Oncogenes and their proteins MCQs With Answer

Oncogenes and their proteins MCQs With Answer

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Introduction

The following MCQ collection on Oncogenes and Their Proteins is designed for M.Pharm students specializing in Advanced Pharmaceutical Biotechnology. It focuses on molecular mechanisms of oncogene activation, functional classes of oncoproteins, common clinical examples, detection methods and targeted therapeutic strategies. Questions probe deeper aspects such as activating mutations (e.g., in RAS), chromosomal translocations (e.g., BCR‑ABL, c‑MYC), gene amplification (e.g., HER2), oncogene addiction, and mechanisms of drug resistance. This set emphasizes conceptual understanding and clinical relevance, helping students prepare for advanced exams and to apply molecular oncology concepts in drug development and therapeutic design.

Q1. Which statement best describes an oncogene?

  • A mutated or overexpressed proto-oncogene whose activity promotes uncontrolled cell proliferation.
  • A gene that normally suppresses tumor formation and requires loss-of-function mutations to promote cancer.
  • A viral gene that always causes cell death upon expression.
  • A DNA repair enzyme that prevents mutations.

Correct Answer: A mutated or overexpressed proto-oncogene whose activity promotes uncontrolled cell proliferation.

Q2. Which of the following lists the primary molecular mechanisms by which proto-oncogenes are activated into oncogenes?

  • Point mutation, gene amplification, chromosomal translocation, insertional mutagenesis causing gain-of-function.
  • Promoter methylation, chromatin condensation, increased DNA repair, decreased translation.
  • Frameshift deletions only, exclusively in tumor suppressor genes.
  • Splice-site mutations that always produce inactive proteins.

Correct Answer: Point mutation, gene amplification, chromosomal translocation, insertional mutagenesis causing gain-of-function.

Q3. The RAS family of oncogenes encode which class of proteins?

  • Small GTPases that cycle between GTP-bound active and GDP-bound inactive forms.
  • Receptor tyrosine kinases that span the cell membrane.
  • Transcriptional co-repressors that inhibit gene expression.
  • DNA helicases involved in replication fork progression.

Correct Answer: Small GTPases that cycle between GTP-bound active and GDP-bound inactive forms.

Q4. The characteristic chromosomal translocation in Burkitt lymphoma involves c-MYC. Which translocation is most typical?

  • t(8;14) translocation placing c-MYC under immunoglobulin heavy chain enhancer.
  • t(9;22) translocation creating BCR-ABL.
  • t(14;18) translocation involving BCL2.
  • t(11;14) translocation involving cyclin D1.

Correct Answer: t(8;14) translocation placing c-MYC under immunoglobulin heavy chain enhancer.

Q5. The Philadelphia chromosome is associated with which fusion oncogene?

  • Reciprocal translocation t(9;22) generating the BCR-ABL fusion oncogene (Philadelphia chromosome).
  • Amplification of HER2/neu on chromosome 17.
  • Point mutation in TP53 leading to loss-of-function.
  • Translocation t(8;14) involving c-MYC.

Correct Answer: Reciprocal translocation t(9;22) generating the BCR-ABL fusion oncogene (Philadelphia chromosome).

Q6. Which molecular target is inhibited by imatinib (Gleevec)?

  • BCR-ABL tyrosine kinase.
  • mTOR serine/threonine kinase.
  • DNA-dependent RNA polymerase II.
  • Histone deacetylase (HDAC).

Correct Answer: BCR-ABL tyrosine kinase.

Q7. HER2/neu (ERBB2) oncogene amplification and overexpression is most commonly associated with which cancer type?

  • Breast cancer (HER2/neu amplification and overexpression).
  • Chronic myeloid leukemia.
  • Colorectal cancer driven exclusively by APC mutations.
  • Glioblastoma multiforme with EGFRvIII only.

Correct Answer: Breast cancer (HER2/neu amplification and overexpression).

Q8. Activating mutations in RAS oncogenes most frequently occur at which codons?

  • Codons 12 and 13 in the RAS gene family.
  • Codon 248 in TP53.
  • Codon 600 in BRAF only.
  • Start codon AUG leading to truncation.

Correct Answer: Codons 12 and 13 in the RAS gene family.

Q9. In genetics of cancer, how do oncogenes typically behave compared with tumor suppressor genes?

  • Oncogenes are typically dominant gain-of-function alleles, while tumor suppressors require loss-of-function of both alleles.
  • Oncogenes are always recessive and require two hits to activate.
  • Tumor suppressors are activated by point mutations that increase function.
  • Oncogenes encode DNA repair proteins and are loss-of-function in cancer.

Correct Answer: Oncogenes are typically dominant gain-of-function alleles, while tumor suppressors require loss-of-function of both alleles.

Q10. Which of the following is a classic example of a viral oncogene derived from a retrovirus?

  • v-src from Rous sarcoma virus, a viral form of the cellular SRC proto-oncogene.
  • p53 encoded by adenovirus that suppresses tumors in humans.
  • HER2 amplified by papillomaviruses.
  • BCR-ABL produced by Epstein-Barr virus integration.

Correct Answer: v-src from Rous sarcoma virus, a viral form of the cellular SRC proto-oncogene.

