Lecture 10: Cancer Flashcards
(130 cards)
1
Q
Which of the following proteins promotes cell cycle progression in cancer?
a) p16
b) Rb
c) Cyclin D
d) p53
A
Answer: c) Cyclin D
2
Q
What is the role of tumor suppressor genes in the development of cancer?
a) Promote cell proliferation
b) Inhibit cell proliferation
c) Activate proto-oncogenes
d) Increase apoptosis
A
Answer: b) Inhibit cell proliferation
3
Q
Which of the following is an example of a proto-oncogene that promotes cell proliferation when mutated?
a) Rb
b) Myc
c) p53
d) Bcl2
A
Answer: b) Myc
4
Q
Gain-of-function mutations in which type of genes are associated with cancer?
a) Tumor suppressor genes
b) Oncogenes
c) DNA repair genes
d) Apoptosis genes
A
Answer: b) Oncogenes
5
Q
Which mutation leads to the loss of function in the retinoblastoma (Rb) gene?
a) Gain-of-function mutation
b) Recessive mutation
c) Dominant mutation
d) Translocation mutation
A
Answer: b) Recessive mutation
6
Q
Which protein is known as the “guardian of the genome” due to its role in DNA damage response?
a) Cyclin D
b) Myc
c) p53
d) Ras
A
Answer: c) p53
7
Q
Which of the following statements is true about proto-oncogenes?
a) They inhibit cell cycle progression.
b) They are dominant traits when mutated.
c) They are recessive traits when mutated.
d) They suppress tumor formation.
A
Answer: b) They are dominant traits when mutated.
8
Q
Which of the following pathways is commonly activated in cancer to promote cell growth and survival?
a) Wnt
b) Ras/RAF/MEK/ERK
c) PI3K/AKT
d) All of the above
A
Answer: d) All of the above
9
Q
What happens when the p16 protein is non-functional in a cell?
a) Cell cycle progression is inhibited.
b) Rb remains active, preventing cell division.
c) Cyclin D-CDK complex becomes overactive.
d) Apoptosis is activated.
A
Answer: c) Cyclin D-CDK complex becomes overactive.
10
Q
Which process is prevented by the overexpression of Bcl2 in cancer cells?
a) Cell division
b) DNA replication
c) Apoptosis
d) Angiogenesis
A
Answer: c) Apoptosis
11
Q
What is the difference between proto-oncogenes and oncogenes?
a) Proto-oncogenes inhibit cell division, oncogenes promote it.
b) Proto-oncogenes promote normal cell division, oncogenes are mutated forms.
c) Proto-oncogenes repair DNA damage, oncogenes cause mutations.
d) Proto-oncogenes are recessive, oncogenes are dominant.
A
Answer: b) Proto-oncogenes promote normal cell division, oncogenes are mutated forms.
12
Q
What role does p53 play in the cell?
a) Promotes DNA replication during the cell cycle.
b) Activates apoptosis in response to DNA damage.
c) Stimulates angiogenesis to supply oxygen to cells.
d) Inhibits Rb to promote cell cycle progression.
A
Answer: b) Activates apoptosis in response to DNA damage.
13
Q
Which of the following is considered a hallmark of cancer?
a) Increased apoptosis
b) Decreased angiogenesis
c) Sustained proliferative signaling
d) Reduced cell division
A
Answer: c) Sustained proliferative signaling
14
Q
Which gene is mutated in chronic myeloid leukemia (CML) as part of the BCR-ABL fusion?
a) Myc
b) Rb
c) ABL
d) Bcl2
A
Answer: c) ABL
15
Q
Loss-of-function mutations in which tumor suppressor gene are associated with retinoblastoma?
a) p53
b) Rb
c) Myc
d) Cyclin D
A
Answer: b) Rb
16
Q
Which of the following is/are TRUE about Rb?
a) The normal function of the product of the Rb gene is to stop the entry of a cell into the S phase.
b) The phosphorylated form of the Rb protein is the active form
c) The Rb protein binds to and inhibits the function of Myc
d) The non-inherited form of the cancer resulting from mutations in the Rb gene is the appearance of tumors in both eyes of the patient
e) 2 of the above
A
a)
17
Q
Which of the following best describes an overactivity mutation in cancer development?
