Chemotherapy of cancer: principles and drug classes MCQs With Answer

Chemotherapy of cancer: principles and drug classes MCQs With Answer

This quiz set is designed for M.Pharm students studying Advanced Pharmacology-II. It focuses on core principles of cancer chemotherapy, major drug classes, mechanisms of action, pharmacokinetic and pharmacodynamic considerations, resistance mechanisms, and clinically important toxicities and preventive strategies. Questions emphasize deeper understanding rather than rote facts, integrating biochemical targets, prodrug activation, cell-cycle specificity, rationale for combinations, and modern targeted and immune-based therapies. Each item includes plausible distractors and a clear correct answer to aid exam preparation and self-assessment. Use these MCQs to test comprehension, clinical reasoning and readiness for advanced professional exams.

Q1. What is the primary cytotoxic mechanism of classical alkylating agents?

• Inhibition of topoisomerase II causing double-strand breaks
• Formation of covalent DNA cross-links by alkylation of guanine leading to strand breakage and inhibition of replication
• Competitive inhibition of nucleotide synthesis enzymes
• Stabilization of microtubules preventing mitotic spindle disassembly

Correct Answer: Formation of covalent DNA cross-links by alkylation of guanine leading to strand breakage and inhibition of replication

Q2. Cyclophosphamide toxicity and activation are best described by which statement?

• Active as administered and causes cardiotoxicity via free radical formation
• Prodrug activated by hepatic CYP to phosphoramide mustard (cytotoxic) and acrolein, with acrolein causing hemorrhagic cystitis
• Directly inhibits dihydrofolate reductase causing mucositis
• Causes dose-dependent pulmonary fibrosis due to metabolite accumulation

Correct Answer: Prodrug activated by hepatic CYP to phosphoramide mustard (cytotoxic) and acrolein, with acrolein causing hemorrhagic cystitis

Q3. Which enzyme is the primary target of methotrexate in cancer chemotherapy?

• Thymidylate synthase
• Dihydrofolate reductase (DHFR)
• Ribonucleotide reductase
• DNA polymerase alpha

Correct Answer: Dihydrofolate reductase (DHFR)

Q4. What is the pharmacologic rationale for leucovorin (folinic acid) rescue after high-dose methotrexate?

• Leucovorin binds methotrexate and increases renal excretion
• Leucovorin is converted to methotrexate and increases efficacy
• Leucovorin provides reduced folates that bypass DHFR to rescue normal cells while tumor cells remain inhibited
• Leucovorin inhibits polyglutamation of methotrexate in tumor cells

Correct Answer: Leucovorin provides reduced folates that bypass DHFR to rescue normal cells while tumor cells remain inhibited

Q5. 5-Fluorouracil (5-FU) exerts antitumor effects primarily by which mechanism?

• Inhibition of dihydrofolate reductase leading to decreased purine synthesis
• Alkylation of DNA bases causing cross-links
• Inhibition of thymidylate synthase and incorporation of fluorinated nucleotides into RNA and DNA
• Microtubule depolymerization leading to mitotic arrest

Correct Answer: Inhibition of thymidylate synthase and incorporation of fluorinated nucleotides into RNA and DNA

Q6. Cytarabine (ara-C) is most active in which phase of the cell cycle and by what mechanism?

• G1 phase; inhibits topoisomerase I
• S phase; converted to Ara-CTP and causes DNA chain termination by incorporation into DNA
• M phase; stabilizes microtubules preventing spindle formation
• G2 phase; cross-links DNA via alkylation

Correct Answer: S phase; converted to Ara-CTP and causes DNA chain termination by incorporation into DNA

Q7. The dose-limiting and clinically significant cardiotoxicity of anthracyclines (e.g., doxorubicin) is primarily due to which mechanism?

• Inhibition of tubulin polymerization in cardiomyocytes
• Free radical generation and iron-dependent oxidative damage combined with topoisomerase IIβ inhibition in cardiomyocytes
• Immune-mediated myocarditis caused by reactive metabolites
• Direct blockade of beta-adrenergic receptors

Correct Answer: Free radical generation and iron-dependent oxidative damage combined with topoisomerase IIβ inhibition in cardiomyocytes

Q8. Which agent is specifically used to reduce anthracycline-related cardiotoxicity and what is its mechanism?

• Amifostine; alkaline urine to increase drug excretion
• Mesna; binds free radicals in myocardium
• Dexrazoxane; chelates iron and inhibits topoisomerase IIβ-mediated DNA damage in cardiomyocytes
• N-acetylcysteine; enhances glutathione to inactivate anthracycline

Correct Answer: Dexrazoxane; chelates iron and inhibits topoisomerase IIβ-mediated DNA damage in cardiomyocytes

Q9. Vincristine’s cytotoxic action and principal dose-limiting toxicity are best described as:

• Microtubule stabilization causing neutropenia
• Microtubule depolymerization causing peripheral neuropathy and constipation
• DNA intercalation causing cardiotoxicity
• Topoisomerase inhibition causing severe diarrhea

Correct Answer: Microtubule depolymerization causing peripheral neuropathy and constipation

Q10. Paclitaxel (a taxane) kills cancer cells primarily by which mechanism?

