C)recessively,mutated or deleted
D)recessively,preserved
E)like sex-linked recessive genes,mutated or deleted

Question 10

____________ is a rare childhood cancer of the eye's retina.

A)Retinal carcinoma
B)Eye cancer
C)Retinal sarcoma
D)Retinoblastoma
E)Retinal epithelioma

Question 11

You are studying two rodent cell lines,one malignant and one normal.You carry out an experiment in which you fuse malignant and normal cells.What happens?

A)All of the hybrid (fused)cells behave like malignant cancer cells.
B)Some of the hybrid cells lose malignant traits.
C)Some of the hybrid cells gained more extreme malignant traits.
D)Most of the hybrids died shortly after fusion.
E)The hybrids began to fuse together spontaneously making giant multinucleate cells.

Question 12

Which one of the following viruses does not appear to be linked to human cancers?

A)hepatitis B virus
B)Epstein-Barr virus
C)herpes virus HHV-8
D)SV40
E)rhinovirus

Question 13

What is the most important property of a cancer cell,whether it is in the body or the culture dish?

A)its chromosome complement
B)its loss of growth control
C)its size
D)its secretions
E)its inability to divide

Question 14

What is the material called serum that is added to culture media?

A)any sugary solution
B)the fluid fraction of the blood
C)the particulate fraction of the blood
D)the combination of the fluid and particulate fractions of the blood
E)any blood that has been in a syringe

Question 15

Chronic infection with what stomach-dwelling bacterium has been associated with certain gastric lymphomas?

A)Escherichia coli
B)Staphylococcus aureus
C)Helicobacter pylori
D)Saccharomyces cerevisiae
E)Helicopter stomachus

Question 16

What do all of the environmental agents that can cause cancer have in common?

A)They can all alter the genome.
B)They are all soluble in water.
C)They are all made of nucleic acids.
D)They are all made of amino acids.
E)They all can alter proteins present in the cell cytoplasm that are responsible for the onset of cancer.

Question 17

Who made the first known correlation between environmental agents and cancer development?

A)Harry Potter
B)Percivall Pott
C)Percival Lowell
D)Charles Darwin
E)Archibald Garrod

Question 18

What enzyme is responsible for maintaining the length of the DNA sequences on the ends of chromosomes (telomeres)?

A)tendrilase
B)telomerase
C)telomere synthase
D)telomere disruptase
E)telomere kinase

Question 19

What is unusual about the inheritance of retinoblastoma,given that it appears to be inherited as a dominant trait?

A)All children who inherited one copy of the RB deletion developed retinoblastoma.
B)Not all children who inherited the RB deletion developed retinoblastoma.
C)No children who inherited the RB deletion developed retinoblastoma.
D)Only boys appear to develop retinoblastoma.
E)Only girls appear to develop retinoblastoma.

Question 20

A single layer of cells that covers a culture dish is called a(n)_________.

A)duolayer
B)imperium
C)monolayer
D)unolayer
E)Unitarian

Question 21

p53 remains in the nucleus,instead of being transported into the cytosol.

A)4 - 5 - 3 - 1 - 6 - 2
B)4 - 3 - 5 - 1 - 6 - 2
C)4 - 3 - 5 - 2 - 1 - 6
D)4 - 1 - 3 - 5 - 6 - 2
E)3 - 5 - 4 - 1 - 6 - 2

Question 22

Raf is a ________ protein kinase that resides at the head of the _______.

A)tyrosine,MAP kinase cascade
B)serine/threonine,MAP kinase cascade
C)tyrosine,glucagon cascade
D)serine/threonine.glucagon cascade
E)serine/threonine,apoptosis cascade

Question 23

What evidence suggested that the elevated sensitivity of cancer cells to radiation therapy and chemotherapy was not due to their more rapid division?

A)Cells that divide more quickly reproduce more effectively.
B)Some cancer cells divide more slowly than their normal counterparts,yet they are still more sensitive to drugs and radiation than are normal cells.
C)Cells that divide more quickly reproduce less effectively.
D)Some cancer cells divide more quickly than their normal counterparts,yet they are still more sensitive to drugs and radiation than are normal cells.
E)Normal cells dividing more slowly than tumor cells are more sensitive to drugs and radiation.

Question 24

How does the behavior of the altered receptor that is the product of the avian erythroblastosis virus differ from the wild type form of the receptor?

