Lecture 10: Cancer

Question 1

Which of the following proteins promotes cell cycle progression in cancer?
a) p16
b) Rb
c) Cyclin D
d) p53

Answer 1

Answer: c) Cyclin D

Question 2

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

Answer 2

Answer: b) Inhibit cell proliferation

Question 3

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

Answer 3

Answer: b) Myc

Question 4

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

Answer 4

Answer: b) Oncogenes

Question 5

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

Answer 5

Answer: b) Recessive mutation

Question 6

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

Answer 6

Answer: c) p53

Question 7

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.

Answer 7

Answer: b) They are dominant traits when mutated.

Question 8

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

Answer 8

Answer: d) All of the above

Question 9

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.

Answer 9

Answer: c) Cyclin D-CDK complex becomes overactive.

Question 10

Which process is prevented by the overexpression of Bcl2 in cancer cells?
a) Cell division
b) DNA replication
c) Apoptosis
d) Angiogenesis

Answer 10

Answer: c) Apoptosis

Question 11

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.

Answer 11

Answer: b) Proto-oncogenes promote normal cell division, oncogenes are mutated forms.

Question 12

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.

Answer 12

Answer: b) Activates apoptosis in response to DNA damage.

Question 13

Which of the following is considered a hallmark of cancer?
a) Increased apoptosis
b) Decreased angiogenesis
c) Sustained proliferative signaling
d) Reduced cell division

Answer 13

Answer: c) Sustained proliferative signaling

Question 14

Which gene is mutated in chronic myeloid leukemia (CML) as part of the BCR-ABL fusion?
a) Myc
b) Rb
c) ABL
d) Bcl2

Answer 14

Answer: c) ABL

Question 15

Loss-of-function mutations in which tumor suppressor gene are associated with retinoblastoma?
a) p53
b) Rb
c) Myc
d) Cyclin D

Answer 15

Answer: b) Rb

Question 16

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

Answer 16

a)

Question 17

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

Answer 17

Answer:
b) A mutation that converts a proto-oncogene into an oncogene, leading to gain of function

Question 18

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

Answer 18

Answer:
b) Unregulated cell division due to lack of inhibitory proteins

Question 19

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

Answer 19

Answer:
b) Promote normal cell growth and division

Question 20

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

Answer 20

Answer:
b) Inhibiting cell proliferation and promoting genomic stability

Question 21

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

Answer 21

Answer:
b) Oncogenes result from gain-of-function mutations in proto-oncogenes

Question 22

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

Answer 22

Answer:
a) One functional copy can usually compensate for the loss of the other

Question 23

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

Answer 23

nswer:
c) p53

Question 24

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

Answer 24

Answer:
b) Multiple genes control cell growth and must be altered for cancer to arise

Question 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 25

Answer:
b) Oncogenes act dominantly when mutated; tumor suppressor genes act recessively

Question 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 26

Answer:
c) Detects DNA damage and can induce cell cycle arrest or apoptosis

Question 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 27

Answer:
b) Activation of the Ras gene causing constant cell proliferation signals

Question 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 28

Answer:
c) Regulate cell cycle checkpoints and initiate DNA repair

Question 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 29

Answer:
b) A mutation that enhances the gene’s normal activity or creates a new function

Question 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 30

Answer:
b) Multiple mutations in various genes that regulate cell growth and division

Question 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 31

Answer:
c) Tumor suppressor genes inhibit cell division; oncogenes promote normal cell growth

Question 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 32

Answer:
c) It leads to the absence of proteins that control cell division

Question 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 33

Answer:
b) p53

Question 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 34

Answer:
b) A trait that requires mutations in both alleles to affect cell function

Question 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 35

Answer: b) Extracellular domain

Question 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 36

Answer: c) The receptor remains unbound, and no signal is transmitted.

Question 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 37

Answer: c) EGFR activation always inhibits cell proliferation.

Question 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 38

Answer: b) EGFR amplification in glioblastoma leads to reduced cell signaling.

Question 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 39

Answer: c) The receptor will become constitutively active, driving unregulated cell growth.

Question 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 40

Answer: a) EGFR will remain inactive even when EGF binds.

Question 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 41

Answer: b) It would stop the continuous growth signals from being transmitted.

Question 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 42

Answer: b) Reduction in tumor growth due to decreased signaling.

Question 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 43

Answer: d) All of the above.

Question 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 44

Answer: b) Downstream signaling pathways will not be activated.

Question 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 45

Answer: b) Prevents entry into the S-phase of the cell cycle

Question 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 46

Answer: b) One

Question 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 47

Answer: b) Two

Question 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 48

Answer: c) It is detected in adulthood

Question 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 49

Answer: c) The cell will enter the S-phase and divide uncontrollably.

