MCQ Quiz- Tumor Suppressors

MCQ Quiz: Tumor Suppressors

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Tumor suppressor genes are the “brakes” of the cell cycle, playing a critical role in preventing cancer by regulating cell division, repairing DNA damage, and initiating programmed cell death. Their inactivation is a fundamental step in the development of many cancers, and understanding their function is crucial for grasping cancer genetics and the rationale behind certain targeted therapies. This quiz for PharmD students will test your knowledge of these essential guardians of the genome, their mechanisms, and their clinical significance in oncology.

1. A “tumor suppressor gene” is a normal gene that primarily functions to:

  • Promote cell growth and proliferation.
  • Inhibit or regulate cell division and prevent the development of tumors.
  • Stimulate the formation of new blood vessels.
  • Cause mutations in the DNA.

Answer: Inhibit or regulate cell division and prevent the development of tumors.

2. The “two-hit hypothesis,” first proposed by Alfred Knudson, applies to the inactivation of:

  • Oncogenes.
  • Tumor suppressor genes.
  • Proto-oncogenes.
  • All genes in the genome.

Answer: Tumor suppressor genes.

3. According to the “two-hit hypothesis,” for a cell to become cancerous through the loss of a tumor suppressor, what must typically happen?

  • A single activating mutation is sufficient.
  • Both copies (alleles) of the tumor suppressor gene must be inactivated.
  • The gene must be amplified.
  • The gene must be translocated to a new chromosome.

Answer: Both copies (alleles) of the tumor suppressor gene must be inactivated.

4. Which of the following is often called the “guardian of the genome” and is the most frequently mutated tumor suppressor gene in human cancers?

  • RB1
  • BRCA1
  • APC
  • p53 (TP53)

Answer: p53 (TP53)

5. The p53 protein plays a critical role in the cellular response to DNA damage by:

  • Halting the cell cycle to allow for DNA repair.
  • Activating DNA repair enzymes.
  • Initiating apoptosis (programmed cell death) if the damage is too severe.
  • All of the above.

Answer: All of the above.

6. In contrast to oncogenes which are activated by a “gain-of-function” mutation, tumor suppressor genes are inactivated by a:

  • Gain-of-function mutation.
  • Loss-of-function mutation.
  • Silent mutation.
  • Frameshift mutation only.

Answer: Loss-of-function mutation.

7. Inherited mutations in tumor suppressor genes are the cause of many hereditary cancer syndromes. For example, an inherited mutation in the RB1 gene causes:

  • Li-Fraumeni syndrome.
  • Hereditary breast and ovarian cancer syndrome.
  • Lynch syndrome.
  • Hereditary retinoblastoma.

Answer: Hereditary retinoblastoma.

8. The Retinoblastoma (RB1) protein is a key tumor suppressor that functions as a major checkpoint in the:

  • G1 phase of the cell cycle.
  • S phase of the cell cycle.
  • G2 phase of the cell cycle.
  • M phase of the cell cycle.

Answer: G1 phase of the cell cycle.

9. The BRCA1 and BRCA2 genes are tumor suppressors that are critically involved in which cellular process?

  • The regulation of angiogenesis.
  • The repair of DNA double-strand breaks via homologous recombination.
  • The metabolism of carcinogens.
  • The control of cell growth signaling.

Answer: The repair of DNA double-strand breaks via homologous recombination.

10. Women who inherit a germline mutation in the BRCA1 or BRCA2 gene have a significantly increased lifetime risk of:

  • Lung and colon cancer.
  • Leukemia and lymphoma.
  • Breast and ovarian cancer.
  • Skin and brain cancer.

Answer: Breast and ovarian cancer.

11. The concept of “synthetic lethality” is the principle behind using PARP inhibitors to treat cancers with a BRCA1/2 mutation. This means:

  • The loss of either the PARP or BRCA function alone is survivable, but the loss of both is lethal to the cancer cell.
  • The PARP inhibitor is only effective when combined with traditional chemotherapy.
  • The drug is synthetically made and is lethal to all cells.
  • The drug only works in tumors that have no mutations.

Answer: The loss of either the PARP or BRCA function alone is tolerable, but the loss of both is lethal to the cancer cell.

