MCQ Quiz- Oncogenes

MCQ Quiz: Oncogenes

by

Oncogenes are the “gas pedals” of cancer, representing mutated or overexpressed versions of normal genes that drive uncontrolled cell growth and proliferation. Understanding these key drivers is the foundation of modern precision oncology and the development of targeted therapies. For pharmacists, knowledge of specific oncogenes and the pathways they control is essential for managing these advanced therapies and providing optimal patient care. This quiz for PharmD students will test your knowledge of the fundamental principles of oncogenes, from their activation to their role as therapeutic targets.

1. A “proto-oncogene” is a normal gene that typically functions to:

  • Suppress tumor growth.
  • Regulate and promote normal cell growth and division.
  • Repair damaged DNA.
  • Initiate apoptosis (programmed cell death).

Answer: Regulate and promote normal cell growth and division.

2. An “oncogene” is a mutated form of a proto-oncogene. The type of mutation that creates an oncogene is typically a(n):

  • Loss-of-function mutation.
  • Gain-of-function mutation.
  • Silent mutation.
  • Null mutation.

Answer: Gain-of-function mutation.

3. Which of the following is a common mechanism for converting a proto-oncogene into an oncogene?

  • Point mutation in the coding sequence.
  • Gene amplification, leading to overexpression.
  • Chromosomal translocation that creates a fusion protein.
  • All of the above.

Answer: All of the above.

4. The action of an oncogene can be compared to a “stuck gas pedal,” while the inactivation of a tumor suppressor gene is like a “failed brake.” Which of the following is a classic oncogene?

  • p53
  • RB1
  • RAS
  • BRCA1

Answer: RAS

5. The RAS family of genes is frequently mutated in many human cancers. The RAS protein is a GTPase that functions as a key switch in which type of pathway?

  • DNA repair
  • Growth factor signaling
  • Apoptosis
  • Cell adhesion

Answer: Growth factor signaling

6. A point mutation in a RAS gene often results in a protein that is:

  • Unable to bind GTP.
  • Stuck in the “ON” or GTP-bound state, leading to constant signaling for cell growth.
  • Stuck in the “OFF” or GDP-bound state.
  • Rapidly degraded by the cell.

Answer: Stuck in the “ON” or GTP-bound state, leading to constant signaling for cell growth.

7. The MYC oncogene codes for a ________ that regulates the expression of many genes involved in cell proliferation.

  • Receptor tyrosine kinase
  • G-protein
  • Transcription factor
  • DNA repair enzyme

Answer: Transcription factor

8. Gene amplification of the HER2 (also known as ERBB2) oncogene is a key driver in some types of which cancer?

  • Lung cancer
  • Colorectal cancer
  • Breast cancer
  • Prostate cancer

Answer: Breast cancer

9. Trastuzumab (Herceptin®) is a targeted therapy that works by:

  • Inhibiting the kinase activity of the HER2 protein.
  • Being a monoclonal antibody that binds to the extracellular domain of the HER2 receptor.
  • Blocking the synthesis of the HER2 protein.
  • Promoting the degradation of the HER2 protein.

Answer: Being a monoclonal antibody that binds to the extracellular domain of the HER2 receptor.

10. The Philadelphia chromosome is a specific chromosomal translocation that creates which fusion oncogene?

  • EML4-ALK
  • TMPRSS2-ERG
  • BCR-ABL
  • NPM-ALK

Answer: BCR-ABL

11. The BCR-ABL fusion protein is a constitutively active _________ that is the hallmark of Chronic Myeloid Leukemia (CML).

  • G-protein
  • Transcription factor
  • Tyrosine kinase
  • DNA polymerase

Answer: Tyrosine kinase

12. Imatinib (Gleevec®) is a tyrosine kinase inhibitor specifically designed to target:

  • EGFR
  • HER2
  • BCR-ABL
  • VEGF

Answer: BCR-ABL

13. The “two-hit hypothesis” applies to the inactivation of ________, not the activation of ________.

  • Oncogenes; tumor suppressor genes.
  • Tumor suppressor genes; oncogenes.
  • Both oncogenes and tumor suppressor genes equally.
  • Neither oncogenes nor tumor suppressor genes.