Question 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 50

Answer: a) One inherited mutated Rb gene and a second mutation in retinal cells

Question 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 51

Answer: d) Develops from two independent mutations in the same retinal cell

Question 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 52

Answer: c) They lack one functional Rb gene copy in all body cells

Question 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 53

Answer: b) Non-hereditary retinoblastoma

Question 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 54

Answer: b) Development of other cancers in adulthood

Question 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 55

Answer: C) Cancer requires the accumulation of multiple mutations over time.

Question 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 56

Answer: C) Cancer risk increases with age due to the accumulation of mutations in dividing cells.

Question 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 57

Answer: C) Multiple mutations accumulate over time after exposure to carcinogens like tobacco.

Question 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 58

Answer: B) Cell division rates decrease, reducing the chances of accumulating mutations.

Question 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 59

Answer: B) There is usually a lag period of 10–20 years before cancer develops.

Question 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 60

Answer: B) DNA damage accumulates and additional mutations occur later, leading to cancer.

Question 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 61

Answer: B) Increasing cell proliferation and preventing cell death.

Question 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 62

Answer: B) No cancer development unless further mutations accumulate.

Question 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 63

Answer: B) Gradual decline due to the lag period for mutations to accumulate.

Question 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 64

Answer: C) 15%

Question 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 65

Answer: D) Circular double-stranded DNA virus

Question 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 66

Answer: B) Viral genome remains as extra-chromosomal DNA producing balanced viral proteins.

Question 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 67

Answer: C) Disruption of the cell cycle and unregulated cell proliferation.

Question 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 68

Answer: B) Integration of viral DNA, disruption of the cell cycle, and accumulation of mutations.

Question 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 69

Answer: C) Directly causes malignant tumors without additional mutations.

Question 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 70

Answer: B) It loses the ability to regulate protein production.

Question 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 71

Answer: B) It remains as extra-chromosomal DNA producing balanced viral proteins.

Question 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 72

Answer: B) Promotes the degradation of p53

Question 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 73

Answer: B) Binds and inhibits E2F, preventing cell cycle progression

Question 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 74

Answer: B) Preventing HPV infection by using immunodominant viral proteins

Question 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 75

Answer: B) p53 will remain active, preventing uncontrolled cell growth

Question 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 76

Answer: A) Rb will bind to E2F, preventing G1-S cyclin transcription

Question 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 77

Answer: C) HPV infection ensures complete cell cycle arrest to protect the host.

Question 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 78

Answer: A) The cell cycle progresses unchecked into the S phase.

Question 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 79

Answer: B) E6 degrades p53; E7 sequesters Rb

Question 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 80

Answer: B) Viral DNA will remain episomal, producing balanced levels of viral proteins.

Question 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 81

Answer: B) Increased inhibition of G1-S cyclin/CDK complexes

Question 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 82

Answer: B) The cell will continue to divide uncontrollably.

Question 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 83

Answer: C) To detect blood in the stool

Question 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 84

Answer: B) APC

Question 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 85

Answer: B) APC

Question 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 86

Answer: B) Tumor suppressor involved in Wnt signaling

Question 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 87

Answer: C) β-catenin is a tumor suppressor. (It is an oncogene.)

Question 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 88

Answer: B) β-catenin levels would increase and lead to cell proliferation.

Question 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 89

Answer: C) Germline mutation in APC

Question 90

Which of the following genes is classified as a tumor suppressor?

A) K-Ras
B) β-catenin
C) APC
D) Cyclin D

Answer 90

Answer: C) APC

Question 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 91

Answer: C) APC loss allows β-catenin accumulation and promotes cell proliferation.

Question 92

Which gene is lost early in the development of colorectal cancer?

a) p53
b) APC
c) K-Ras
d) Smad4

Answer 92

Answer: b) APC

Question 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 93

Answer: b) Inhibits the Wnt signaling pathway

Question 94

Which oncogene is activated during the progression of early adenomas?

a) Smad4
b) p53
c) K-Ras
d) APC

Answer 94

Answer: c) K-Ras

Question 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 95

Answer: b) Accumulation of β-catenin and hyperplasia

Question 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

Answer 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
Answer: b) Activation of K-Ras

Question 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 97

Answer: b) Loss of p53 activity occurs in the intermediate adenoma stage (it occurs later in carcinoma development).

Question 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 98

Answer: b) APC

Question 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 99

Answer: c) Inactivation of APC

Question 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 100

Answer: C) Fusion with blood cells

Question 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 101

Answer: B) Loss of cell-to-cell adhesion, allowing detachment

Question 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 102

Answer: B) VHL ligase

Question 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 103

Answer: C) It promotes endothelial cell sprouting.

Question 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 104

Answer: C) Elevated levels of HIF and angiogenesis

Question 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 105

Answer: B) Increased secretion of VEGF

Question 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 106

Answer: C) VEGF directly inhibits HIF in hypoxic conditions

Question 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 107

Answer: B) It directly degrades VEGF