Anticancer Drugs — MCQs

Anticancer Drugs Indian Medical PG Practice Questions and MCQs

Question 191: Which of the following anticancer drugs is excreted by the lungs?

A. 5-Fluorouracil (Correct Answer)
B. Cyclophosphamide
C. Doxorubicin
D. Cisplatin

Explanation: **Explanation:** **Correct Answer: A. 5-Fluorouracil (5-FU)** 5-Fluorouracil is a pyrimidine analog that undergoes extensive hepatic metabolism. The rate-limiting enzyme, **dihydropyrimidine dehydrogenase (DPD)**, converts 5-FU into dihydrofluorouracil [1]. Ultimately, it is broken down into **carbon dioxide (CO₂)**, urea, and α-fluoro-β-alanine. The CO₂ produced during this metabolic degradation is primarily **excreted through the lungs**. This unique pharmacokinetic property is the basis for the "13C-FU breath test" used to assess DPD activity in patients. **Analysis of Incorrect Options:** * **B. Cyclophosphamide:** This alkylating agent is a prodrug activated by hepatic CYP450 enzymes. Its metabolites, including the toxic byproduct **acrolein** (which causes hemorrhagic cystitis), are primarily excreted via the **kidneys**. * **C. Doxorubicin:** This anthracycline antibiotic is metabolized by the liver and is predominantly excreted via the **biliary system** (feces). Dose adjustment is required in patients with hepatic dysfunction. * **D. Cisplatin:** This platinum compound is cleared almost exclusively by the **kidneys** through glomerular filtration and tubular secretion [2]. It is notorious for causing nephrotoxicity. **High-Yield Clinical Pearls for NEET-PG:** * **DPD Deficiency:** Patients with a genetic deficiency of dihydropyrimidine dehydrogenase (DPD) are at high risk for severe, life-threatening toxicity (mucositis, myelosuppression) when given 5-FU. * **Hand-Foot Syndrome:** A common dermatological side effect associated with 5-FU and its oral prodrug, Capecitabine. * **Rescue Agent:** **Uridine triacetate** is the specific antidote for 5-FU overdose or toxicity.

Question 192: What is the drug of choice for chronic myeloid leukemia (CML)?

A. Hydroxyurea
B. Imatinib (Correct Answer)
C. Infliximab
D. Interferon alfa (IFN)

Explanation: **Explanation:** **Correct Option: B. Imatinib** Imatinib is the first-line drug of choice for Chronic Myeloid Leukemia (CML). The underlying pathophysiology of CML involves the **Philadelphia chromosome [t(9;22)]**, which creates the **BCR-ABL fusion gene**. This gene encodes a constitutively active **tyrosine kinase** enzyme that drives uncontrolled myeloid proliferation. Imatinib acts as a selective **Tyrosine Kinase Inhibitor (TKI)** by binding to the ATP-binding site of the BCR-ABL protein, effectively "switching off" the signal for cell division. **Analysis of Incorrect Options:** * **A. Hydroxyurea:** Previously used to rapidly reduce high white blood cell counts (leukapheresis effect), it is now considered a palliative treatment. It does not target the underlying genetic defect and cannot induce cytogenetic remission. * **C. Infliximab:** This is a monoclonal antibody against **TNF-alpha**. It is used in autoimmune conditions like Rheumatoid Arthritis and Crohn’s disease, not in leukemia. * **D. Interferon-alfa:** This was the treatment of choice before the advent of TKIs. It is now reserved for specific cases, such as CML during pregnancy, where TKIs are contraindicated due to teratogenicity. **High-Yield Clinical Pearls for NEET-PG:** * **Mechanism:** Imatinib is a 2-phenylaminopyrimidine derivative. * **Resistance:** Resistance to Imatinib often occurs due to the **T315I mutation**. In such cases, **Ponatinib** is the drug of choice. * **Second-generation TKIs:** Dasatinib and Nilotinib are used if Imatinib is not tolerated or if there is resistance. * **Side Effects:** A characteristic side effect of Imatinib is **periorbital edema** and fluid retention.