Answer: Tumor suppressor genes; oncogenes.

14. An “acutely transforming” RNA tumor virus can cause cancer rapidly because it carries a viral oncogene (v-onc), which is a hijacked and mutated version of a cellular:

  • Proto-oncogene.
  • Tumor suppressor gene.
  • DNA repair gene.
  • Apoptotic gene.

Answer: Proto-oncogene.

15. “Insertional mutagenesis” by a retrovirus can lead to cancer by:

  • Integrating the provirus next to a proto-oncogene, causing its overexpression due to the strong viral promoter.
  • Delivering a viral oncogene.
  • Inactivating a tumor suppressor gene.
  • Both A and C are possible.

Answer: Both A and C are possible.

16. The SRC gene, the first oncogene discovered, codes for a:

  • Membrane-bound receptor.
  • Non-receptor tyrosine kinase involved in cell signaling.
  • Transcription factor.
  • G-protein.

Answer: Non-receptor tyrosine kinase involved in cell signaling.

17. A “driver mutation” is a mutation in an oncogene or tumor suppressor gene that:

  • Is a random, passenger mutation with no effect.
  • Directly contributes to the cancer phenotype.
  • Only occurs in non-cancerous cells.
  • Is easy to treat.

Answer: Directly contributes to the cancer phenotype.

18. The development of targeted therapies against oncogenes is the foundation of:

  • Traditional cytotoxic chemotherapy.
  • Palliative care.
  • Precision or personalized medicine.
  • Surgical oncology.

Answer: Precision or personalized medicine.

19. A pharmacist’s knowledge of “growth factor” signaling pathways is critical for understanding how:

  • Oncogenes hijack these pathways to drive cancer growth.
  • Antibiotics work.
  • Anticoagulants prevent blood clots.
  • Diuretics lower blood pressure.

Answer: Oncogenes hijack these pathways to drive cancer growth.

20. A key leadership role for an oncology pharmacist is to:

  • Advocate for the appropriate molecular testing to identify oncogenic drivers for targeted therapy.
  • Make all final treatment decisions.
  • Manage the hospital’s overall budget.
  • Perform surgery.

Answer: Advocate for the appropriate molecular testing to identify oncogenic drivers for targeted therapy.

21. A “business plan” for a new biotech company would likely focus on developing a novel inhibitor for a recently discovered:

  • Oncogene.
  • Housekeeping gene.
  • Tumor suppressor gene.
  • DNA repair gene.

Answer: Oncogene.

22. A “forging ahead” mindset in oncology means that pharmacists must:

  • Continuously learn about new oncogenes and the targeted therapies developed to inhibit them.
  • Rely only on their knowledge of older, traditional chemotherapies.
  • Resist the use of personalized medicine.
  • Focus only on the dispensing of medications.

Answer: Continuously learn about new oncogenes and the targeted therapies developed to inhibit them.

23. The “financials” of developing a drug against a specific oncogene are characterized by:

  • High research and development costs.
  • A long and risky development timeline.
  • A potentially high price for the final product.
  • All of the above.

Answer: All of the above.

24. The “regulation” of a new targeted therapy that inhibits an oncogene, along with its required companion diagnostic test, is the responsibility of the:

  • DEA
  • FDA
  • CMS
  • EPA

Answer: The FDA

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

  • Identify all patients with a specific oncogenic mutation who might be eligible for a new clinical trial.
  • Track the pharmacy’s inventory.
  • Schedule patient appointments.
  • Create a marketing brochure.

Answer: Identify all patients with a specific oncogenic mutation who might be eligible for a new clinical trial.