a) A mutation that inactivates a tumor suppressor gene, leading to loss of function
b) A mutation that converts a proto-oncogene into an oncogene, leading to gain of function
c) A mutation that repairs DNA damage, preventing cancer progression
d) A mutation that results in increased apoptosis of cancer cells
A
Answer:
b) A mutation that converts a proto-oncogene into an oncogene, leading to gain of function
18
Q
What is the primary consequence of an underactivity mutation (loss of function) in tumor suppressor genes?
a) Increased production of oncogene proteins
b) Unregulated cell division due to lack of inhibitory proteins
c) Enhanced DNA repair mechanisms
d) Activation of immune responses against tumor cells
A
Answer:
b) Unregulated cell division due to lack of inhibitory proteins
19
Q
Proto-oncogenes normally function to:
a) Suppress tumor formation by inhibiting cell division
b) Promote normal cell growth and division
c) Repair damaged DNA in the cell
d) Trigger cell death (apoptosis) in abnormal cells
A
Answer:
b) Promote normal cell growth and division
20
Q
Tumor suppressor genes play a critical role in:
a) Accelerating the cell cycle to promote growth
b) Inhibiting cell proliferation and promoting genomic stability
c) Enhancing the function of oncogenes
d) Encoding proteins that directly cause mutations
A
Answer:
b) Inhibiting cell proliferation and promoting genomic stability
21
Q
Which statement is true regarding the role of oncogenes in cancer?
a) Oncogenes are mutated tumor suppressor genes that have lost function
b) Oncogenes result from gain-of-function mutations in proto-oncogenes
c) Oncogenes repair DNA and prevent cancer progression
d) Oncogenes require mutations in both alleles to contribute to cancer
A
Answer:
b) Oncogenes result from gain-of-function mutations in proto-oncogenes
22
Q
A loss-of-function mutation in both copies of a tumor suppressor gene is typically necessary for cancer development because:
a) One functional copy can usually compensate for the loss of the other
b) Tumor suppressor genes are dominant over oncogenes
c) Tumor suppressor genes promote cell growth when mutated
d) Single mutations always result in cell death
A
Answer:
a) One functional copy can usually compensate for the loss of the other
23
Q
Which of the following is an example of a tumor suppressor gene commonly associated with cancer when mutated?
a) Ras
b) Myc
c) p53
d) HER2
A
nswer:
c) p53
24
Q
Why can’t a single gene mutation typically cause cancer on its own?
a) Cancer requires both genetic and environmental factors to develop
b) Multiple genes control cell growth and must be altered for cancer to arise
c) The immune system immediately eliminates cells with single mutations
d) Single gene mutations are always repaired by the cell
A
Answer:
b) Multiple genes control cell growth and must be altered for cancer to arise
25
Which characteristic distinguishes oncogenes from tumor suppressor genes in terms of mutation effects?
a) Oncogenes require loss-of-function mutations; tumor suppressor genes require gain-of-function
b) Oncogenes act dominantly when mutated; tumor suppressor genes act recessively
c) Both oncogenes and tumor suppressor genes act recessively when mutated
d) Oncogenes are inherited; tumor suppressor genes are not
Answer:
b) Oncogenes act dominantly when mutated; tumor suppressor genes act recessively
26
The gene p53 is often called the "guardian of the genome" because it:
a) Promotes cell cycle progression regardless of DNA damage
b) Repairs mutations in oncogenes to prevent cancer
c) Detects DNA damage and can induce cell cycle arrest or apoptosis
d) Enhances the function of proto-oncogenes to protect the cell
Answer:
c) Detects DNA damage and can induce cell cycle arrest or apoptosis
27
An example of an overactivity mutation leading to cancer is:
a) Loss of both copies of the Rb gene
b) Activation of the Ras gene causing constant cell proliferation signals
c) Deletion of the p53 gene resulting in impaired DNA repair
d) Inactivation of DNA repair enzymes leading to mutations
Answer:
b) Activation of the Ras gene causing constant cell proliferation signals
28
Tumor suppressor genes are important in cancer prevention because they:
a) Code for proteins that directly kill cancer cells
b) Stimulate the immune system to attack tumors
c) Regulate cell cycle checkpoints and initiate DNA repair
d) Increase angiogenesis to supply nutrients to cells
Answer:
c) Regulate cell cycle checkpoints and initiate DNA repair
29
Which of the following best describes the concept of "gain of function" in oncogenes?
