MCQ Quiz- DNA Repair Mechanisms

MCQ Quiz: A Guide to DNA Repair Mechanisms

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The integrity of our DNA is under constant assault from both internal metabolic processes and external environmental agents. To survive, cells have evolved a sophisticated and overlapping set of DNA repair mechanisms to correct this damage, preventing mutations that can lead to diseases like cancer. For pharmacists, understanding these pathways is crucial for grasping the mechanisms of certain anticancer drugs and the genetic basis of many diseases. This quiz for PharmD students will test your knowledge of the major DNA repair pathways and the key enzymes involved.

1. The primary purpose of DNA repair mechanisms is to:

  • Increase the rate of evolution.
  • Introduce new genetic diversity.
  • Maintain the integrity of the genome by correcting errors and damage.
  • Regulate the cell cycle.

Answer: Maintain the integrity of the genome by correcting errors and damage.

2. A patient has a genetic defect in the Nucleotide Excision Repair (NER) pathway. They would be extremely sensitive to which of the following?

  • X-rays
  • Alkylating agents
  • UV radiation from sunlight
  • Reactive oxygen species

Answer: UV radiation from sunlight

3. “Mismatch Repair” (MMR) is a system that primarily corrects:

  • Double-strand breaks.
  • Errors made by DNA polymerase during replication, such as mismatched base pairs.
  • Bulky adducts on the DNA.
  • Uracil in the DNA strand.

Answer: Errors made by DNA polymerase during replication, such as mismatched base pairs.

4. The first step in “Base Excision Repair” (BER) for a damaged base like uracil is performed by which enzyme?

  • AP Endonuclease
  • DNA Ligase
  • DNA Polymerase
  • DNA Glycosylase

Answer: DNA Glycosylase

5. After a DNA glycosylase removes a damaged base, it creates an “apurinic/apyrimidinic” (AP) site. Which enzyme then cuts the phosphodiester backbone at this site?

  • DNA Ligase
  • AP Endonuclease
  • DNA Photolyase
  • DNA Polymerase

Answer: AP Endonuclease

6. “Nucleotide Excision Repair” (NER) differs from Base Excision Repair (BER) in that NER:

  • Repairs only single-base damage.
  • Removes a single damaged base.
  • Removes a larger patch of nucleotides surrounding a bulky, helix-distorting lesion.
  • Does not require DNA ligase.

Answer: Removes a larger patch of nucleotides surrounding a bulky, helix-distorting lesion.

7. Pyrimidine dimers, a common form of DNA damage caused by UV light, are primarily repaired in humans by:

  • Photoreactivation.
  • Nucleotide Excision Repair.
  • Mismatch Repair.
  • Base Excision Repair.

Answer: Nucleotide Excision Repair.

8. Which of the following is the most dangerous type of DNA lesion for a cell?

  • A single nucleotide mismatch.
  • A deaminated cytosine.
  • A double-strand break.
  • An AP site.

Answer: A double-strand break.

9. “Non-Homologous End Joining” (NHEJ) is a pathway that repairs double-strand breaks. A key characteristic of this pathway is that it is:

  • Highly accurate and error-free.
  • Dependent on a sister chromatid for a template.
  • Fast but “quick and dirty,” often resulting in small insertions or deletions (error-prone).
  • Only active during the S phase of the cell cycle.

Answer: Fast but “quick and dirty,” often resulting in small insertions or deletions (error-prone).

10. “Homologous Recombination” (HR) is the other major pathway for repairing double-strand breaks. Its key characteristic is that it is:

  • Highly accurate because it uses an undamaged sister chromatid as a template.
  • Very fast but highly error-prone.
  • The preferred repair method in the G1 phase of the cell cycle.
  • Does not require any specialized enzymes.

Answer: Highly accurate because it uses an undamaged sister chromatid as a template.

11. The proteins BRCA1 and BRCA2, which are famously mutated in hereditary breast and ovarian cancers, are key players in which DNA repair pathway?