12. The APC (Adenomatous Polyposis Coli) gene is a tumor suppressor that is most famously mutated in:

  • Familial adenomatous polyposis (FAP) and many sporadic colorectal cancers.
  • Melanoma.
  • Glioblastoma.
  • Chronic myeloid leukemia.

Answer: Familial adenomatous polyposis (FAP) and many sporadic colorectal cancers.

13. In addition to mutation, a tumor suppressor gene can be silenced by which “epigenetic” mechanism?

  • Gene amplification.
  • Hypermethylation of its promoter region.
  • Histone acetylation.
  • A chromosomal translocation.

Answer: Hypermethylation of its promoter region.

14. A key difference between an oncogene and a tumor suppressor gene is that an oncogene’s mutation acts in a ________ manner, while a tumor suppressor’s mutation acts in a ________ manner.

  • Recessive; dominant
  • Dominant; recessive
  • Both are dominant.
  • Both are recessive.

Answer: Dominant; recessive

15. A pharmacist’s knowledge of “oncogenes” and tumor suppressors is the foundation of understanding:

  • How cancer develops at a molecular level.
  • The rationale for targeted therapies.
  • The basis of hereditary cancer risk.
  • All of the above.

Answer: All of the above.

16. The use of “gene therapy” could one day be used to treat cancer by:

  • Introducing a functional copy of a mutated tumor suppressor gene back into cancer cells.
  • Activating a known oncogene.
  • Inhibiting all DNA repair.
  • Deleting all tumor suppressor genes.

Answer: Introducing a functional copy of a mutated tumor suppressor gene back into cancer cells.

17. A “forging ahead” mindset in pharmacy means embracing personalized medicine, such as using the status of a patient’s __________ to guide therapy.

  • Tumor suppressor genes (e.g., BRCA status for a PARP inhibitor)
  • Insurance plan
  • Social circle
  • Marital status

Answer: Tumor suppressor genes (e.g., BRCA status for a PARP inhibitor)

18. A “business plan” for a new cancer diagnostics company might focus on developing a more sensitive test for detecting mutations in:

  • Key tumor suppressor genes like p53.
  • All genes in the genome.
  • Housekeeping genes.
  • Genes for metabolic enzymes.

Answer: Key tumor suppressor genes like p53.

19. A pharmacist’s “leadership” is shown when they advocate for:

  • The routine use of genetic testing for hereditary cancer syndromes in high-risk patients.
  • The use of fewer genetic tests.
  • The discontinuation of all targeted therapies.
  • A return to traditional chemotherapy for all cancers.

Answer: The routine use of genetic testing for hereditary cancer syndromes in high-risk patients.

20. The “regulation” of a new genetic test that identifies mutations in tumor suppressor genes is the responsibility of the:

  • DEA
  • FDA (often through its oversight of lab-developed tests and in vitro diagnostics).
  • CMS
  • EPA

Answer: The FDA (often through its oversight of lab-developed tests and in vitro diagnostics).

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

  • Identify all patients with a BRCA mutation to ensure they have been counseled on risk-reducing strategies.
  • Track the pharmacy’s inventory of all drugs.
  • Schedule patient appointments.
  • Create a marketing plan.

Answer: Identify all patients with a BRCA mutation to ensure they have been counseled on risk-reducing strategies.

22. A “Clinical Decision Support” system could be designed to alert a physician if they are prescribing a drug that is ineffective in tumors with a specific _________ mutation.

  • Tumor suppressor gene
  • Growth factor receptor
  • DNA polymerase
  • Ribosomal subunit

Answer: Tumor suppressor gene

23. A “negotiation” with a payer for an expensive PARP inhibitor would be strongest if the patient has a documented mutation in:

  • A gene like BRCA1 or BRCA2.
  • The p53 gene.
  • The RB1 gene.
  • Any tumor suppressor gene.

Answer: A gene like BRCA1 or BRCA2.

24. The “service” of genetic counseling is critical when a patient is found to have a germline mutation in a tumor suppressor gene in order to:

  • Explain the implications for their own cancer risk and the risk to their family members.
  • Prescribe the appropriate chemotherapy.
  • Administer the genetic test.
  • Bill for the service.

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

25. A “policy” decision to recommend routine HPV vaccination is a public health measure to prevent cancers caused by the virus’s ability to inactivate which two tumor suppressors?

