Anticancer Drugs Practice Questions

Q: Irreversible ototoxicity is caused by which of the following drugs?

Cisplatin. **Explanation:** **Cisplatin** is a potent platinum-based alkylating agent used for various solid tumors. Its most characteristic dose-limiting toxicities are **nephrotoxicity** and **ototoxicity**. The ototoxicity is typically **bilateral, progressive, and irreversible**. It occurs because cisplatin induces the formation of reactive oxygen species (ROS) in the stria vascularis and hair cells of the cochlea, leading to permanent cell death. It initially affects high-frequency hearing (tinnitus is an early sign) before progressing to lower frequencies. **Analysis of Incorrect Options:** * **Cyclophosphamide:** Known primarily for **hemorrhagic cystitis** (due to the metabolite acrolein) and bone marrow suppression. It does not cause significant ototoxicity. * **Bleomycin:** Its most notorious side effect is **pulmonary fibrosis** and skin hyperpigmentation. It is "myelosuppressive-sparing" and does not affect hearing. * **Chlorambucil:** An alkylating agent used mainly in Chronic Lymphocytic Leukemia (CLL). Its primary toxicity is myelosuppression and potential secondary malignancies; it is not associated with ototoxicity. **Clinical Pearls for NEET-PG:** * **Amifostine:** A cytoprotective agent (free radical scavenger) that can be used to reduce cisplatin-induced nephrotoxicity. * **Vigorous Hydration:** The primary preventive measure for cisplatin-induced renal damage. * **Emetogenic Potential:** Cisplatin is the most highly emetogenic chemotherapy drug (requires NK1 receptor antagonists like Aprepitant). * **Other Ototoxic Drugs:** Remember the mnemonic "SALTA" (Salicylates, Aminoglycosides, Loop diuretics, Thalidomide, Antimalarials/Anticancer like Cisplatin).

Q: A patient undergoing chemotherapy for two weeks for a mediastinal tumor develops high-frequency hearing loss. What is the most probable cause of this condition?

Cisplatin. ### Explanation **Correct Option: A. Cisplatin** Cisplatin is a potent platinum-based alkylating agent used for various solid tumors (e.g., testicular, lung, and mediastinal tumors). Its most characteristic dose-limiting toxicities are **nephrotoxicity** and **ototoxicity**. * **Mechanism of Ototoxicity:** Cisplatin causes the generation of reactive oxygen species (ROS) in the **stria vascularis** and destroys the **outer hair cells** of the organ of Corti. * **Clinical Presentation:** It typically presents as bilateral, irreversible, **high-frequency hearing loss** (tinnitus is often the first sign). This aligns perfectly with the patient's symptoms. **Why Incorrect Options are Wrong:** * **B. Etoposide:** A topoisomerase II inhibitor primarily associated with **myelosuppression** and secondary leukemias. It does not cause hearing loss. * **C. Doxorubicin:** An anthracycline antibiotic famous for **cardiotoxicity** (dilated cardiomyopathy) due to free radical generation in the myocardium. * **D. Methotrexate:** An antimetabolite (folate antagonist) known for **mucositis**, bone marrow suppression, and hepatotoxicity. It is not ototoxic. **High-Yield Clinical Pearls for NEET-PG:** * **Amifostine:** A cytoprotective agent (free radical scavenger) used to reduce cisplatin-induced nephrotoxicity. * **Vigorous Hydration:** The primary strategy to prevent cisplatin-induced renal damage. * **Emetic Potential:** Cisplatin is the most highly emetogenic chemotherapy drug (requires NK1 receptor antagonists like Aprepitant). * **Other Ototoxic Drugs:** Loop diuretics (Furosemide), Aminoglycosides (Gentamicin), and Vancomycin. When combined with Cisplatin, the risk of permanent deafness increases significantly.

Q: Which of the following drugs inhibits de novo synthesis of purines?