  • Mismatch Repair
  • Base Excision Repair
  • Nucleotide Excision Repair
  • Homologous Recombination

Answer: Homologous Recombination

12. The enzyme “DNA photolyase,” found in many organisms but not placental mammals, is an example of “direct reversal” repair because it:

  • Removes a damaged base, creating an AP site.
  • Uses light energy to directly reverse the bonds forming a pyrimidine dimer.
  • Removes a patch of DNA.
  • Fills in a gap with new DNA.

Answer: Uses light energy to directly reverse the bonds forming a pyrimidine dimer.

13. In prokaryotic mismatch repair, how does the system distinguish the newly synthesized strand (with the error) from the parent strand?

  • By the presence of nicks in the new strand.
  • The parent strand is methylated, while the new strand is not yet methylated.
  • The parent strand is shorter.
  • The new strand is bound by more proteins.

Answer: The parent strand is methylated, while the new strand is not yet methylated.

14. The “enzymes of DNA metabolism” like DNA polymerase and DNA ligase are essential for:

  • DNA replication.
  • The final steps of most DNA repair pathways.
  • Molecular cloning techniques.
  • All of the above.

Answer: All of the above.

15. A patient with the genetic disease Xeroderma Pigmentosum has defects in which DNA repair pathway, making them highly susceptible to skin cancer?

  • Mismatch Repair
  • Base Excision Repair
  • Nucleotide Excision Repair
  • Homologous Recombination

Answer: Nucleotide Excision Repair

16. The mechanism of action of many “chemotherapeutic” agents involves:

  • Causing extensive DNA damage to induce apoptosis in rapidly dividing cancer cells.
  • Enhancing the cell’s DNA repair capacity.
  • Preventing all DNA damage.
  • Correcting mutations in cancer cells.

Answer: Causing extensive DNA damage to induce apoptosis in rapidly dividing cancer cells.

17. PARP inhibitors are a class of targeted oncology drugs that are particularly effective in tumors with a pre-existing defect in which repair pathway?

  • Mismatch Repair
  • Base Excision Repair
  • Nucleotide Excision Repair
  • Homologous Recombination (e.g., BRCA-mutated cancers)

Answer: Homologous Recombination (e.g., BRCA-mutated cancers)

18. The concept of “synthetic lethality,” exploited by PARP inhibitors, means that:

  • A defect in one DNA repair pathway is tolerable, but defects in two pathways simultaneously is lethal to the cell.
  • The drug is only lethal when synthesized in a lab.
  • The drug kills both healthy and cancer cells equally.
  • The drug is a combination of two different lethal agents.

Answer: A defect in one DNA repair pathway is tolerable, but defects in two pathways simultaneously is lethal to the cell.

19. Which of the following is a type of “direct reversal” repair?

  • The removal of a methyl group from O⁶-methylguanine by a methyltransferase enzyme.
  • The removal of a uracil base by a glycosylase.
  • The repair of a double-strand break by NHEJ.
  • The removal of a bulky adduct by NER.

Answer: The removal of a methyl group from O⁶-methylguanine by a methyltransferase enzyme.

20. A pharmacist’s knowledge of “DNA structure” is fundamental to understanding how:

  • DNA damage (like a pyrimidine dimer) can distort the double helix.
  • A drug can intercalate into the DNA.
  • Repair enzymes recognize and bind to the DNA.
  • All of the above.

Answer: All of the above.

21. The Ku proteins (Ku70/Ku80) are key sensors that recognize and bind to the ends of a DNA double-strand break to initiate which pathway?

  • Homologous Recombination
  • Non-Homologous End Joining
  • Mismatch Repair
  • Nucleotide Excision Repair

Answer: Non-Homologous End Joining

22. A key leadership role for a pharmacist in an oncology setting is to:

  • Understand how resistance to DNA-damaging agents can arise from upregulation of DNA repair pathways.
  • Make all decisions about chemotherapy regimens.
  • Compound all sterile preparations.
  • Manage the clinic’s schedule.

Answer: Understand how resistance to DNA-damaging agents can arise from upregulation of DNA repair pathways.