a) A mutation that reduces the gene's normal activity
b) A mutation that enhances the gene's normal activity or creates a new function
c) A mutation that deletes the gene entirely
d) A mutation that has no effect on gene function
Answer:
b) A mutation that enhances the gene's normal activity or creates a new function
30
What is required for a cell to become cancerous in terms of gene mutations?
a) A single mutation in any gene
b) Multiple mutations in various genes that regulate cell growth and division
c) Only environmental factors without any genetic mutations
d) Activation of tumor suppressor genes alone
Answer:
b) Multiple mutations in various genes that regulate cell growth and division
31
How do tumor suppressor genes differ from oncogenes in their normal, non-mutated state?
a) Tumor suppressor genes promote cell division; oncogenes inhibit it
b) Tumor suppressor genes repair DNA; oncogenes do not have a normal function
c) Tumor suppressor genes inhibit cell division; oncogenes promote normal cell growth
d) Both have no role in normal cells and are only active in cancer cells
Answer:
c) Tumor suppressor genes inhibit cell division; oncogenes promote normal cell growth
32
Which of the following is a characteristic of a loss-of-function mutation in tumor suppressor genes?
a) It is dominant and requires only one mutated allele
b) It results in overproduction of regulatory proteins
c) It leads to the absence of proteins that control cell division
d) It enhances the cell's ability to undergo apoptosis
Answer:
c) It leads to the absence of proteins that control cell division
33
Which gene, when functioning normally, helps repair DNA damage and can induce apoptosis if the damage is irreparable?
a) BRCA1
b) p53
c) HER2
d) Myc
Answer:
b) p53
34
In the context of cancer genetics, a recessive trait refers to:
a) A trait that manifests when at least one allele is mutated
b) A trait that requires mutations in both alleles to affect cell function
c) A dominant mutation in a proto-oncogene
d) An inherited mutation that always leads to cancer
Answer:
b) A trait that requires mutations in both alleles to affect cell function
35
Which part of the EGFR receptor binds to the growth factor? a) Cytoplasmic domain
b) Extracellular domain
c) Transmembrane domain
d) Phosphorylation domain
Answer: b) Extracellular domain
36
What happens when EGFR is in its normal inactive state?
a) The receptor undergoes phosphorylation.
b) It continuously activates intracellular signaling pathways.
c) The receptor remains unbound, and no signal is transmitted.
d) The extracellular domain binds to intracellular signaling molecules.
Answer: c) The receptor remains unbound, and no signal is transmitted.
37
Which of the following statements about EGFR is FALSE?
a) EGFR is a transmembrane receptor involved in cell signaling.
b) A truncated EGFR receptor does not require EGF binding to activate intracellular signaling.
c) EGFR activation always inhibits cell proliferation.
d) Mutations in EGFR can lead to uncontrolled cell growth in cancer.
Answer: c) EGFR activation always inhibits cell proliferation.
38
Which of the following is FALSE about glioblastoma?
a) EGFR mutations are common oncogenic events in glioblastoma.
b) EGFR amplification in glioblastoma leads to reduced cell signaling.
c) EGFR mutations can cause constitutive (always active) signaling.
d) Targeting EGFR can be a therapeutic strategy for glioblastoma.
Answer: b) EGFR amplification in glioblastoma leads to reduced cell signaling.
39
If the extracellular domain of EGFR is deleted, what will most likely happen?
a) The receptor will fail to activate, causing reduced cell signaling.
b) The receptor will remain inactive even when EGF is present.
c) The receptor will become constitutively active, driving unregulated cell growth.
d) The receptor will degrade and cease functioning.
Answer: c) The receptor will become constitutively active, driving unregulated cell growth.
40
If the cytoplasmic domain of EGFR is inhibited by a drug, what will happen?
a) EGFR will remain inactive even when EGF binds.
b) EGFR will continuously activate signaling pathways.
c) EGFR will cause an increase in apoptosis.
d) The extracellular domain will no longer bind EGF.
Answer: a) EGFR will remain inactive even when EGF binds.