Mycophenolate. **Mycophenolate mofetil** is the correct answer because it is a potent, selective, and reversible inhibitor of **Inosine Monophosphate Dehydrogenase (IMPDH)**. This enzyme is the rate-limiting step in the **de novo synthesis of guanosine nucleotides (purines)**. Unlike other cells that can use the salvage pathway, T and B lymphocytes are critically dependent on de novo synthesis for proliferation. By blocking this pathway, Mycophenolate effectively exerts a cytostatic effect on lymphocytes. **Analysis of Incorrect Options:** * **Cyclosporine & Tacrolimus:** These are **Calcineurin inhibitors**. They bind to cyclophilin and FKBP-12 respectively, preventing the activation of NFAT (Nuclear Factor of Activated T-cells). This inhibits the transcription of IL-2, blocking T-cell activation rather than purine synthesis [1]. * **Infliximab:** This is a chimeric monoclonal antibody that binds to and neutralizes **TNF-α** (Tumor Necrosis Factor-alpha). It is used in inflammatory conditions like Crohn’s disease and Rheumatoid Arthritis but does not interfere with nucleotide synthesis. **High-Yield Clinical Pearls for NEET-PG:** * **Drug of Choice:** Mycophenolate is widely used for prophylaxis of transplant rejection (especially renal) and in SLE (Lupus Nephritis). * **Side Effects:** The most common side effects are **GI distress** (nausea, diarrhea) and **myelosuppression**. * **Teratogenicity:** It is associated with "Mycophenolate embryopathy" (ear and facial abnormalities); thus, it is contraindicated in pregnancy. * **Comparison:** Unlike Azathioprine (which is also a purine antimetabolite), Mycophenolate does not require activation by HGPRT and is not affected by Allopurinol.

Q: Which of the following is an anti-CD20 monoclonal antibody?

Tositumomab. **Explanation:** **Tositumomab** is a murine IgG1 monoclonal antibody directed against the **CD20 antigen**, which is primarily expressed on the surface of normal and malignant B-lymphocytes. It is often used as a radiopharmaceutical (Iodine-131 tositumomab) for the treatment of relapsed or refractory follicular lymphoma. By binding to CD20, it induces cell death through antibody-dependent cell-mediated cytotoxicity (ADCC), complement-dependent cytotoxicity (CDC), and apoptosis. **Analysis of Incorrect Options:** * **Alemtuzumab (Option A):** This is a monoclonal antibody directed against **CD52**, found on B and T lymphocytes. It is used in Chronic Lymphocytic Leukemia (CLL) and Multiple Sclerosis. * **Bevacizumab (Option B):** This is an angiogenesis inhibitor that targets **VEGF (Vascular Endothelial Growth Factor)**, not a surface cluster of differentiation (CD) marker. It is used in colorectal, lung, and renal cancers. * **Gemtuzumab (Option C):** This is an antibody-drug conjugate directed against **CD33**, which is expressed on leukemic blasts in Acute Myeloid Leukemia (AML). **High-Yield Clinical Pearls for NEET-PG:** * **CD20 Inhibitors:** Other high-yield anti-CD20 antibodies include **Rituximab** (chimeric), **Ofatumumab** (human), and **Obinutuzumab**. * **Mnemonic for CD Markers:** * **C**-D**20** = **R**ituximab (**20** looks like **R** flipped). * **C**-D**33** = **G**emtuzumab (**3** looks like **G**). * **C**-D**52** = **A**lemtuzumab (**5-2** = 3; but remember it as the "A" drug). * **Trastuzumab** targets **HER2/neu** (ErbB2) and is a classic question for breast cancer management.

Q: What is the mechanism of action of tacrolimus?

Calcineurin inhibitor. **Explanation:** **Mechanism of Action (Correct Answer: B)** Tacrolimus (FK506) is a potent immunosuppressant that belongs to the class of **Calcineurin Inhibitors**. It binds to an intracellular protein called **FK-binding protein (FKBP-12)**. This tacrolimus-FKBP complex then inhibits calcineurin, a phosphatase responsible for dephosphorylating the **Nuclear Factor of Activated T-cells (NFAT)**. Without dephosphorylation, NFAT cannot enter the nucleus to promote the transcription of **Interleukin-2 (IL-2)** and other cytokines, thereby preventing T-lymphocyte activation. **Analysis of Incorrect Options:** * **A. Folate antagonist:** This describes drugs like **Methotrexate**, which inhibit dihydrofolate reductase (DHFR) to interfere with DNA synthesis. * **C. Antimetabolite:** This refers to drugs like **5-Fluorouracil, Azathioprine, or Cytarabine** that mimic natural substrates to inhibit nucleic acid synthesis. * **D. CD 20 antibody:** This is the mechanism of **Rituximab**, a monoclonal antibody used in B-cell lymphomas and certain autoimmune conditions. **High-Yield Clinical Pearls for NEET-PG:** * **Clinical Use:** Primary drug for preventing organ rejection in liver, kidney, and heart transplants; also used topically for atopic dermatitis. * **Side Effects:** Nephrotoxicity (most common), neurotoxicity (tremors, seizures), and **post-transplant diabetes mellitus (PTDM)**. * **Comparison:** Unlike Cyclosporine (which binds to Cyclophilin), Tacrolimus is more potent and does **not** typically cause gingival hyperplasia or hirsutism. * **Metabolism:** It is metabolized by **CYP3A4**; therefore, grapefruit juice and macrolides can increase its toxicity.