A)The altered receptor behaves in the same way as the wild-type receptor.
B)The altered receptor constitutively stimulates cell growth in the presence and absence of the growth factor.
C)The altered receptor stimulates cell growth in the presence of the growth factor,but not in its absence.
D)The altered receptor constitutively represses growth and cell proliferation in the presence and absence of the growth factor.
E)The altered receptor stimulates cell growth in the absence of the growth factor,but not in its presence.

Question 25

If Raf is mutated so that it is "on" constitutively,what is the effect on the cell?

A)The cells stop dividing.
B)The cells differentiate.
C)The cells dedifferentiate.
D)The cells lose growth control.
E)The cells increase in volume permanently.

Question 26

The avian erythroblastosis virus contains an oncogene called erbB that encodes ___________.

A)an altered EGF receptor that is missing part of the extracellular domain that binds to the growth factor
B)an altered insulin receptor that binds insulin with lower affinity
C)an altered transcription factor that turns on hemoglobin synthesis
D)an elongated auxiliary protein of the cytoskeleton
E)an underexpressed nuclear protein

Question 27

You culture cells and selectively block MYC gene expression.What is the effect on the cells?

A)Cell progression through the cycle continues unabated.
B)Cell progression through G₁ is blocked.
C)The cells arrest in the middle of mitosis.
D)The cells arrest in the middle of meiosis.
E)The cells arrest in the middle of S phase.

Question 28

The first oncogene discovered was _____,which codes for a _______.

A)MYC,tyrosine protein kinase
B)SRC,tyrosine protein kinase
C)SRC,serine/threonine protein kinase
D)MYC,serine/threonine protein kinase
E)SRC,intermediary metabolism regulatory protein

Question 29

What was the initial explanation for the sensitivity of cancer cells to radiation therapy and chemotherapy as compared to normal cells?

A)Cancer cells are sensitive to radiation and chemotherapy because they divide more rapidly.
B)Cancer cells are less resistant to drugs or radiation because once they sustain genetic damage,they either progress through the cell cycle while repair is incomplete and they may undergo apoptosis.
C)Cancer cells are sensitive to radiation and chemotherapy because they divide more slowly.
D)Cancer cells are less resistant to drugs or radiation because once they sustain genetic damage,they either arrest the cell cycle until repair is complete or undergo apoptosis.
E)Cancer cells are sensitive to radiation and chemotherapy because they will not undergo apoptosis.

Question 30

How does PTEN affect the balance between proapoptotic and antiapoptotic signals?

A)PTEN removes the phosphate group from the 3-position of PIP₃ converting it to PI(4,5)P₂,which cannot activate PKB (AKT)and thus throws the balance in an antiapoptotic direction.
B)PTEN removes the phosphate group from the 3-position of PIP₃ converting it to PI(4,5)P₂,which cannot activate PKB (AKT)and thus throws the balance in a proapoptotic direction.
C)PTEN cuts a phosphate group off of PKB,which throws the balance in a proapoptotic direction.
D)PTEN cuts a phosphate group off of PKB,which throws the balance in an antiapoptotic direction.
E)PTEN adds a phosphate group to PKB,which throws the balance in a proapoptotic direction.

Question 31

What is the oncogene that is most often mutated in human tumors and what does it encode?

A)the RAS gene,a GTP-binding protein that serves as an on-off switch for a key cell signaling pathway that controls cell proliferation
B)the RAS gene,a DNA polymerase that replicates DNA for dividing cells
C)the MYC gene,an RNA polymerase that transcribes mRNA encoding proteins needed for cell division
D)the RB gene,a GTP-binding protein that serves as an on-off switch for a key cell signaling pathway that controls cell proliferation
E)the MYC gene,a protein kinase that enhances cell differentiation

Question 32

Whether a cell lives or dies after a particular event depends to a large degree on ________ between ________ and _________ signals.

A)the differences,mitotic,cytokinetic
B)the balance,mitotic,cytokinetic
C)the balance,proapoptotic,antiapoptotic
D)the differences,on,off
E)the similarities,proapoptotic,antiapoptotic

Question 33

The sis oncogene of the simian sarcoma virus was derived from what normal cellular gene?