41
If EGFR mutations lead to constitutive activation, what would be the effect of blocking downstream signaling pathways?
a) It would prevent the overactive EGFR from binding EGF.
b) It would stop the continuous growth signals from being transmitted.
c) It would lead to overproduction of growth factor ligands.
d) It would inhibit EGF binding to the receptor.
Answer: b) It would stop the continuous growth signals from being transmitted.
42
Which of the following is most likely to occur if EGFR inhibitors are administered to a patient with glioblastoma?
a) Increased cell proliferation.
b) Reduction in tumor growth due to decreased signaling.
c) Amplification of EGFR gene mutations.
d) Increased activation of the extracellular domain.
Answer: b) Reduction in tumor growth due to decreased signaling.
43
If EGFR inhibitors fail to reduce tumor growth, which of the following could explain the resistance?
a) Mutations in EGFR that block inhibitor binding.
b) Overproduction of EGF ligand.
c) Activation of alternative growth pathways, such as Ras or PI3K.
d) All of the above.
Answer: d) All of the above.
44
If a drug blocks phosphorylation of the cytoplasmic domain of EGFR, which of the following will occur?
a) EGF will fail to bind the receptor.
b) Downstream signaling pathways will not be activated.
c) The receptor will become constitutively active.
d) The receptor will remain bound to the cell membrane.
Answer: b) Downstream signaling pathways will not be activated.
45
What is the function of the Rb protein in normal cells?
a) Promotes uncontrolled cell growth
b) Prevents entry into the S-phase of the cell cycle
c) Repairs DNA damage
d) Signals apoptosis in cancer cells
Answer: b) Prevents entry into the S-phase of the cell cycle
46
In hereditary retinoblastoma, how many mutations are required in the same cell for cancer to develop?
a) None
b) One
c) Two
d) Three
Answer: b) One
47
In non-hereditary retinoblastoma, how many mutations are required in the same cell for cancer to develop?
a) One
b) Two
c) Three
d) None
Answer: b) Two
48
Which of the following statements about hereditary retinoblastoma is false?
a) It typically affects both eyes.
b) Individuals inherit one mutated Rb gene copy.
c) It is detected in adulthood.
d) Individuals with hereditary Rb have a higher risk of developing other cancers later in life.
Answer: c) It is detected in adulthood
49
If the Rb protein is inhibited in a retinal cell, what will most likely happen?
a) The cell will fail to enter the S-phase.
b) The cell will undergo programmed cell death (apoptosis).
c) The cell will enter the S-phase and divide uncontrollably.
d) The cell will repair mutations in the DNA.
Answer: c) The cell will enter the S-phase and divide uncontrollably.
50
A child with hereditary retinoblastoma develops tumors in both eyes. What is the most likely cause?
a) One inherited mutated Rb gene and a second mutation in retinal cells
b) Two independent mutations in the same retinal cell
c) Inherited two mutated copies of the Rb gene
d) Exposure to radiation during infancy
Answer: a) One inherited mutated Rb gene and a second mutation in retinal cells
51
Which of the following is a characteristic of non-hereditary retinoblastoma?
a) Multiple tumors affecting both eyes
b) Increased risk of other cancers later in life
c) Caused by a single mutation in the Rb gene
d) Develops from two independent mutations in the same retinal cell
Answer: d) Develops from two independent mutations in the same retinal cell
52
Why are individuals with hereditary retinoblastoma at higher risk for developing cancers like osteogenic sarcoma?
a) They inherit both mutated copies of the Rb gene.
b) They undergo treatments like radiation therapy.
c) They lack one functional Rb gene copy in all body cells.
d) Cancer cells spread from the retina to other parts of the body.
Answer: c) They lack one functional Rb gene copy in all body cells
53
If a tumor in the retina of a child is diagnosed and genetic testing reveals both Rb genes are mutated, what type of retinoblastoma is most likely?
a) Hereditary retinoblastoma
b) Non-hereditary retinoblastoma
c) Retinoblastoma caused by radiation
d) Retinoblastoma caused by infection
Answer: b) Non-hereditary retinoblastoma
54
If a treatment eliminates retinal tumors in a child with hereditary retinoblastoma, what long-term risk remains?
a) Recurrence of retinal tumors
b) Development of other cancers in adulthood
c) Total blindness
d) Mutation of other tumor suppressor genes
Answer: b) Development of other cancers in adulthood
55
Why is a single mutation in a single gene not enough to cause cancer?