Question 193: Which of the following antineoplastic drugs causes hepatotoxicity?

A. 6-mercaptopurine (Correct Answer)
B. 5-fluorouracil
C. Doxorubicin
D. Etoposide

Explanation: **Explanation:** **6-Mercaptopurine (6-MP)** is a thiopurine antimetabolite that acts as a purine analogue. It is a well-known cause of **hepatotoxicity**, which typically manifests as cholestatic jaundice, elevated transaminases, or even hepatic necrosis. The toxicity is often dose-related and is linked to its metabolism by the enzyme **Thiopurine Methyltransferase (TPMT)**. Patients with genetic deficiencies in TPMT are at a significantly higher risk of severe bone marrow suppression and hepatotoxicity when treated with standard doses of 6-MP or its prodrug, Azathioprine. **Analysis of Incorrect Options:** * **5-Fluorouracil (5-FU):** Primarily associated with gastrointestinal toxicity (mucositis, diarrhea) and **Hand-Foot Syndrome** (palmar-plantar erythrodysesthesia). It is not typically associated with significant hepatotoxicity. * **Doxorubicin:** An anthracycline antibiotic famous for its **cardiotoxicity** (dilated cardiomyopathy) due to free radical generation. Its main dose-limiting toxicity is myelosuppression. * **Etoposide:** A topoisomerase II inhibitor. Its primary adverse effects are myelosuppression and alopecia; it is also associated with a risk of secondary leukemia. **High-Yield NEET-PG Pearls:** * **TPMT Testing:** Always screen for TPMT activity before starting 6-MP to prevent life-threatening toxicity. * **Drug Interaction:** **Allopurinol** inhibits Xanthine Oxidase (the enzyme that degrades 6-MP). Co-administration leads to toxic levels of 6-MP; therefore, the dose of 6-MP must be reduced by 50-75%. * **Other Hepatotoxic Chemo Agents:** Methotrexate (cirrhosis/fibrosis), L-asparaginase, and Busulfan (Veno-occlusive disease).

Question 194: Cyclophosphamide is classified as which of the following types of drugs?

A. Alkylating agent (Correct Answer)
B. Antitumor antibiotic
C. Monoclonal antibody
D. Antimetabolite

Explanation: **Explanation:** **1. Why Alkylating Agent is Correct:** Cyclophosphamide belongs to the **Nitrogen Mustard** group of alkylating agents. It is a **prodrug** that requires activation in the liver by **Cytochrome P450 (CYP2B6)** enzymes into its active metabolites: **4-hydroxycyclophosphamide** and **aldophosphamide**. These eventually break down into **phosphoramide mustard** (the active cytotoxic moiety) and **acrolein**. The phosphoramide mustard forms covalent bonds with DNA, specifically at the **N7 position of guanine**, leading to DNA cross-linking, strand breakage, and inhibition of DNA synthesis. **2. Why Other Options are Incorrect:** * **Antitumor Antibiotics:** These are derived from *Streptomyces* bacteria (e.g., Doxorubicin, Bleomycin). They act via intercalation or free radical production, not direct alkylation. * **Monoclonal Antibodies:** These are targeted biological agents (e.g., Rituximab, Trastuzumab) that bind to specific cell surface antigens. * **Antimetabolites:** These are S-phase specific drugs (e.g., Methotrexate, 5-Fluorouracil) that interfere with the synthesis of nucleic acids by mimicking natural substrates. **3. Clinical Pearls for NEET-PG:** * **Dose-Limiting Toxicity:** Bone marrow suppression. * **Specific Toxicity:** **Hemorrhagic Cystitis**, caused by the metabolite **Acrolein**. This is prevented by aggressive hydration and the administration of **MESNA** (2-Mercaptoethane sulfonate), which neutralizes acrolein in the bladder. * **Other Side Effects:** SIADH (Hyponatremia), Alopecia, and Gonadal suppression (Infertility). * **Clinical Uses:** It is a versatile drug used in the CHOP regimen for Lymphomas, Breast cancer, and as an immunosuppressant in Nephrotic syndrome and Wegener’s Granulomatosis.