A)the Ras gene
B)the gene for platelet-derived growth factor (PDGF)
C)the gene for the insulin receptor
D)the gene for the glucagon receptor
E)the gene for epidermal growth factor

Question 34

Patients suffering from familial adenomatous polyposis coli have typically been found to have _________,which is the site of the _________.

A)a small chromosome 15 deletion,RP tumor-suppressor gene
B)a small chromosome 5 deletion,APC oncogene
C)a small chromosome 5 duplication,APC tumor-suppressor gene
D)a small chromosome 5 deletion,APC tumor-suppressor gene
E)a small chromosome 6 deletion,APC tumor-suppressor gene

Question 35

You study two cell lines.In one,the MDM2 protein is overexpressed;in the other the p53 protein is absent.What difference would you expect in the behavior of these two cell lines?

A)In cells containing overexpressed MDM2,p53 levels will be low;in cells lacking the TP53 gene,p53 levels are also low;thus there is no difference in behavior.
B)In cells containing overexpressed MDM2,p53 levels will be high;in cells lacking the TP53 gene,p53 levels are low;thus there is a drastic difference in behavior.
C)In cells containing overexpressed MDM2,p53 levels will be high;in cells lacking the TP53 gene,p53 levels are high;thus there is no difference.
D)In cells containing overexpressed MDM2,p53 levels will be low;in cells lacking the TP53 gene,p53 levels are high;thus there is no drastic difference.
E)None of these are correct.

Question 36

What virus seems to be related to the development of Burkitt's lymphoma in African patients,while it is associated only with minor infections,like mononucleosis,in the Western world?

A)avian erythroblastosis virus
B)simian sarcoma virus
C)rhinovirus
D)Epstein-Barr virus
E)parvovirus

Question 37

What part of the cell cycle does the pRB protein help to regulate?

A)the S - G₂ transition
B)the G₁ - S transition
C)the G₂ - M transition
D)the G₀ - G₁ transition
E)the M - G₂ transition

Question 38

What happens quite often to the number of normal receptors in the plasma membranes of malignant cells as compared to normal cells?

A)Malignant cells usually have the same number of receptors in their plasma membranes as normal cells.
B)Malignant cells usually have a much larger number of plasma membrane receptors than normal cells.
C)Malignant cells usually have a much smaller number of plasma membrane receptors than normal cells.
D)Malignant cells usually have no plasma membrane receptors,while normal cells have them.
E)None of these are correct.

Question 39

Under what circumstances are tumor cells likely to undergo apoptosis when they have sustained damage to DNA?

A)if they have a functioning RP gene.
B)if they have a functioning TP53 gene
C)if they have a non-functioning RP gene.
D)if they have a non-functioning TP53gene
E)if they have a non-functioning BAX gene

Question 40

_____________ is an inherited disease in which individuals develop many (hundreds or thousands)of premalignant polyps from epithelial cells lining the colon wall.

A)Familial adenomatous polyposis coli
B)Familial hypercholesterolemia
C)Inherited adenomitis
D)Familial polypsoidemia
E)Inherited polypoma intestines

Question 41

The cancer vaccine Provenge has been designed to teach a person's immune cells to attack what cancer?

A)chronic lymphocytic leukemia
B)Kaposi's sarcoma
C)colorectal cancer
D)bladder cancer
E)prostate cancer

Question 42

What is the name for tiny regulatory RNAs that negatively regulate the expression of target mRNAs?

A)tRNAs
B)microRNAs
C)mtRNAs
D)macroRNAs
E)rRNAs

Question 43

What is a xenograft?

A)transplanting cells in the presence of xenon
B)transplant of cells from one organism to an organism of a different species
C)mixing cells from two different species in a culture dish
D)a transplant that does not have a good histocompatibility antigen match
E)a skin graft from one organism to another within the same species

Question 44

__________ is an approach that tries to get the immune system more involved in the fight against cancer.

A)Immunotherapy
B)Gene therapy
C)Inhibition of cancer-promoting proteins
D)Inhibition of angiogenesis
E)Hyposensitization

Question 45

With respect to cancer genetics and the cancer genome,what are passenger genes?