A) Mutations are repaired by DNA repair systems before causing damage.
B) A single mutation does not disrupt enough cellular processes to result in cancer.
C) Cancer requires the accumulation of multiple mutations over time.
D) Mutations only occur in non-dividing cells.
Answer: C) Cancer requires the accumulation of multiple mutations over time.
56
What does the graph showing cancer incidence with age suggest?
A) Cancer risk decreases as you age because cells divide less frequently.
B) Cancer risk remains constant regardless of age.
C) Cancer risk increases with age due to the accumulation of mutations in dividing cells.
D) Cancer is unrelated to age.
Answer: C) Cancer risk increases with age due to the accumulation of mutations in dividing cells.
57
What does the lag period between smoking exposure and lung cancer incidence indicate?
A) Cancer develops immediately after exposure to carcinogens.
B) A single mutation caused by smoking is sufficient to cause cancer.
C) Multiple mutations accumulate over time after exposure to carcinogens like tobacco.
D) Smoking does not cause cancer directly.
Answer: C) Multiple mutations accumulate over time after exposure to carcinogens like tobacco.
58
What might explain the drop in cancer incidence after age 80–85?
A) The body's immune system becomes stronger with age.
B) Cell division rates decrease, reducing the chances of accumulating mutations.
C) Mutations are less likely to occur as DNA becomes more stable with age.
D) Cancer incidence is unrelated to cell division rates.
Answer: B) Cell division rates decrease, reducing the chances of accumulating mutations.
59
Which of the following is true about cancer caused by environmental mutagens?
A) One exposure is sufficient to cause cancer.
B) There is usually a lag period of 10–20 years before cancer develops.
C) Mutagens only cause cancer if exposure happens in childhood.
D) Cancer risk is independent of the number of mutations.
Answer: B) There is usually a lag period of 10–20 years before cancer develops.
60
If a carcinogen exposure only lasts for a limited time, why might cancer develop years later?
A) The carcinogen triggers immediate immune suppression.
B) DNA damage accumulates and additional mutations occur later, leading to cancer.
C) Cells exposed to carcinogens stop dividing immediately.
D) Cancer cannot occur after exposure ends.
Answer: B) DNA damage accumulates and additional mutations occur later, leading to cancer.
61
What are the two main processes involved in cancer development?
A) Inhibiting cell division and increasing cell death.
B) Increasing cell proliferation and preventing cell death.
C) Blocking angiogenesis and reducing inflammation.
D) Reducing mutation rates and slowing cell cycles.
Answer: B) Increasing cell proliferation and preventing cell death.
62
If exposure to asbestos leads to a single mutation in a lung cell but no additional mutations occur, what is the likely outcome?
A) Immediate cancer development.
B) No cancer development unless further mutations accumulate.
C) The cell will undergo apoptosis and prevent cancer.
D) The mutation will repair itself automatically.
Answer: B) No cancer development unless further mutations accumulate.
63
If cigarette consumption were reduced drastically today, how might the incidence of lung cancer change over the next 20 years?
A) Immediate drop in lung cancer cases.
B) Gradual decline due to the lag period for mutations to accumulate.
C) No change in lung cancer rates.
D) Increase in lung cancer cases due to pre-existing mutations.
Answer: B) Gradual decline due to the lag period for mutations to accumulate.
64
What percentage of cancers are thought to arise due to mechanisms involving viruses and bacterial parasites?
A) 5%
B) 10%
C) 15%
D) 20%
Answer: C) 15%
65
What type of virus is the papillomavirus?
A) Single-stranded RNA virus
B) Single-stranded DNA virus
C) Circular double-stranded RNA virus
D) Circular double-stranded DNA virus
Answer: D) Circular double-stranded DNA virus
66
What happens during the initial infection of papillomavirus?
A) Viral DNA integrates into the host's genome immediately.
B) Viral genome remains as extra-chromosomal DNA producing balanced viral proteins.
C) Viral proteins immediately cause malignant tumor formation.
D) The virus causes extensive cell death in cervical epithelial cells.
Answer: B) Viral genome remains as extra-chromosomal DNA producing balanced viral proteins.