23. A “business plan” for a new biotech company might focus on developing a novel inhibitor of a key DNA repair enzyme as a(n):

  • New antibiotic.
  • New anticancer agent.
  • New antiviral agent.
  • New anti-inflammatory agent.

Answer: New anticancer agent.

24. The “forging ahead” mindset in pharmacy means embracing personalized medicine, such as using a patient’s __________ status to select an effective therapy.

  • Tumor DNA repair
  • Insurance
  • Social
  • Marital

Answer: Tumor DNA repair

25. A “policy” debate in pharmacogenomics could center on whether insurance should cover testing for mutations in __________ for cancer risk assessment.

  • All genes.
  • The BRCA1 and BRCA2 genes.
  • The CYP2D6 gene.
  • The MTHFR gene.

Answer: The BRCA1 and BRCA2 genes.

26. The high fidelity of DNA replication is due to the proofreading activity of DNA polymerase and the subsequent action of which repair system?

  • Nucleotide Excision Repair
  • Mismatch Repair
  • Base Excision Repair
  • Non-Homologous End Joining

Answer: Mismatch Repair

27. Deamination of cytosine is a common form of spontaneous DNA damage that converts it to:

  • Thymine
  • Guanine
  • Adenine
  • Uracil

Answer: Uracil

28. If a deaminated cytosine (uracil) is not repaired before replication, it will lead to what type of mutation?

  • A C-G base pair will be converted to a T-A base pair.
  • A deletion of the base pair.
  • An insertion of a new base pair.
  • A double-strand break.

Answer: A C-G base pair will be converted to a T-A base pair.

29. The process of “special recombination” like V(D)J recombination involves the creation of a double-strand break that is repaired by which pathway?

  • Non-Homologous End Joining
  • Homologous Recombination
  • Mismatch Repair
  • Base Excision Repair

Answer: Non-Homologous End Joining

30. The ultimate reason we study DNA repair mechanisms in pharmacy is that:

  • They are central to understanding cancer biology and the mechanisms of many anticancer drugs.
  • They are interesting but have no clinical relevance.
  • They are the primary target of all antibiotics.
  • They are easy to understand.

Answer: They are central to understanding cancer biology and the mechanisms of many anticancer drugs.

31. In Base Excision Repair, after the AP endonuclease cuts the backbone, which two enzymes complete the repair?

  • DNA Polymerase and DNA Ligase
  • Helicase and Primase
  • RAG1 and RAG2
  • Topoisomerase and Gyrase

Answer: DNA Polymerase and DNA Ligase

32. The “SOS response” in bacteria is an inducible DNA repair system that is:

  • Highly accurate.
  • Error-prone, allowing the cell to survive but at the cost of introducing mutations.
  • A form of direct reversal.
  • The same as nucleotide excision repair.

Answer: Error-prone, allowing the cell to survive but at the cost of introducing mutations.

33. Homologous recombination is most active during which phases of the eukaryotic cell cycle, when a sister chromatid is available?

  • G1 and M
  • S and G2
  • G0 and G1
  • M and G2

Answer: S and G2

34. A key part of the “Introduction to Pharmacy Informatics” is understanding how an EHR can be used to store a patient’s genetic information, such as their status for which DNA repair genes?

  • BRCA1/BRCA2
  • CYP2C19
  • VKORC1
  • SLCO1B1

Answer: BRCA1/BRCA2

35. A “Clinical Decision Support” system could be designed to alert a physician if they are prescribing a PARP inhibitor to a patient who does not have a documented mutation in:

  • A mismatch repair gene.
  • A homologous recombination gene like BRCA1/2.
  • A base excision repair gene.
  • A nucleotide excision repair gene.

Answer: A homologous recombination gene like BRCA1/2.

36. An “analytics and reporting system” could be used in a cancer center to track:

  • The percentage of eligible patients who receive genetic testing for hereditary cancer syndromes.
  • The outcomes of patients treated with PARP inhibitors.
  • The incidence of specific DNA repair gene mutations in their patient population.
  • All of the above.

Answer: All of the above.