  • BRCA1 and BRCA2
  • p53 and RB1
  • APC and MSH2
  • PTEN and NF1

Answer: p53 and RB1

26. A pharmacist’s knowledge of “DNA repair mechanisms” is critical because:

  • Many key tumor suppressor genes (like BRCA1/2 and the MMR genes) are part of these pathways.
  • It is not relevant to tumor suppressor function.
  • All tumor suppressors are transcription factors.
  • All tumor suppressors are cell cycle regulators.

Answer: Many key tumor suppressor genes (like BRCA1/2 and the MMR genes) are part of these pathways.

27. The field of “epigenetics” is highly relevant to tumor suppressors because:

  • Epigenetic silencing (like promoter hypermethylation) is a common, non-mutational way to inactivate a tumor suppressor gene.
  • Epigenetics only affects oncogenes.
  • The two fields are unrelated.
  • All epigenetic marks activate tumor suppressors.

Answer: Epigenetic silencing (like promoter hypermethylation) is a common, non-mutational way to inactivate a tumor suppressor gene.

28. The “molecular biology technique” of DNA sequencing is essential for:

  • Identifying the “second hit” or mutation in a tumor suppressor gene.
  • Measuring the level of a protein.
  • Cloning an entire organism.
  • Separating DNA fragments by size.

Answer: Identifying the “second hit” or mutation in a tumor suppressor gene.

29. A “chemotherapeutic” like an HDAC inhibitor can be thought of as a drug that can indirectly:

  • Reactivate epigenetically silenced tumor suppressor genes.
  • Cause mutations in tumor suppressor genes.
  • Enhance the function of oncogenes.
  • Repair damaged DNA.

Answer: Reactivate epigenetically silenced tumor suppressor genes.

30. The ultimate reason pharmacists study tumor suppressors is because their inactivation is:

  • A fundamental and required step in the development of most cancers, providing key insights into both risk and treatment.
  • An interesting but clinically minor phenomenon.
  • The cause of all infectious diseases.
  • The primary target for all antibiotics.

Answer: A fundamental and required step in the development of most cancers, providing key insights into both risk and treatment.

31. Li-Fraumeni syndrome is a rare hereditary cancer syndrome caused by a germline mutation in which tumor suppressor gene?

  • RB1
  • APC
  • BRCA1
  • TP53

Answer: TP53

32. The “cell cycle” is a key process regulated by tumor suppressors. The G1-S checkpoint is primarily controlled by:

  • p53
  • RB1
  • Both p53 and RB1
  • Neither p53 nor RB1

Answer: Both p53 and RB1

33. The “apoptosis” pathway is a form of programmed cell death that is often initiated by:

  • The p53 tumor suppressor in response to severe DNA damage.
  • An oncogene like RAS.
  • A growth factor.
  • The RB1 protein.

Answer: The p53 tumor suppressor in response to severe DNA damage.

34. A “human resources” department in a cancer center would need to recruit genetic counselors with expertise in:

  • Hereditary cancer syndromes caused by tumor suppressor mutations.
  • Marketing.
  • Finance.
  • Only human relations.

Answer: Hereditary cancer syndromes caused by tumor suppressor mutations.

35. A “health disparity” could arise if a patient from an underserved population is not offered _________ even if they meet the criteria.

  • Standard chemotherapy.
  • Genetic counseling and testing for a hereditary tumor suppressor syndrome.
  • A routine blood test.
  • An antiemetic.

Answer: Genetic counseling and testing for a hereditary tumor suppressor syndrome.

36. The “cloning” of a tumor suppressor gene like p53 allows researchers to:

  • Study its normal function in a controlled lab setting.
  • Produce large quantities of the p53 protein for structural analysis.
  • Investigate the effects of specific mutations.
  • All of the above.

Answer: All of the above.

37. The “enzymes of DNA metabolism” are linked to tumor suppressors because many of these genes, like BRCA1, code for:

  • Proteins that are part of the DNA repair enzymatic machinery.
  • The enzymes themselves.
  • The substrates for these enzymes.
  • The inhibitors of these enzymes.

Answer: Proteins that are part of the DNA repair enzymatic machinery.

38. The “special recombination” pathway of homologous recombination is dependent on the function of which tumor suppressors?