Question 195: Bleomycin toxicity primarily involves which organ?

A. Liver
B. Bone marrow
C. Skin
D. Lungs (Correct Answer)

Explanation: **Explanation:** **Bleomycin** is a cytotoxic antibiotic that acts by generating free radicals (superoxide and hydroxyl radicals) which cause single- and double-stranded DNA breaks. **Why Lungs (Option D) is correct:** The toxicity of Bleomycin is uniquely organ-specific. The drug is inactivated by the enzyme **bleomycin hydrolase**. However, this enzyme is found in very low concentrations in the **lungs and skin**. Consequently, the lungs are unable to effectively metabolize the drug, leading to the accumulation of free radicals. This results in oxidative damage, inflammation, and eventually **Pulmonary Fibrosis**. This is a classic dose-limiting toxicity (typically occurring at cumulative doses >400 units). **Why other options are incorrect:** * **A. Liver:** Bleomycin does not exhibit significant hepatotoxicity. * **B. Bone marrow:** This is a high-yield distinction. Unlike most cytotoxic drugs, Bleomycin is **"bone marrow sparing"** (minimal myelosuppression), making it ideal for combination regimens like ABVD for Hodgkin lymphoma. * **C. Skin:** While Bleomycin does cause skin toxicity (hyperpigmentation, erythema, and "flagellate dermatitis"), **pulmonary toxicity** is the more severe, life-threatening, and clinically primary concern tested in exams. **High-Yield Clinical Pearls for NEET-PG:** * **Flagellate Dermatitis:** A characteristic whip-like skin rash associated with Bleomycin. * **Cell Cycle Phase:** It is **G2 phase-specific**. * **Monitoring:** Patients on Bleomycin require baseline and periodic **Pulmonary Function Tests (PFTs)**; a decrease in DLCO (Diffusion Capacity) is an early sign of toxicity. * **Oxygen Warning:** Exposure to high concentrations of inspired oxygen (FiO2) can exacerbate Bleomycin-induced lung injury.

Question 196: Stocking and glove neuropathy is seen in which of the following chemotherapeutic agents?

A. Vinblastine
B. Paclitaxel (Correct Answer)
C. Etoposide
D. Mitoxantrone

Explanation: **Explanation:** **Correct Option: B (Paclitaxel)** Paclitaxel, a taxane, acts by stabilizing microtubules and preventing their disassembly (arresting cells in the M-phase). Its most characteristic dose-limiting toxicity is **peripheral neuropathy**, typically presenting in a **"stocking and glove" distribution**. This occurs because taxanes interfere with microtubule-dependent axonal transport, leading to distal axonal degeneration. Sensory symptoms (numbness, tingling, and burning pain) usually precede motor involvement. **Analysis of Incorrect Options:** * **A. Vinblastine:** While Vinca alkaloids (like Vincristine) are notorious for neurotoxicity, Vinblastine is primarily associated with **bone marrow suppression** (Vin**b**lastine **b**lasts the **b**one marrow). Vincristine is more commonly linked to peripheral neuropathy than Vinblastine. * **C. Etoposide:** This is a Topoisomerase II inhibitor. Its major side effects are myelosuppression and alopecia. It is also associated with an increased risk of secondary leukemia. * **D. Mitoxantrone:** An anthracenedione used in prostate cancer and MS. Its primary concern is **cardiotoxicity** (though less than Doxorubicin) and it can cause a harmless blue-green discoloration of urine and sclera. **High-Yield Clinical Pearls for NEET-PG:** * **Microtubule Inhibitors:** Remember "Vincas prevent assembly, Taxanes prevent disassembly." * **Other drugs causing Peripheral Neuropathy:** Vincristine, Cisplatin, Oxaliplatin (cold-induced), Thalidomide, and Bortezomib. * **Paclitaxel Pre-medication:** To prevent hypersensitivity reactions (due to the Cremophor EL vehicle), patients are pre-treated with Dexamethasone, H1 blockers, and H2 blockers.