Q: Red discoloration of urine is seen with which of the following medications?

Doxorubicin. **Explanation:** **Doxorubicin** (and its analog Daunorubicin) is an Anthracycline antibiotic used in cancer chemotherapy. The correct answer is Doxorubicin because it is a **naturally red-colored compound**. After administration, the drug and its metabolites are excreted via the kidneys, leading to a benign but striking **red discoloration of the urine** (chromaturia). Patients should be counseled about this side effect to prevent unnecessary alarm. **Analysis of Incorrect Options:** * **Methotrexate:** An antimetabolite (folate antagonist) primarily known for causing myelosuppression, mucositis, and hepatotoxicity. It does not typically change urine color. * **Cytarabine (Ara-C):** A pyrimidine antagonist used in leukemias. Its major dose-limiting toxicity is myelosuppression and cerebellar ataxia at high doses. * **Cisplatin:** A platinum compound known for its significant **nephrotoxicity** and ototoxicity. While it affects the kidneys, it does not cause red discoloration of urine. **High-Yield Clinical Pearls for NEET-PG:** * **Cardiotoxicity:** The most serious side effect of Doxorubicin is cumulative, dose-dependent cardiotoxicity (dilated cardiomyopathy). **Dexrazoxane** is the iron-chelating agent used to prevent this. * **Mechanism:** Anthracyclines work by inhibiting **Topoisomerase II**, intercalating DNA, and generating free radicals. * **Other "Red" Drugs:** Apart from Doxorubicin, **Rifampin** (antitubercular) and **Clofazimine** (antileprotic) are classic causes of red/orange discoloration of body fluids. * **Cyclophosphamide:** Contrast this with Doxorubicin; Cyclophosphamide causes **Hemorrhagic Cystitis** (bloody urine), which is prevented by **MESNA**.

Q: Which type of alkylating antineoplastic drug is Lomustine?

Nitrosoureas. **Explanation:** Alkylating agents are a class of antineoplastic drugs that act by attaching alkyl groups to DNA, leading to cross-linking and strand breaks. **Lomustine (CCNU)** belongs to the **Nitrosourea** sub-class. **Why Nitrosoureas is correct:** Nitrosoureas, including **Lomustine, Carmustine (BCNU), and Semustine**, are highly lipid-soluble, non-ionized compounds. This characteristic allows them to readily cross the **blood-brain barrier (BBB)**. Consequently, they are the drugs of choice for treating primary brain tumors (e.g., glioblastoma multiforme) and meningeal leukemia. **Analysis of Incorrect Options:** * **Nitrogen mustards:** This group includes drugs like Cyclophosphamide, Ifosfamide, and Mechlorethamine. While they are alkylating agents, their chemical structure and clinical applications differ from nitrosoureas. * **Alkyl sulfonate:** The classic example is **Busulfan**, primarily used in Chronic Myeloid Leukemia (CML) and known for causing pulmonary fibrosis. * **Triazine:** This group includes **Dacarbazine and Temozolomide**. While Temozolomide also crosses the BBB, Lomustine is chemically classified specifically as a nitrosourea. **High-Yield Clinical Pearls for NEET-PG:** * **Mechanism:** Nitrosoureas require non-enzymatic activation to form carbonium ions that alkylate DNA. * **Toxicity:** A unique feature of nitrosoureas is **delayed myelosuppression** (occurring 4–6 weeks after administration). * **Mnemonic:** Remember the "mustines" (**Car**mustine, **Lo**mustine, **Se**mustine) are **Nitrosoureas** that go to the **CNS**.