Q11. Which targeted drug is best known for inhibiting mutant EGFR in non-small cell lung cancer?

  • Erlotinib (EGFR tyrosine kinase inhibitor).
  • Trastuzumab (HER2 monoclonal antibody).
  • Bevacizumab (VEGF inhibitor).
  • Prednisone (glucocorticoid receptor agonist).

Correct Answer: Erlotinib (EGFR tyrosine kinase inhibitor).

Q12. What does the concept of “oncogene addiction” describe?

  • Tumor dependency on a single overactive oncogene for survival and proliferation.
  • Normal cells’ reliance on proto-oncogenes for differentiation.
  • Viral dependence on host oncogenes for replication only.
  • Redundant signaling pathways that make tumors drug-resistant.

Correct Answer: Tumor dependency on a single overactive oncogene for survival and proliferation.

Q13. Which oncoprotein class includes c-MYC and functions primarily as a transcription factor?

  • Transcription factors such as the MYC family (e.g., c‑MYC, N‑MYC).
  • Receptor tyrosine kinases localized to the plasma membrane only.
  • Extracellular matrix proteases unrelated to transcription.
  • Mitochondrial electron transport chain proteins.

Correct Answer: Transcription factors such as the MYC family (e.g., c‑MYC, N‑MYC).

Q14. What is the primary biochemical role of GAPs (GTPase-activating proteins) in RAS signaling?

  • They accelerate GTP hydrolysis on RAS, turning RAS from active to inactive state.
  • They facilitate exchange of GDP for GTP to activate RAS.
  • They phosphorylate downstream MAP kinases directly.
  • They ubiquitinate RAS for proteasomal degradation.

Correct Answer: They accelerate GTP hydrolysis on RAS, turning RAS from active to inactive state.

Q15. Which laboratory technique is commonly used to detect gene amplification of an oncogene in tumor samples?

  • Fluorescence in situ hybridization (FISH) to detect gene amplification.
  • Western blot for total protein only without gene copy information.
  • ELISA for circulating antibodies against oncogenes.
  • Gram staining of tumor tissue.

Correct Answer: Fluorescence in situ hybridization (FISH) to detect gene amplification.

Q16. Which of the following is an example of a non-receptor tyrosine kinase oncogene commonly activated by chromosomal rearrangement?

  • ABL (as part of the BCR-ABL fusion) is a non-receptor tyrosine kinase commonly activated by chromosomal translocation.
  • HER2 is a non-receptor tyrosine kinase activated by mitochondrial mutation.
  • RAS is a non-receptor tyrosine kinase activated by gene fusion only.
  • MYC is a receptor tyrosine kinase localized to the membrane.

Correct Answer: ABL (as part of the BCR-ABL fusion) is a non-receptor tyrosine kinase commonly activated by chromosomal translocation.

Q17. Gain-of-function mutations in c-KIT are clinically associated with which tumor type and targeted by which drug class?

  • Gastrointestinal stromal tumors (GIST) with activating c-KIT mutations, targeted by tyrosine kinase inhibitors such as imatinib.
  • Breast carcinomas targeted only by aromatase inhibitors.
  • Melanomas exclusively treated with alkylating agents and not targeted drugs.
  • Lymphomas cured by antibiotics due to bacterial etiology.

Correct Answer: Gastrointestinal stromal tumors (GIST) with activating c-KIT mutations, targeted by tyrosine kinase inhibitors such as imatinib.

Q18. Which categories correctly classify common oncoproteins by molecular function?

  • Growth factors, receptor/non-receptor tyrosine kinases, small GTPases, transcription factors, and cell-cycle regulators.
  • Only mitochondrial enzymes and ribosomal proteins are oncoproteins.
  • Oncoproteins are exclusively viral proteins and never cellular proteins.
  • Ion channels only, with no involvement of kinases or transcription factors.

Correct Answer: Growth factors, receptor/non-receptor tyrosine kinases, small GTPases, transcription factors, and cell-cycle regulators.

Q19. What is insertional mutagenesis as it relates to oncogene activation?

  • Activation of a proto-oncogene when viral promoter/enhancer sequences integrate near or within the gene, increasing its expression.
  • Deletion of the entire genome by insertion of a transposon that removes oncogenes.
  • Random insertion of tRNA genes that always silences oncogenes.
  • Integration of bacterial plasmids that encode tumor suppressors.

Correct Answer: Activation of a proto-oncogene when viral promoter/enhancer sequences integrate near or within the gene, increasing its expression.

Q20. Which mechanisms commonly underlie acquired resistance to kinase inhibitors targeting oncogenic proteins?

  • Secondary (gatekeeper) mutations in the kinase domain, activation of bypass signaling pathways, or gene amplification of the oncogene.
  • Immediate degradation of the drug by serum albumin only, irrespective of tumor genotype.
  • Permanent cure after first dose, with no possible resistance mechanisms.
  • Exclusive activation of apoptotic pathways that increase drug sensitivity over time.

Correct Answer: Secondary (gatekeeper) mutations in the kinase domain, activation of bypass signaling pathways, or gene amplification of the oncogene.

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