A)genes that are subject to mutation but have no effect on the phenotype of a cancer cell
B)genes that are not subject to mutation and have no effect on the phenotype of a cancer cell
C)genes that are subject to mutation but have a large effect on the phenotype of a cancer cell
D)genes that are subject to mutation but have no effect on the genotype of a cancer cell
E)genes that are subject to mutation but have no effect on the phenotype of an egg cell

Question 46

Which of the following enzymes is known to be expressed at a high level in the cancer cells of patients suffering from acute myeloid leukemia and at low levels in the cancer cells of patients suffering from acute lymphoblastic leukemia?

A)cholesterase
B)catalase
C)adenylyl cyclase
D)phosphodiesterase
E)protein kinase A

Question 47

The genes involved in tumorigenesis constitute a specific subset of the genome whose products are involved in which of the following activities?

A)progression of a cell through the cell cycle
B)adhesion of a cell to its neighbors
C)apoptosis
D)repair of DNA damage
E)All of these are correct.

Question 48

The BCL-2 oncogene is the oncogene most closely linked to _________;it encodes a membrane-bound ____________.

A)apoptosis,protein that normally acts to activate apoptosis
B)apoptosis,protein that normally acts to inhibit apoptosis
C)uncontrolled proliferation,protein that normally acts to inhibit apoptosis
D)uncontrolled proliferation,protein that normally acts to activate apoptosis
E)apoptosis,protein that binds to the insulin receptor tyrosine kinase

Question 49

Against what protein is the treatment for metastatic colon cancer Vectibix directed?

A)pRB
B)p53
C)the EGF receptor
D)VEGF
E)Her2

Question 50

Because they act to _______ tumorigenesis,the miR-15a and miR-16 miRNAs can be thought of as _________.

A)enhance,tumor suppressors
B)inhibit,oncogenes
C)enhance,oncogenes
D)inhibit,tumor suppressors
E)delete,parts of the mismatch repair mechanism

Question 51

Mutant forms of which of the following genes have been associated with melanomas and colorectal cancers,respectively?

A)APC and BRAF
B)BRAF and CCMD
C)BRAF and APC
D)CCMD and APC
E)ZUNI and BRAF

Question 52

For what disease is the human monoclonal antibody Arzerra likely to be approved for treatment?

A)acute lymphocytic leukemia
B)chronic lymphocytic leukemia
C)ALS (Lou Gehrig's disease)
D)multiple sclerosis
E)glioblastoma

Question 53

The cancer vaccine Provenge has been designed to teach a person's immune cells to attack what enzyme?

A)prostatic acid phosphatase
B)alkaline phosphatase
C)catalase
D)telomerase
E)reverse transcriptase

Question 54

Which of the following is a biomarker that may at some point could reveal the presence of cancer through a blood test or screening?

A)mutant DNA
B)abnormal carbohydrates
C)distinctive metabolites
D)presence of cancer cells
E)All of these are correct.

Question 55

How are drug companies trying to combat the ability of the BCL-2 gene to lower the effectiveness of chemotherapy?

A)They are trying to develop drugs that stabilize cancer cells.
B)They are trying to develop drugs that make cancer cells more likely to undergo apoptosis.
C)They are trying to develop drugs that cause cancer cells to revert to normal embryonic cells.
D)They are trying to develop drugs that cause cancer cells to dedifferentiate.
E)They are trying to develop drugs that cause cancer cells to differentiate.

Question 56

Which of the following is presently being used as a screening procedure for cancer?

A)mammography for detecting breast cancer
B)Pap smears for detecting cervical cancer
C)PSA determinations for detecting prostate cancer
D)colonoscopy for detecting colorectal cancer
E)All of these are correct.

Question 57

The cancer vaccine GRNVAC1 has been designed to teach a person's immune cells to attack what enzyme?

A)prostatic acid phosphatase
B)alkaline phosphatase
C)catalase
D)telomerase
E)reverse transcriptase

Question 58

If any of the proteins involved in mismatch repair are damaged,the mutation rate and cancer risk will rise;this is called the ___________.

A)stability phenotype
B)mutator phenotype
C)mutator genotype
D)alteration phenotype
E)alteration genotype

Question 59

After the DNAs attached to the glass slide of a microarray are exposed to a probe,how are they usually visualized?

A)The cDNA probes are fluorescently labeled.
B)The mRNA probes are fluorescently labeled.
C)The cDNA probes are radioactively labeled.
D)The cDNA probes are labeled with ferritin.
E)The mRNA probes are labeled with ferritin.