• Inhibition of topoisomerase II leading to double-strand breaks
• Stabilization of microtubules and prevention of their depolymerization, causing mitotic arrest
• Competitive inhibition of thymidylate synthase
• Formation of DNA cross-links through alkylation

Correct Answer: Stabilization of microtubules and prevention of their depolymerization, causing mitotic arrest

Q11. Irinotecan’s antitumor activity depends on its conversion to SN-38; what is the drug’s primary molecular target and a characteristic toxicity?

• Topoisomerase I inhibition; severe delayed diarrhea due to SN-38
• Topoisomerase II inhibition; cardiotoxicity due to free radicals
• Microtubule stabilization; peripheral neuropathy
• Dihydrofolate reductase inhibition; mucositis

Correct Answer: Topoisomerase I inhibition; severe delayed diarrhea due to SN-38

Q12. Etoposide is classified as which type of topoisomerase inhibitor and what is its main consequence on DNA?

• Topoisomerase I inhibitor causing single-strand DNA repair inhibition
• Topoisomerase II inhibitor causing reversible protein-linked DNA double-strand breaks that lead to cell death
• Topoisomerase IV inhibitor leading to plasmid circularization
• Topoisomerase III inhibitor blocking Holliday junction resolution

Correct Answer: Topoisomerase II inhibitor causing reversible protein-linked DNA double-strand breaks that lead to cell death

Q13. Bleomycin’s pulmonary toxicity is more likely because of which pharmacologic reason?

• High expression of bleomycin hydrolase in lung causes toxic metabolite accumulation
• Low activity of bleomycin hydrolase in lung tissue leading to accumulation of active drug and oxidative damage
• Direct alkylation of pulmonary surfactant by bleomycin
• Induction of collagen synthesis causing fibrosis via TGF-β secretion

Correct Answer: Low activity of bleomycin hydrolase in lung tissue leading to accumulation of active drug and oxidative damage

Q14. Cisplatin’s major dose-limiting toxicities and key preventive measure include which pairing?

• Pulmonary fibrosis; pretreatment with corticosteroids
• Nephrotoxicity and ototoxicity; vigorous hydration, diuresis and amifostine or mannitol
• Cardiotoxicity; dexrazoxane
• Severe hemorrhagic cystitis; mesna and hyperhydration

Correct Answer: Nephrotoxicity and ototoxicity; vigorous hydration, diuresis and amifostine or mannitol

Q15. Imatinib exerts anticancer effects by which mechanism and on which target?

• Monoclonal antibody against EGFR blocking ligand binding
• Small-molecule tyrosine kinase inhibitor targeting BCR-ABL, KIT and PDGFR
• Proteasome inhibitor that increases pro-apoptotic proteins
• Antimetabolite inhibiting thymidylate synthase

Correct Answer: Small-molecule tyrosine kinase inhibitor targeting BCR-ABL, KIT and PDGFR

Q16. Trastuzumab (Herceptin) targets HER2-positive breast cancer; what is a major clinical toxicity and an important monitoring parameter?

• Severe neuropathy; baseline and periodic nerve conduction studies
• Cardiotoxicity (reduced LVEF); baseline and serial echocardiography or MUGA scans
• Renal failure; monitoring serum creatinine weekly
• Pulmonary fibrosis; routine DLCO measurement

Correct Answer: Cardiotoxicity (reduced LVEF); baseline and serial echocardiography or MUGA scans

Q17. Immune checkpoint inhibitors (e.g., anti-PD-1/PD-L1) cause a pattern of toxicities best described as:

• Classical cytotoxic chemotherapy toxicities like alopecia and neutropenia only
• Immune-related adverse events such as colitis, hepatitis, pneumonitis, and endocrinopathies due to loss of peripheral tolerance
• Immediate hypersensitivity reactions only
• Selective nephrotoxicity mediated by complement activation

Correct Answer: Immune-related adverse events such as colitis, hepatitis, pneumonitis, and endocrinopathies due to loss of peripheral tolerance

Q18. In tumor lysis syndrome prevention for high-risk patients receiving cytotoxic therapy, which agent converts uric acid to the more soluble allantoin and is preferred in established TLS?

• Allopurinol
• Rasburicase
• Probenecid
• Febuxostat

Correct Answer: Rasburicase

Q19. A common mechanism of multidrug resistance (MDR) in cancer cells involves:

• Increased expression of DNA repair enzymes only
• Upregulation of efflux pumps such as P-glycoprotein (MDR1/ABCB1) that export structurally unrelated chemotherapeutic drugs
• Complete absence of cell cycle checkpoints leading to drug sensitivity
• Loss of metabolic activation enzymes making prodrugs more potent

Correct Answer: Upregulation of efflux pumps such as P-glycoprotein (MDR1/ABCB1) that export structurally unrelated chemotherapeutic drugs

Q20. Which principle best describes the rationale for standard combination chemotherapy regimens?

• Use of agents with identical mechanisms to maximize a single-pathway blockade
• Combining agents with different mechanisms, non-overlapping dose-limiting toxicities and activity in different cell-cycle phases to increase tumor kill and reduce resistance
• Administering all drugs on the same day to exploit peak plasma concentrations
• Using only cell-cycle-specific agents because nonspecific drugs have no role in combinations

Correct Answer: Combining agents with different mechanisms, non-overlapping dose-limiting toxicities and activity in different cell-cycle phases to increase tumor kill and reduce resistance

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