67
What is the result of viral DNA integrating into the host chromosome in papillomavirus infections?
A) Balanced production of viral replication proteins.
B) Immediate death of the infected cell.
C) Disruption of the cell cycle and unregulated cell proliferation.
D) Formation of antibodies against the virus.
Answer: C) Disruption of the cell cycle and unregulated cell proliferation.
68
What leads to the formation of a malignant tumor in papillomavirus-induced cervical cancer?
A) Continuous viral replication without integration into host DNA.
B) Integration of viral DNA, disruption of the cell cycle, and accumulation of mutations.
C) Overproduction of antibodies against the virus.
D) Immune suppression caused by viral proteins.
Answer: B) Integration of viral DNA, disruption of the cell cycle, and accumulation of mutations.
69
Which of the following is NOT a characteristic of papillomavirus?
A) Circular double-stranded DNA virus.
B) Leads to balanced production of viral replication proteins in initial stages.
C) Directly causes malignant tumors without additional mutations.
D) Can integrate into the host genome and disrupt cell cycle control.
Answer: C) Directly causes malignant tumors without additional mutations.
70
If the viral genome integrates into the host chromosome, what happens to its ability to regulate protein production?
A) It increases regulation of viral proteins.
B) It loses the ability to regulate protein production.
C) It stops producing viral proteins altogether.
D) It becomes more balanced in protein production.
Answer: B) It loses the ability to regulate protein production.
71
What usually happens to the viral genome in benign infections of papillomavirus?
A) It integrates into the host genome.
B) It remains as extra-chromosomal DNA producing balanced viral proteins.
C) It destroys the host cell's nucleus.
D) It induces widespread mutations in the host DNA.
Answer: B) It remains as extra-chromosomal DNA producing balanced viral proteins.
72
Which of the following best describes the role of the E6 protein in HPV-induced cancer?
A) Prevents Rb from binding E2F
B) Promotes the degradation of p53
C) Activates transcription of the p21 gene
D) Blocks the transcription of G1-S cyclins
Answer: B) Promotes the degradation of p53
73
What is the function of the Rb protein in uninfected epithelial cells?
A) Activates E2F to promote cell proliferation
B) Binds and inhibits E2F, preventing cell cycle progression
C) Degrades p53 to inhibit apoptosis
D) Stimulates G1-S cyclin transcription
Answer: B) Binds and inhibits E2F, preventing cell cycle progression
74
The HPV vaccine works by:
A) Targeting E6 and E7 proteins directly
B) Preventing HPV infection by using immunodominant viral proteins
C) Blocking the degradation of Rb and p53
D) Inhibiting G1-S cyclin transcription
Answer: B) Preventing HPV infection by using immunodominant viral proteins
75
If E6 protein production is inhibited in an HPV-infected cell, what will most likely happen?
A) p53 will be degraded, allowing unchecked cell proliferation
B) p53 will remain active, preventing uncontrolled cell growth
C) E2F will be released, leading to increased transcription of G1-S cyclins
D) Cell cycle progression will remain unaffected
Answer: B) p53 will remain active, preventing uncontrolled cell growth
76
In a patient infected with HPV, which of the following changes might occur if E7 is rendered non-functional?
A) Rb will bind to E2F, preventing G1-S cyclin transcription
B) p53 will be degraded, leading to reduced p21 production
C) G1-S cyclins will be overexpressed, pushing the cell into the S phase
D) Cell proliferation will remain uncontrolled
Answer: A) Rb will bind to E2F, preventing G1-S cyclin transcription
77
Which of the following statements is false about HPV proteins and their roles?
A) E6 promotes the degradation of p53.
B) E7 sequesters Rb, allowing E2F to activate G1-S cyclin transcription.
C) HPV infection ensures complete cell cycle arrest to protect the host.
D) E6 and E7 together disrupt normal cell cycle control.
Answer: C) HPV infection ensures complete cell cycle arrest to protect the host.
78
What happens when p53 is unable to bind the promoter of the p21 gene due to HPV infection?
A) The cell cycle progresses unchecked into the S phase.
B) G1-S cyclin/CDK complexes are inhibited.
C) Rb prevents E2F from activating transcription.
D) Apoptosis is triggered, protecting the cell from uncontrolled growth.