Question 60

William Coley,a New York physician in the late 1800s,studied spontaneous remissions of terminal cancer cases.He read that one man,who had an inoperable neck tumor,had gone into remission after what event?

A)after a cold
B)after changing his diet drastically
C)after a streptococcal infection beneath his skin
D)after a rigorous exercise regimen
E)after taking multiple vitamins

Question 61

If you could treat a tumor with an antibody against a factor that attracts blood vessels to the tumor,what might happen?

Question 62

The development of chronic myelogenous leukemia tumor-resistance to Gleevec appears to usually be caused by mutations in the ABL portion of the fusion gene.Therefore,what is thought to be the best drug regimen for treating CML?

A)a cocktail of several different inhibitors that target different parts of the Abl protein
B)a cocktail of several different inhibitors that target the same parts of the Abl protein
C)a cocktail of several different inhibitors that target common domains of different proteins
D)a cocktail of several different inhibitors that target the different parts of different proteins
E)an aperetif

Question 63

If patients with advanced CML are initially treated with Gleevec,they generally develop resistance to the drug within a few months.What seems to cause the resistance?

A)mutations in the BCR portion of the fusion gene
B)mutations in the ABL portion of the fusion gene
C)ABL gene deletion
D)ABL gene amplification
E)BCR gene amplification

Question 64

Which screening test just being developed will be able to screen based on the relative levels of various proteins in the blood?

A)genomics
B)Pap smear
C)colonoscopy
D)proteomics
E)astronomics

Question 65

Normal cells greatly slow their rates of cell division after filling a culture dish with a layer one cell deep (a monolayer).If a circular group of cells is removed from the middle of the filled culture dish,the cells on the edges of the "wound" will begin to divide,fill the space and then stop dividing again.How does the behavior of transformed cells differ?

Question 66

Which screening test just being developed will be able to warn us of the types of cancer to which we may be most susceptible by looking for the presence of specific genes associated with various types of cancer?

A)genomics
B)Pap smear
C)colonoscopy
D)proteomics
E)astronomics

Question 67

Judah Folkmann suggested that solid tumors __________.

A)might be destroyed by enhancing their ability to form new blood vessels
B)might be dissipated by enhancing the ability of cancer cells to separate from each other
C)might be destroyed by inhibiting their ability to form new blood vessels
D)might be enlarged by breaking down neighboring tissues
E)might be desiccated by osmotic action

Question 68

__________ is new blood vessel formation.

A)Vesselogeny
B)Angiogenesis
C)Formational vessels
D)Angiotension
E)Venogenesis

Question 69

About 25% of breast cancers are composed of cells that overexpress the HER2 gene.What property does the overexpression of this gene confer upon the tumor cells?

A)The tumor cells are more responsive to Herceptin stimulation in the body.
B)The tumor cells are less responsive to Herceptin stimulation.
C)The tumor cells are more likely to undergo apoptosis.
D)These cells are especially sensitive to growth factor stimulation.
E)These cells are especially resistant to growth factor stimulation.

Question 70

Against what form of cancer is Mylotarg most effective?

A)acute myeloid leukemia
B)breast cancer
C)non-Hodgkins B-cell lymphoma
D)Hodgkins disease
E)pancreatic cancer

Question 71

After his initial discoveries and for the rest of his life,Coley tried to develop a ______ extract that when injected under the skin would stimulate a patient's immune system to destroy their malignancy.His approach called ________ worked against some uncommon__________.

A)bacterial,Coley's toxin,soft-tissue carcinomas
B)bacterial,Coley's solution,soft-tissue sarcomas
C)viral,Coley's toxin,soft-tissue sarcomas
D)bacterial,Coley's toxin,soft-tissue sarcomas
E)human cytoplasmic,Coley's cure,soft-tissue hepatomas

Question 72

________ is a humanized antibody directed against a cell surface receptor called _____ that binds a growth factor responsible for stimulating the proliferation of breast cancer cells.

A)Ascriptin,Asc3
B)Herceptin,Her2
C)Apcolin,Apc2
D)Herceptin.Raf
E)Rafinolin,Raf

Question 73

Which molecule do Bexxar and Zevalin antibodies attack?

A)collagen
B)CD20
C)myeloid protein
D)actin
E)EGF receptor

Question 74

What is the difference between a benign tumor and a malignant tumor?