Q: Methotrexate is often used as a chemotherapeutic agent to treat patients with leukemia. This drug is effective because it inhibits cells in which phase of the cell cycle?

S phase. **Explanation:** **Mechanism of Action (Why S phase is correct):** Methotrexate (MTX) is a folate antagonist and a classic example of a **Cell Cycle Specific (CCS)** drug. It works by competitively inhibiting the enzyme **Dihydrofolate Reductase (DHFR)**. This inhibition prevents the conversion of dihydrofolate to tetrahydrofolate (the active form). Tetrahydrofolate is a crucial cofactor required for the synthesis of thymidylate and purine nucleotides. Since DNA synthesis and replication occur exclusively during the **S phase (Synthesis phase)** of the cell cycle, MTX exerts its cytotoxic effect by halting DNA production during this specific window. **Analysis of Incorrect Options:** * **G1 phase (Gap 1):** This is the pre-synthetic phase where organelles and proteins are produced. While some drugs like L-asparaginase act here, MTX does not target the metabolic processes specific to G1. * **G2 phase (Gap 2):** This phase involves the synthesis of RNA and proteins required for spindle formation. Drugs like **Bleomycin** and **Etoposide** primarily act in the G2 phase. * **M phase (Mitosis):** This involves physical cell division. Drugs that target microtubules, such as **Vinca alkaloids** (Vincristine, Vinblastine) and **Taxanes** (Paclitaxel), are specific to the M phase. **High-Yield Clinical Pearls for NEET-PG:** * **Rescue Therapy:** High-dose MTX toxicity is managed with **Leucovorin (Folinic acid)**, which bypasses the blocked DHFR enzyme to provide a source of reduced folate to healthy cells. * **Resistance:** Most common mechanism of resistance is a change in the affinity of DHFR or decreased uptake by the folate carrier. * **Adverse Effects:** Nephrotoxicity (due to crystalluria), Hepatotoxicity (cirrhosis with long-term use), and Pulmonary fibrosis. * **Other Uses:** Apart from leukemia, it is a first-line Disease-Modifying Antirheumatic Drug (DMARD) for Rheumatoid Arthritis and is used for Ectopic Pregnancy and Psoriasis.

Q: Pulmonary fibrosis is a known side effect of which of the following anticancer drugs?

Bleomycin. Explanation: **Bleomycin** [1] is the correct answer because it is classically associated with dose-dependent **pulmonary fibrosis** [1]. The underlying mechanism involves the drug’s inability to be metabolized in the lungs. While most tissues contain "Bleomycin hydrolase," the lungs and skin lack this enzyme, leading to the accumulation of the drug. This results in the generation of free radicals that cause oxidative damage [1] to alveolar cells, eventually progressing to interstitial fibrosis. **Analysis of Incorrect Options:** * **Methotrexate (A):** While it can cause "Methotrexate-induced pneumonitis" (an acute hypersensitivity reaction), it is more famously known for **bone marrow suppression** [2], hepatotoxicity, and mucositis. * **Vincristine (B):** This microtubule inhibitor [3] is primarily associated with **peripheral neuropathy** (paresthesia, loss of reflexes) and autonomic dysfunction (constipation/paralytic ileus). It is notably bone marrow-sparing. * **Cyclophosphamide (D):** Its hallmark toxicity is **hemorrhagic cystitis** due to the metabolite **Acrolein**. While chronic high doses can rarely cause fibrosis, it is not the classic association tested in this context. **High-Yield Clinical Pearls for NEET-PG:** * **Monitoring:** Patients on Bleomycin should undergo regular **Pulmonary Function Tests (PFTs)**; a decrease in DLCO (Diffusing capacity of the lungs for carbon monoxide) is an early sign of toxicity. * **The "B" Rule:** Remember **B**leomycin and **B**usulfan both cause Pulmonary Fi**B**rosis. * **Skin Toxicity:** Bleomycin also causes **flagellate hyperpigmentation** [1] (linear streaks on the trunk). * **Cell Cycle:** Bleomycin acts in the **G2 phase** [1] of the cell cycle.

Q: Which enzyme deficiency leads to serious side effects with 5-Fluorouracil?