Answer: A) The cell cycle progresses unchecked into the S phase.
79
Which of the following combinations correctly describes the interaction of E6 and E7 with host proteins?
A) E6 binds E2F; E7 degrades p53
B) E6 degrades p53; E7 sequesters Rb
C) E6 binds Rb; E7 degrades p21
D) E6 activates G1-S cyclins; E7 blocks p53
Answer: B) E6 degrades p53; E7 sequesters Rb
80
If the HPV vaccine prevents the integration of viral DNA into host chromosomes, what would be the outcome?
A) E6 and E7 will continue to disrupt Rb and p53 functions.
B) Viral DNA will remain episomal, producing balanced levels of viral proteins.
C) Viral infection will have no effect on host cell proliferation.
D) The host will become immune to all viral infections.
Answer: B) Viral DNA will remain episomal, producing balanced levels of viral proteins.
81
Which of the following would not directly result from the inactivation of p53 by E6?
A) Decreased transcription of the p21 gene
B) Increased inhibition of G1-S cyclin/CDK complexes
C) Reduced cellular apoptosis
D) Unchecked progression through the G1-S checkpoint
Answer: B) Increased inhibition of G1-S cyclin/CDK complexes
82
In a cell with functional Rb and p53, but overexpressing E2F, what might you expect?
A) The cell will arrest in the G1 phase.
B) The cell will continue to divide uncontrollably.
C) p53 will degrade Rb, allowing progression into the S phase.
D) E2F will be sequestered, preventing transcription of S-phase genes.
Answer: B) The cell will continue to divide uncontrollably.
83
What is the primary purpose of the FIT test in colorectal cancer screening?
A) To check for genetic mutations in the stool
B) To detect antibodies specific to cancer cells
C) To detect blood in the stool
D) To determine the stage of colorectal cancer
Answer: C) To detect blood in the stool
84
Which gene mutation is most commonly associated with colorectal cancer according to the lecture ?
A) K-Ras
B) APC
C) p53
D) β-catenin
Answer: B) APC
85
Familial Adenomatous Polyposis Coli (FAP) is associated with mutations in which gene?
A) K-Ras
B) APC
C) Smad4
D) TGFβ receptor II
Answer: B) APC
86
What role does APC play in colorectal cancer?
A) Oncogene promoting cell proliferation
B) Tumor suppressor involved in Wnt signaling
C) DNA repair protein
D) Growth factor receptor
Answer: B) Tumor suppressor involved in Wnt signaling
87
Which of the following statements is FALSE about colorectal cancer?
A) It originates from the epithelial lining of the colon and rectum.
B) APC is involved in Wnt signaling and is frequently mutated.
C) β-catenin is a tumor suppressor.
D) Colorectal cancer is typically diagnosed after the age of 55.
Answer: C) β-catenin is a tumor suppressor. (It is an oncogene.)
88
If APC is inactivated, which of the following would likely happen?
A) Wnt signaling would decrease.
B) β-catenin levels would increase and lead to cell proliferation.
C) p53 would compensate for the loss of APC.
D) Cell proliferation would decrease.
Answer: B) β-catenin levels would increase and lead to cell proliferation.
89
A patient has a family history of colorectal cancer associated with an inherited mutation. What is the most likely explanation?
A) Activation of the K-Ras oncogene
B) Loss of function in mismatch repair genes
C) Germline mutation in APC
D) Somatic mutation in β-catenin
Answer: C) Germline mutation in APC
90
Which of the following genes is classified as a tumor suppressor?
A) K-Ras
B) β-catenin
C) APC
D) Cyclin D
Answer: C) APC
91
Which of the following statements about the mechanism of colorectal cancer development is TRUE?
A) K-Ras is a tumor suppressor that prevents uncontrolled cell division.
B) β-catenin activation results in decreased Wnt signaling.
C) APC loss allows β-catenin accumulation and promotes cell proliferation.
D) TGFβ receptor II mutations enhance DNA mismatch repair.
Answer: C) APC loss allows β-catenin accumulation and promotes cell proliferation.
