Anticancer Drugs — MCQs

Anticancer Drugs Indian Medical PG Practice Questions and MCQs

Question 21: 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?

A. Cisplatin (Correct Answer)
B. Etoposide
C. Doxorubicin
D. Methotrexate

Explanation: ### 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.

Question 22: Which of the following drugs inhibits de novo synthesis of purines?

A. Cyclosporine
B. Tacrolimus
C. Mycophenolate (Correct Answer)
D. Infliximab

Explanation: **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.

Question 23: Which of the following is an anti-CD20 monoclonal antibody?

A. Alemtuzumab
B. Bevacizumab
C. Gemtuzumab
D. Tositumomab (Correct Answer)

Explanation: **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.

Question 24: What is the mechanism of action of tacrolimus?

A. Folate antagonist
B. Calcineurin inhibitor (Correct Answer)
C. Antimetabolite
D. CD 20 antibody

Explanation: **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.

Question 25: Red discoloration of urine is seen with which of the following medications?

A. Methotrexate
B. Cytarabine
C. Doxorubicin (Correct Answer)
D. Cisplatin

Explanation: **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**.

Question 26: Which type of alkylating antineoplastic drug is Lomustine?

A. Nitrogen mustards
B. Nitrosoureas (Correct Answer)
C. Alkyl sulfonate
D. Triazine

Explanation: **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**.

Question 27: 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?

A. G1 phase
B. S phase (Correct Answer)
C. G2 phase
D. M phase

Explanation: **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.

Question 28: Pulmonary fibrosis is a known side effect of which of the following anticancer drugs?

A. Methotrexate
B. Vincristine
C. Bleomycin (Correct Answer)
D. Cyclophosphamide

Explanation: 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.

Question 29: Which enzyme deficiency leads to serious side effects with 5-Fluorouracil?

A. CYP2D6
B. Dihydropyrimidine dehydrogenase (Correct Answer)
C. Uridine diphosphate
D. Purine

Explanation: **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 30: All of the following are true about sargramustin except?

A. It is a G-CSF analog (Correct Answer)
B. It is used in cases of neutropenia
C. Chronic usage can lead to bone pain
D. It can also lead to flu-like symptoms

Explanation: ### Explanation **Concept:** The primary distinction to understand here is between **G-CSF** (Granulocyte Colony-Stimulating Factor) and **GM-CSF** (Granulocyte-Macrophage Colony-Stimulating Factor). **Why Option A is the correct answer (The "Except"):** **Sargramostim** is a recombinant **GM-CSF** analog, not a G-CSF analog [1]. It stimulates the proliferation and differentiation of a broader range of progenitor cells, including neutrophils, monocytes/macrophages, and eosinophils [2]. In contrast, drugs like **Filgrastim** and **Pegfilgrastim** are G-CSF analogs, which act more selectively on the neutrophil lineage. **Analysis of other options:** * **Option B (Used in neutropenia):** This is a true statement. Sargramostim is clinically indicated to accelerate myeloid recovery following intensive chemotherapy, bone marrow transplantation, or in cases of drug-induced neutropenia [1], [3]. * **Option C (Bone pain):** This is a true statement and a common side effect. Rapid expansion of the bone marrow in response to colony-stimulating factors leads to medullary pressure, manifesting as bone pain (often in the sternum or pelvis). * **Option D (Flu-like symptoms):** This is a true statement. GM-CSF (Sargramostim) is generally more toxic than G-CSF [2]. It can cause a "first-dose reaction" and systemic symptoms like fever, myalgia, arthralgia, and lethargy, mimicking a flu-like syndrome. **NEET-PG High-Yield Pearls:** * **Filgrastim:** G-CSF (Selective for Neutrophils). * **Sargramostim:** GM-CSF (Broad acting: Neutrophils + Macrophages). * **Oprelvekin (IL-11):** Used for Thrombocytopenia (stimulates megakaryocytes). * **Romiplostim/Eltrombopag:** Thrombopoietin receptor agonists used in ITP. * **Side Effect Distinction:** Sargramostim is more likely to cause **Capillary Leak Syndrome** (edema, pleural/pericardial effusions) compared to Filgrastim.

Practice by Chapter

Principles of Cancer Chemotherapy

Practice Questions

Alkylating Agents

Practice Questions

Antimetabolites

Practice Questions

Antitumor Antibiotics

Practice Questions

Plant Alkaloids

Practice Questions

Topoisomerase Inhibitors

Practice Questions

Hormonal Agents

Practice Questions

Targeted Therapy

Practice Questions

Immunotherapy

Practice Questions

Management of Chemotherapy Side Effects

Practice Questions

Want unlimited practice?

Get full access to all questions, explanations, and performance tracking.

Start For Free