Question 197: Which of the following immunosuppressive agents acts primarily by inhibiting helper T cells?

A. Cyclosporine (Correct Answer)
B. Azathioprine
C. Cytarabine
D. Cycloserine

Explanation: **Explanation:** **Correct Answer: A. Cyclosporine** Cyclosporine is a potent immunosuppressant classified as a **Calcineurin Inhibitor**. Its primary mechanism involves binding to the intracellular protein **Cyclophilin**. This complex inhibits Calcineurin, a phosphatase required for the dephosphorylation and activation of the **Nuclear Factor of Activated T-cells (NFAT)**. Consequently, the transcription of **Interleukin-2 (IL-2)** is blocked. Since IL-2 is the primary cytokine responsible for the proliferation and activation of **Helper T-cells (CD4+ cells)**, Cyclosporine effectively suppresses T-cell-mediated immunity. **Analysis of Incorrect Options:** * **B. Azathioprine:** This is a purine antimetabolite (prodrug of 6-Mercaptopurine). It inhibits DNA synthesis, affecting the proliferation of both T and B lymphocytes non-specifically, rather than acting primarily as a signaling inhibitor in helper T-cells. * **C. Cytarabine:** An antimetabolite (Pyrimidine analog) used primarily in chemotherapy for Acute Myeloid Leukemia (AML). It inhibits DNA polymerase and is not used as a primary immunosuppressant for T-cell inhibition. * **D. Cycloserine:** An antitubercular drug (second-line) that inhibits bacterial cell wall synthesis by acting as an analog of D-alanine. It has no role in immunosuppression. **High-Yield Clinical Pearls for NEET-PG:** * **Side Effects of Cyclosporine:** Remember the "5 H's"—**H**irsutism, **H**yperplasia of gums (gingival hypertrophy), **H**ypertension, **H**yperlipidemia, and **H**epatotoxicity. It is also notably **Nephrotoxic**. * **Drug Interactions:** Cyclosporine is metabolized by **CYP3A4**; its levels increase with Grapefruit juice and Macrolides. * **Comparison:** Unlike Cyclosporine, **Tacrolimus** binds to **FKBP-12** but shares the same mechanism of inhibiting Calcineurin. Tacrolimus does *not* cause hirsutism or gingival hyperplasia.

Question 198: Which antimetabolite antineoplastic agent is used in the treatment of mesothelioma?

A. 6-thioguanine
B. 5-FU
C. Busulfan
D. Pemetrexed (Correct Answer)

Explanation: **Explanation:** **Pemetrexed** is the correct answer. It is a multi-targeted antifolate antimetabolite that inhibits three key enzymes in folate metabolism: **thymidylate synthase (TS)**, **dihydrofolate reductase (DHFR)**, and **glycinamide ribonucleotide formyltransferase (GARFT)**. Its primary clinical indication is in the treatment of **malignant pleural mesothelioma** (in combination with Cisplatin) and non-small cell lung cancer (NSCLC). **Analysis of Incorrect Options:** * **A. 6-thioguanine:** A purine analog used primarily in the treatment of acute leukemias (AML). It does not have a role in solid tumors like mesothelioma. * **B. 5-FU (5-Fluorouracil):** A pyrimidine analog used extensively for GI tract cancers (colorectal, gastric) and breast cancer, but it is not the standard of care for mesothelioma. * **C. Busulfan:** An **alkylating agent** (specifically an alkyl sulfonate), not an antimetabolite. It is primarily used in chronic myeloid leukemia (CML) and as a conditioning agent before bone marrow transplantation. **High-Yield Clinical Pearls for NEET-PG:** * **Supplementation:** To reduce the hematologic and GI toxicity of Pemetrexed, patients must be pre-treated with **Vitamin B12 and Folic Acid**. * **Skin Reactions:** Dexamethasone is often given to prevent the cutaneous rash associated with Pemetrexed. * **Mechanism:** Unlike Methotrexate (which primarily inhibits DHFR), Pemetrexed’s inhibition of TS and GARFT makes it more effective against a broader range of solid tumors. * **Drug of Choice:** Pemetrexed + Cisplatin is the first-line chemotherapy regimen for unresectable mesothelioma.