  • p53 and RB1
  • BRCA1 and BRCA2
  • APC and MSH2
  • PTEN and NF1

Answer: BRCA1 and BRCA2

39. A pharmacist’s understanding of “DNA methylation and imprinting” is crucial because:

  • Imprinting is a normal process of silencing one allele, similar to one “hit” on a tumor suppressor.
  • DNA methylation is a common way to achieve the “second hit” that inactivates a tumor suppressor.
  • Both A and B are correct.
  • Neither A nor B is correct.

Answer: Both A and B are correct.

40. A pharmacist’s communication with a “caregiver” is critical when explaining the implications of an inherited mutation in a:

  • Tumor suppressor gene, as it affects the cancer risk for other family members.
  • An oncogene.
  • A metabolic enzyme.
  • A drug transporter.

Answer: A tumor suppressor gene, as it affects the cancer risk for other family members.

41. The “RNA tumor viruses” can cause cancer by:

  • Inactivating tumor suppressor genes like p53 and RB1 (as seen with HPV, a DNA virus, but a similar principle).
  • Integrating their genome and disrupting a tumor suppressor gene.
  • Both A and B are mechanisms by which viruses can contribute to cancer.
  • They cannot inactivate tumor suppressors.

Answer: Both A and B are mechanisms by which viruses can contribute to cancer.

42. The “Eukaryotic RNA processing” course is relevant because a mutation in a splice site of a __________ can lead to an inactive protein.

  • Tumor suppressor gene
  • Oncogene
  • Housekeeping gene
  • All of the above

Answer: All of the above

43. A key “human factor” to consider when designing a report for a genetic test on tumor suppressors is:

  • To make the report as complex and difficult to understand as possible.
  • To present the information clearly and unambiguously to avoid misinterpretation by the clinician.
  • To use a small font size.
  • To hide the most important results.

Answer: To present the information clearly and unambiguously to avoid misinterpretation by the clinician.

44. An “Electronic Health Record” (EHR) that is “forging ahead” would have a dedicated, structured field for a patient’s:

  • Family history of cancer.
  • Germline mutation status for key tumor suppressor genes.
  • Both A and B.
  • Neither A nor B.

Answer: Both A and B.

45. The “protein synthesis and translational control” of a tumor suppressor gene can be altered by:

  • Mutations in the coding sequence.
  • A mutation in the promoter that prevents transcription.
  • MicroRNAs that target the tumor suppressor’s mRNA for degradation.
  • All of the above.

Answer: All of the above.

46. A pharmacist’s “advocacy” could involve supporting policies that mandate insurance coverage for:

  • Genetic testing for high-risk patients with a family history suggestive of a tumor suppressor gene mutation.
  • All cosmetic procedures.
  • Over-the-counter vitamins.
  • Experimental therapies with no evidence of efficacy.

Answer: Genetic testing for high-risk patients with a family history suggestive of a tumor suppressor gene mutation.

47. A “drug class review” by a P&T committee would be essential for evaluating the role of which new class of drugs that targets a tumor suppressor pathway?

  • PARP inhibitors.
  • Beta-blockers.
  • Statins.
  • ACE inhibitors.

Answer: PARP inhibitors.

48. In which “practice setting” is a pharmacist most likely to have a deep, specialized knowledge of tumor suppressor genes?

  • A community pharmacy.
  • A precision oncology or cancer genetics clinic.
  • A mail-order pharmacy.
  • A supermarket pharmacy.

Answer: A precision oncology or cancer genetics clinic.

49. An effective leader in an oncology pharmacy would:

  • Ensure that all staff are competent in the principles of targeted therapy related to tumor suppressors.
  • Focus only on the financial aspects of the pharmacy.
  • Avoid implementing new technologies.
  • Discourage collaboration with oncologists.

Answer: Ensure that all staff are competent in the principles of targeted therapy related to tumor suppressors.

50. The ultimate principle of why pharmacists study tumor suppressors is that they are:

  • A fundamental “brake” on cell division whose failure is a key step in cancer, making them critical for understanding risk, diagnosis, and modern therapeutics.
  • A type of oncogene.
  • Only relevant to a few rare types of cancer.
  • An interesting but clinically minor topic.

Answer: A fundamental “brake” on cell division whose failure is a key step in cancer, making them critical for understanding risk, diagnosis, and modern therapeutics.

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