Dihydropyrimidine dehydrogenase. **Explanation:** **1. Why Dihydropyrimidine dehydrogenase (DPD) is correct:** 5-Fluorouracil (5-FU) is a pyrimidine antimetabolite used in treating solid tumors (e.g., colorectal and breast cancer). **DPD is the rate-limiting enzyme responsible for the catabolism (breakdown) of over 80% of administered 5-FU** into inactive metabolites. If a patient has a genetic deficiency of DPD, 5-FU is not cleared efficiently, leading to toxic accumulation. This results in severe, potentially life-threatening side effects, including profound myelosuppression, severe mucositis, and neurotoxicity. **2. Why the other options are incorrect:** * **CYP2D6:** This is a Cytochrome P450 enzyme involved in the metabolism of drugs like Tamoxifen, codeine, and beta-blockers. It does not play a role in 5-FU metabolism. * **Uridine diphosphate (UDP):** While 5-FU is converted into active metabolites like F-dUMP and FUTP (which involve uridine pathways), the *deficiency* of UDP itself is not the clinical marker for 5-FU toxicity. (Note: Uridine triacetate is actually used as an antidote for 5-FU overdose). * **Purine:** 5-FU is a **pyrimidine** analogue, not a purine. Enzymes related to purine metabolism (like TPMT) are relevant for drugs like 6-Mercaptopurine, not 5-FU. **3. High-Yield Clinical Pearls for NEET-PG:** * **Mechanism of Action:** 5-FU inhibits **Thymidylate Synthase**, leading to "thymineless death" of cells. * **Antidote:** **Uridine triacetate** is the specific FDA-approved antidote for 5-FU or Capecitabine overdose/toxicity. * **Hand-Foot Syndrome:** A common dermatological side effect associated with 5-FU and its prodrug, Capecitabine. * **Comparison:** While **DPD** deficiency affects 5-FU, **TPMT** (Thiopurine Methyltransferase) deficiency leads to toxicity with **6-Mercaptopurine** and **Azathioprine**.

Question 1

Irreversible ototoxicity is caused by which of the following drugs?

Accepted Answer

Cisplatin

Answer

Cyclophosphamide

Answer

Bleomycin

Answer

Chlorambucil

Question 2

A patient undergoing chemotherapy for two weeks for a mediastinal tumor develops high-frequency hearing loss. What is the most probable cause of this condition?

Accepted Answer

Cisplatin

Answer

Etoposide

Answer

Doxorubicin

Answer

Methotrexate

Question 3

Which of the following drugs inhibits de novo synthesis of purines?

Accepted Answer

Mycophenolate

Answer

Cyclosporine

Answer

Tacrolimus

Answer

Infliximab

Question 4

Which of the following is an anti-CD20 monoclonal antibody?

Accepted Answer

Tositumomab

Answer

Alemtuzumab

Answer

Bevacizumab

Answer

Gemtuzumab

Question 5

What is the mechanism of action of tacrolimus?

Accepted Answer

Calcineurin inhibitor

Answer

Folate antagonist

Answer

Antimetabolite

Answer

CD 20 antibody

Question 6

Red discoloration of urine is seen with which of the following medications?

Accepted Answer

Doxorubicin

Answer

Methotrexate

Answer

Cytarabine

Answer

Cisplatin

Question 7

Which type of alkylating antineoplastic drug is Lomustine?

Accepted Answer

Nitrosoureas

Answer

Nitrogen mustards

Answer

Alkyl sulfonate

Answer

Triazine

Question 8

Methotrexate is often used as a chemotherapeutic agent to treat patients with leukemia. This drug is effective because it inhibits cells in which phase of the cell cycle?

Accepted Answer

S phase

Answer

G1 phase

Answer

G2 phase

Answer

M phase

Question 9

Pulmonary fibrosis is a known side effect of which of the following anticancer drugs?

Accepted Answer

Bleomycin

Answer

Methotrexate

Answer

Vincristine

Answer

Cyclophosphamide

Question 10

Which enzyme deficiency leads to serious side effects with 5-Fluorouracil?

Accepted Answer

Dihydropyrimidine dehydrogenase

Answer

CYP2D6

Answer

Uridine diphosphate

Answer

Purine

Anticancer Drugs — MCQs

Anticancer Drugs — MCQs

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