Question 199: Nilutamide is an:

A. Anti-convulsant
B. Anti-androgen (Correct Answer)
C. Anti-progestin
D. Anti-oestrogen

Explanation: ### Explanation **Correct Option: B (Anti-androgen)** **Mechanism and Rationale:** Nilutamide is a **pure, non-steroidal anti-androgen** [1, 2]. It acts by competitively blocking the androgen receptors in target tissues [1, 3]. By inhibiting the binding of testosterone and its active metabolite, dihydrotestosterone (DHT), it prevents the growth-stimulating effects of androgens on prostate cancer cells [1, 3]. It is primarily used in the management of metastatic prostate cancer, often in combination with surgical or chemical castration (LHRH agonists) to achieve **Combined Androgen Blockade (CAB)** [1, 2]. **Analysis of Incorrect Options:** * **A. Anti-convulsant:** These drugs (e.g., Phenytoin, Valproate) stabilize neuronal membranes to prevent seizures. Nilutamide has no action on GABA or sodium channels. * **C. Anti-progestin:** Drugs like Mifepristone block progesterone receptors and are used for medical abortion or Cushing’s syndrome. * **D. Anti-oestrogen:** These include Selective Estrogen Receptor Modulators (SERMs) like Tamoxifen or pure antagonists like Fulvestrant, used primarily in breast cancer. **High-Yield Clinical Pearls for NEET-PG:** * **The "-utamide" Suffix:** Remember Flutamide, Bicalutamide, and Nilutamide as the classic non-steroidal anti-androgens. Enzalutamide is a newer, more potent second-generation agent. * **Specific Side Effect:** Nilutamide is uniquely associated with **impaired dark adaptation** (night blindness) and **disulfiram-like reactions** with alcohol. It can also cause interstitial pneumonitis. * **Clinical Use:** It is specifically indicated to prevent the "testosterone flare" seen when starting GnRH agonists (like Leuprolide) in prostate cancer patients.

Question 200: Encorafenib was approved by FDA recently for which condition?

A. Prostate cancer
B. Melanoma (Correct Answer)
C. Smallpox
D. Chickenpox

Explanation: **Explanation:** **Encorafenib** is a potent, small-molecule **BRAF inhibitor** (specifically targeting the V600E mutation). It works by inhibiting the MAP kinase pathway (RAS-RAF-MEK-ERK), which is constitutively active in many cancers, leading to uncontrolled cell proliferation. 1. **Why Melanoma is correct:** Encorafenib was FDA-approved (in combination with Binimetinib, a MEK inhibitor) for the treatment of patients with **unresectable or metastatic melanoma** harboring the **BRAF V600E or V600K mutations**. Combining a BRAF inhibitor (Encorafenib) with a MEK inhibitor (Binimetinib) is the standard of care to delay the development of drug resistance and reduce skin-related toxicities (like squamous cell carcinomas) seen with BRAF monotherapy. 2. **Why other options are incorrect:** * **Prostate Cancer:** Managed primarily with hormonal therapy (GnRH analogs like Leuprolide, anti-androgens like Enzalutamide) or taxanes (Docetaxel). * **Smallpox and Chickenpox:** These are viral infections. Smallpox is treated with antivirals like **Tecovirimat**, while Chickenpox (VZV) is managed with **Acyclovir**. Encorafenib has no antiviral properties. **High-Yield Clinical Pearls for NEET-PG:** * **The "BEACON" Regimen:** Encorafenib is also approved (in combination with Cetuximab) for **Metastatic Colorectal Cancer** with BRAF V600E mutations. * **Mechanism:** It has a longer dissociation half-life (>30 hours) compared to other BRAF inhibitors like Vemurafenib or Dabrafenib, potentially leading to more sustained target inhibition. * **Side Effects:** Common adverse effects include fatigue, nausea, and skin rashes. Unlike earlier BRAF inhibitors, it has a lower incidence of photosensitivity.

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

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