Anticancer Drugs Practice Questions

Q: Pemetrexed, a drug useful in breast cancer, belongs to which of the following categories?

Antimetabolite. **Explanation:** **Pemetrexed** is a multi-targeted **antimetabolite** (Option D). Antimetabolites are cell-cycle specific drugs that act primarily during the **S-phase** by interfering with DNA and RNA synthesis. Pemetrexed works by inhibiting three key enzymes involved in folate metabolism: 1. **Thymidylate synthase (TS)** 2. **Dihydrofolate reductase (DHFR)** 3. **Glycinamide ribonucleotide formyltransferase (GARFT)** By inhibiting these enzymes, it prevents the formation of precursor purine and pyrimidine nucleotides, thereby halting DNA synthesis and inducing apoptosis in cancer cells. **Why other options are incorrect:** * **A. Antitumor agents (Antibiotics):** These are derived from microorganisms (e.g., Doxorubicin, Bleomycin) and typically act by intercalating DNA or causing strand breaks, not by mimicking metabolites. * **B. Alkylating agents:** These drugs (e.g., Cyclophosphamide, Cisplatin) work by forming covalent bonds with DNA, leading to cross-linking and strand breakage. They are cell-cycle non-specific. * **C. Hormonal agents:** These include Tamoxifen or Anastrozole, which modulate hormone receptors or synthesis in hormone-dependent cancers. **High-Yield Clinical Pearls for NEET-PG:** * **Indications:** Primarily used in **Malignant Pleural Mesothelioma** (in combination with Cisplatin) and **Non-Small Cell Lung Cancer (NSCLC)**. * **Toxicity Management:** To reduce hematologic and GI toxicity, patients must be pre-treated with **Vitamin B12 and Folic Acid** supplementation. * **Skin Reactions:** Dexamethasone is often co-administered to prevent pemetrexed-induced cutaneous rashes.

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

5-Fluorouracil. **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.

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

Imatinib. **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.

Q: Which of the following antineoplastic drugs causes hepatotoxicity?

6-mercaptopurine. **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).

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

Alkylating agent. **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.

Q: Bleomycin toxicity primarily involves which organ?

Lungs. **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.

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

Paclitaxel. **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.

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

Cyclosporine. **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.

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

Pemetrexed. **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.

Q: Nilutamide is an:

Anti-androgen. ### 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 1

Pemetrexed, a drug useful in breast cancer, belongs to which of the following categories?

Accepted Answer

Antimetabolite

Answer

Antitumor agent

Answer

Alkylating agent

Answer

Hormonal agent

Question 2

Which of the following anticancer drugs is excreted by the lungs?

Accepted Answer

5-Fluorouracil

Answer

Cyclophosphamide

Answer

Doxorubicin

Answer

Cisplatin

Question 3

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

Accepted Answer

Imatinib

Answer

Hydroxyurea

Answer

Infliximab

Answer

Interferon alfa (IFN)

Question 4

Which of the following antineoplastic drugs causes hepatotoxicity?

Accepted Answer

6-mercaptopurine

Answer

5-fluorouracil

Answer

Doxorubicin

Answer

Etoposide

Question 5

Cyclophosphamide is classified as which of the following types of drugs?

Accepted Answer

Alkylating agent

Answer

Antitumor antibiotic

Answer

Monoclonal antibody

Answer

Antimetabolite

Question 6

Bleomycin toxicity primarily involves which organ?

Accepted Answer

Lungs

Answer

Liver

Answer

Bone marrow

Answer

Skin

Question 7

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

Accepted Answer

Paclitaxel

Answer

Vinblastine

Answer

Etoposide

Answer

Mitoxantrone

Question 8

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

Accepted Answer

Cyclosporine

Answer

Azathioprine

Answer

Cytarabine

Answer

Cycloserine

Question 9

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

Accepted Answer

Pemetrexed

Answer

6-thioguanine

Answer

5-FU

Answer

Busulfan

Question 10

Nilutamide is an:

Accepted Answer

Anti-androgen

Answer

Anti-convulsant

Answer

Anti-progestin

Answer

Anti-oestrogen

Anticancer Drugs — MCQs

Anticancer Drugs — MCQs

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