37. The “regulation” of a new diagnostic test to identify mutations in DNA repair genes is the responsibility of the:

  • DEA
  • FDA
  • CMS
  • EPA

Answer: FDA

38. A “negotiation” with a payer for an expensive PARP inhibitor would be strengthened by:

  • Evidence from clinical trials showing a significant survival benefit in patients with specific DNA repair defects.
  • The high cost of the drug alone.
  • The novelty of the drug’s mechanism.
  • The personal preference of the physician.

Answer: Evidence from clinical trials showing a significant survival benefit in patients with specific DNA repair defects.

39. A pharmacist’s knowledge of “human resources” in an oncology clinic would involve ensuring that staff who handle DNA-damaging chemotherapy agents:

  • Receive appropriate safety training.
  • Are aware of the long-term health risks.
  • Know how to handle spills correctly.
  • All of the above.

Answer: All of the above.

40. A key “leadership” challenge in a cancer research institute is:

  • Securing funding for research into novel DNA repair inhibitors.
  • Managing a team of highly specialized scientists.
  • Fostering a collaborative environment.
  • All of the above.

Answer: All of the above.

41. The “enzymes of DNA metabolism” are the core machinery of DNA repair. A DNA glycosylase is an enzyme that breaks which type of bond?

  • Phosphodiester bond
  • Hydrogen bond
  • Glycosidic bond (between the base and the sugar)
  • Peptide bond

Answer: Glycosidic bond (between the base and the sugar)

42. A key “policy” issue is deciding which DNA repair gene mutations are clinically actionable and should be included in:

  • Standard genetic screening panels.
  • Newborn screening.
  • Direct-to-consumer genetic tests.
  • All of the above.

Answer: All of the above.

43. The “service” of genetic counseling is critical when a patient tests positive for a mutation in a DNA repair gene like BRCA1 in order to:

  • Explain the implications for their cancer risk and the risk for their family members.
  • Prescribe a PARP inhibitor.
  • Perform the genetic test.
  • Bill for the service.

Answer: Explain the implications for their cancer risk and the risk for their family members.

44. A “health disparity” could be created if genetic testing for mutations in DNA repair genes is:

  • Only accessible or offered to affluent, White populations.
  • Covered by all insurance plans.
  • Offered with culturally competent counseling.
  • Used to guide therapy for all patients.

Answer: Only accessible or offered to affluent, White populations.

45. A “first response” to a toxic exposure to a DNA-damaging agent (e.g., a chemical spill) would prioritize:

  • Decontamination and ensuring the safety of the responder.
  • Immediately starting chemotherapy.
  • Taking a detailed family history.
  • Performing a genetic test.

Answer: Decontamination and ensuring the safety of the responder.

46. The “cloning” of a specific human DNA repair gene into bacteria allows researchers to:

  • Produce large quantities of the enzyme for study.
  • Analyze its structure and function.
  • Screen for drugs that might inhibit the enzyme.
  • All of the above.

Answer: All of the above.

47. The “molecular biology technique” of PCR can be used to:

  • Amplify a specific DNA repair gene from a patient’s DNA sample to screen for mutations.
  • Repair a double-strand break.
  • Measure the level of a protein.
  • Clone an entire organism.

Answer: Amplify a specific DNA repair gene from a patient’s DNA sample to screen for mutations.

48. In “prokaryotic DNA replication,” the proofreading function is a form of immediate repair performed by:

  • DNA Polymerase I
  • DNA Polymerase III
  • DNA Ligase
  • Both A and B

Answer: Both A and B

49. The “special recombination” pathway of V(D)J recombination intentionally creates a double-strand break that is then repaired by the error-prone ________ pathway to generate diversity.

  • Homologous Recombination
  • Non-Homologous End Joining
  • Mismatch Repair
  • Base Excision Repair

Answer: Non-Homologous End Joining

50. The ultimate reason for a pharmacist to understand DNA repair mechanisms is that their failure is a fundamental cause of _______, and their manipulation is a key strategy in _______.

  • Heart disease; cardiology
  • Infection; infectious disease
  • Cancer; oncology
  • Diabetes; endocrinology

Answer: Cancer; oncology

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