92
Which gene is lost early in the development of colorectal cancer?
a) p53
b) APC
c) K-Ras
d) Smad4
Answer: b) APC
93
What is the primary role of the APC gene in the colon?
a) Promotes cell proliferation
b) Inhibits the Wnt signaling pathway
c) Activates p53
d) Triggers metastasis
Answer: b) Inhibits the Wnt signaling pathway
94
Which oncogene is activated during the progression of early adenomas?
a) Smad4
b) p53
c) K-Ras
d) APC
Answer: c) K-Ras
95
If the APC gene is inactivated, what would most likely happen in the colon?
a) Reduced cell proliferation
b) Accumulation of β-catenin and hyperplasia
c) Increased DNA repair activity
d) Loss of epithelial integrity
Answer: b) Accumulation of β-catenin and hyperplasia
96
A patient has a colorectal carcinoma with no mutation in APC. What mutation is most likely present in this case?
a) Loss of Smad4
b) Activation of K-Ras
c) Overexpression of p53
d) Inactivation of TGFβ receptor
A patient has a colorectal carcinoma with no mutation in APC. What mutation is most likely present in this case?
a) Loss of Smad4
b) Activation of K-Ras
c) Overexpression of p53
d) Inactivation of TGFβ receptor
Answer: b) Activation of K-Ras
97
Which of the following statements about colorectal cancer is FALSE?
a) APC mutations occur early in the development of colorectal cancer.
b) Loss of p53 activity occurs in the intermediate adenoma stage.
c) K-Ras activation promotes benign polyp growth.
d) TGFβ receptor loss is associated with metastasis.
Answer: b) Loss of p53 activity occurs in the intermediate adenoma stage (it occurs later in carcinoma development).
98
A patient with Familial Adenomatous Polyposis (FAP) is being monitored. Which gene is most likely mutated in this patient?
a) p53
b) APC
c) K-Ras
d) TGFβ receptor
Answer: b) APC
99
If β-catenin accumulation is observed in a colon biopsy, what is the likely explanation?
a) Loss of K-Ras
b) Overexpression of p53
c) Inactivation of APC
d) Activation of Smad4
Answer: c) Inactivation of APC
100
Which of the following steps is NOT part of the metastatic process?
A) Local invasion
B) Crossing the basal lamina
C) Fusion with blood cells
D) Colonization at a new site
Answer: C) Fusion with blood cells
101
What happens when the E-cadherin protein is lost in cancer cells?
A) Increased adhesion to neighboring cells
B) Loss of cell-to-cell adhesion, allowing detachment
C) Prevention of angiogenesis
D) Increased stability of the basal lamina
Answer: B) Loss of cell-to-cell adhesion, allowing detachment
102
Which protein is primarily responsible for degrading HIF under normal oxygen levels?
A) VEGF
B) VHL ligase
C) E-cadherin
D) HIF itself
Answer: B) VHL ligase
103
Which statement about VEGF is TRUE?
A) It inhibits angiogenesis.
B) It prevents the spread of cancer cells.
C) It promotes endothelial cell sprouting.
D) It degrades HIF under hypoxic conditions.
Answer: C) It promotes endothelial cell sprouting.
104
If VHL ligase were inactivated in a cancer cell, what would happen?
A) Increased degradation of HIF
B) Decreased angiogenesis
C) Elevated levels of HIF and angiogenesis
D) Inhibition of VEGF production
Answer: C) Elevated levels of HIF and angiogenesis
105
In a tumor located in low-oxygen tissue, which event is most likely to occur first?
A) HIF degradation by VHL
B) Increased secretion of VEGF
C) Stabilization of E-cadherin
D) Decrease in endothelial cell proliferation
Answer: B) Increased secretion of VEGF
106
Which of the following statements about metastasis is FALSE?
A) Angiogenesis is necessary for tumor growth at new sites.
B) Fewer than 1 in 1000 cancer cells survive in the bloodstream.
C) VEGF directly inhibits HIF in hypoxic conditions.
D) Loss of adhesion proteins is a prerequisite for metastasis.
Answer: C) VEGF directly inhibits HIF in hypoxic conditions
107
Which of the following is FALSE regarding VHL ligase?
A) It is a tumor suppressor.
B) It directly degrades VEGF.
C) It tags HIF for degradation under normal oxygen conditions.
D) Its loss can lead to increased angiogenesis.
Answer: B) It directly degrades VEGF
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