26. A “Clinical Decision Support” system is critical for the safe use of oncogene-targeted therapies to:

  • Alert a prescriber if they order a drug for which the patient lacks the targetable oncogenic mutation.
  • Manage complex drug-drug interactions.
  • Provide dosing guidance based on organ function.
  • All of the above.

Answer: All of the above.

27. A “negotiation” with a payer for an expensive new drug that targets a rare oncogene would require a strong case based on:

  • Evidence of clinical efficacy from trials.
  • The drug’s high price alone.
  • The novelty of the drug’s target.
  • The personal preference of the oncologist.

Answer: Evidence of clinical efficacy from trials.

28. A pharmacist’s knowledge of “DNA structure and DNA-protein interactions” is fundamental to understanding how:

  • Oncogenic transcription factors bind to DNA to regulate gene expression.
  • A drug binds to its protein target.
  • Both A and B are correct.
  • Neither A nor B is correct.

Answer: Both A and B are correct.

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

  • Amplify a specific oncogene from a tumor biopsy to test for mutations.
  • Measure a patient’s cholesterol.
  • Treat cancer directly.
  • Separate proteins by size.

Answer: Amplify a specific oncogene from a tumor biopsy to test for mutations.

30. The ultimate reason pharmacists must understand oncogenes is because they are:

  • The central drivers of many cancers and the primary targets for a large and growing class of precision medicines.
  • An interesting but clinically irrelevant topic.
  • Only important for basic science researchers.
  • The cause of all infectious diseases.

Answer: The central drivers of many cancers and the primary targets for a large and growing class of precision medicines.

31. The MAPK pathway (RAS-RAF-MEK-ERK) is an example of a:

  • DNA repair pathway.
  • Signal transduction cascade that is often constitutively activated by oncogenes.
  • Metabolic pathway.
  • Cell cycle checkpoint.

Answer: Signal transduction cascade that is often constitutively activated by oncogenes.

32. The “service” an oncology pharmacist provides includes counseling a patient on:

  • The specific oncogene their therapy is targeting.
  • How to manage the unique side effects of that targeted therapy.
  • The importance of adherence.
  • All of the above.

Answer: All of the above.

33. The “policy” of requiring a “companion diagnostic” test to be approved alongside a targeted drug is to ensure that:

  • The drug is only given to patients whose tumors have the specific oncogenic target.
  • The drug company can charge more for the test.
  • The drug is used in as many patients as possible.
  • The test is available over-the-counter.

Answer: The drug is only given to patients whose tumors have the specific oncogenic target.

34. A “human resources” department in a precision oncology company would need to recruit scientists with deep expertise in:

  • Cancer biology and oncogenic signaling pathways.
  • Marketing.
  • Finance.
  • Only human relations.

Answer: Cancer biology and oncogenic signaling pathways.

35. A “health disparity” could be worsened if:

  • Molecular testing for targetable oncogenes is not equitably available to all patient populations.
  • All patients have equal access to targeted therapies.
  • A new, low-cost generic drug becomes available.
  • A pharmacy provides free screenings.

Answer: Molecular testing for targetable oncogenes is not equitably available to all patient populations.

36. “Acquired resistance” to a drug that targets an oncogene often occurs when:

  • The cancer cell develops a secondary mutation in the oncogene or activates a bypass pathway.
  • The patient stops taking the medication.
  • The drug’s dose is too high.
  • The patient is not adherent.

Answer: The cancer cell develops a secondary mutation in the oncogene or activates a bypass pathway.

37. A pharmacist’s knowledge of “chemotherapeutics” must now encompass:

  • Only traditional cytotoxic agents.
  • A vast and growing number of oral and IV agents that target specific oncogenes.
  • Only hormonal therapies.
  • Only immunotherapies.

Answer: A vast and growing number of oral and IV agents that target specific oncogenes.

38. The “Eukaryotic and Prokaryotic Transcription” principles are relevant because:

  • Oncogenes like MYC are transcription factors that regulate the expression of other genes.
  • It is not relevant.
  • All oncogenes are enzymes.
  • All oncogenes are receptors.

Answer: Oncogenes like MYC are transcription factors that regulate the expression of other genes.

39. In which “practice setting” is a pharmacist’s expertise on oncogenes most utilized?

  • A standard community pharmacy.
  • A specialty pharmacy or academic cancer center.
  • A mail-order pharmacy.
  • A supermarket pharmacy.

Answer: A specialty pharmacy or academic cancer center.

40. A “drug class review” by a P&T committee for a group of new EGFR inhibitors would be an example of:

  • An evidence-based process to make formulary decisions about drugs targeting the same oncogene.
  • A marketing presentation.
  • A basic dispensing task.
  • A legal proceeding.

Answer: An evidence-based process to make formulary decisions about drugs targeting the same oncogene.

41. The concept of “addiction” can be applied to cancer cells, which can become “addicted” to the signaling from a single, dominant:

  • Oncogene.
  • Tumor suppressor gene.
  • DNA repair pathway.
  • Metabolic enzyme.

Answer: Oncogene.

42. A pharmacist’s “advocacy” for a patient with a rare oncogenic mutation might involve:

  • Helping to enroll them in a clinical trial for an experimental targeted therapy.
  • Insisting they receive standard chemotherapy.
  • Telling them there are no treatment options.
  • Focusing only on the cost of their current medications.

Answer: Helping to enroll them in a clinical trial for an experimental targeted therapy.

43. The “human factors” of managing oral oncolytics that target oncogenes include a high risk of:

  • Patient error due to complex dosing and the need for adherence.
  • The drugs being too safe.
  • The pharmacy workflow being too simple.
  • A lack of side effects to monitor.

Answer: Patient error due to complex dosing and the need for adherence.

44. An “Electronic Health Record” (EHR) is essential for precision oncology because it must:

  • Store a patient’s specific tumor mutation (oncogene) data in a structured format to guide therapy.
  • Hide the results of molecular tests from the clinical team.
  • Make it difficult to order targeted therapies.
  • Increase the risk of prescribing errors.

Answer: Store a patient’s specific tumor mutation (oncogene) data in a structured format to guide therapy.

45. The “epigenetics” field is relevant to oncogenes because:

  • Epigenetic changes, like hypomethylation, can lead to the inappropriate expression of an oncogene.
  • Oncogenes are a type of epigenetic mark.
  • The two fields are unrelated.
  • All epigenetic changes silence oncogenes.

Answer: Epigenetic changes, like hypomethylation, can lead to the inappropriate expression of an oncogene.

46. “Cloning” is a molecular biology technique that is essential for:

  • Studying the function of a newly discovered oncogene.
  • Producing monoclonal antibody drugs that target the products of oncogenes.
  • Both A and B.
  • Neither A nor B.

Answer: Both A and B.

47. A pharmacist’s communication with a “caregiver” about a targeted therapy should include:

  • The name of the oncogene the drug is targeting.
  • How to manage specific side effects, like the EGFR rash.
  • The importance of not missing a dose.
  • All of the above.

Answer: All of the above.

48. The “enzymes of DNA metabolism” are a different class of cancer drug targets, but the signaling pathways driven by oncogenes often influence:

  • The cell’s decision to divide, which involves DNA replication.
  • The cell’s ability to repair DNA damage.
  • Both A and B.
  • Neither A nor B.

Answer: Both A and B.

49. “DNA repair mechanisms” are crucial because a failure in this system can lead to the mutations that create:

  • Oncogenes.
  • Tumor suppressor genes.
  • Normal cells.
  • A healthy immune system.

Answer: Oncogenes.

50. The ultimate principle of why pharmacists study oncogenes is because they are:

  • A fundamental mechanism of cancer and the key to developing and managing personalized cancer therapies.
  • An interesting but clinically minor topic.
  • The cause of all human diseases.
  • The target of all antibiotics.

Answer: A fundamental mechanism of cancer and the key to developing and managing personalized cancer therapies

Leave a Comment