Anticancer Drugs Practice Questions

Q: Pulmonary fibrosis is a complication of which of the following drugs?

Busulfan. **Explanation:** **1. Why Busulfan is Correct:** Busulfan is an alkylating agent primarily used in chronic myeloid leukemia (CML) and as a conditioning agent before bone marrow transplantation [2]. Its most notorious long-term side effect is **"Busulfan Lung,"** characterized by chronic interstitial pulmonary fibrosis. The mechanism involves oxidative stress and direct damage to alveolar epithelial cells, leading to fibroblast proliferation. Clinically, this presents as progressive dyspnea and a dry cough, often occurring months to years after starting therapy. **2. Analysis of Incorrect Options:** * **A. Methotrexate:** While Methotrexate can cause lung injury, it typically presents as an **acute hypersensitivity pneumonitis** (reversible) rather than chronic progressive fibrosis. * **B. Doxorubicin:** The dose-limiting toxicity of this anthracycline is **Cardiotoxicity** (dilated cardiomyopathy/congestive heart failure) due to free radical generation in the myocardium [1]. * **C. Cisplatin:** The primary dose-limiting toxicities for Cisplatin are **Nephrotoxicity** (acute tubular necrosis) and **Ototoxicity** (high-frequency hearing loss). It is not typically associated with pulmonary fibrosis. **3. NEET-PG High-Yield Pearls:** * **Mnemonic for Pulmonary Fibrosis (BBAM):** **B**leomycin (most common) [1], **B**usulfan, **A**miodarone, **M**ethotrexate/Nitrofurantoin. * **Bleomycin:** Causes fibrosis by inducing oxidative damage; it is the most frequently tested drug for this side effect [1]. * **Monitoring:** Patients on Busulfan or Bleomycin should undergo periodic **Pulmonary Function Tests (PFTs)**; a decrease in DLCO (Diffusing capacity of the lungs for carbon monoxide) is an early indicator of toxicity. * **Busulfan other side effects:** Skin hyperpigmentation (Addisonian-like pigmentation) and profound myelosuppression [2].

Q: Which of the following drugs used in the treatment of lung cancer is also used in the treatment of ovarian carcinoma?

Cisplatin. **Explanation:** **Cisplatin** is the correct answer because it is a cornerstone platinum-based alkylating agent used in the treatment of various solid tumors [1], [2]. Its mechanism involves forming intra-strand cross-links in DNA, which inhibits replication and triggers apoptosis [1], [3]. * **Why Cisplatin is correct:** It is a first-line agent for **Non-Small Cell Lung Cancer (NSCLC)** and **Small Cell Lung Cancer (SCLC)**, typically used in combination with etoposide or gemcitabine. Simultaneously, it (or its analog Carboplatin) is the standard of care for **Epithelial Ovarian Carcinoma**, often paired with Paclitaxel [1], [3]. **Analysis of Incorrect Options:** * **Methotrexate:** A folate antagonist primarily used in leukemias, lymphomas, osteosarcoma, and choriocarcinoma. While used in some lung protocols historically, it is not a standard treatment for ovarian cancer. * **Cyclophosphamide:** An alkylating agent (nitrogen mustard) used for breast cancer, lymphomas, and nephrotic syndrome. While it has activity in ovarian cancer, it is not a primary choice for lung cancer compared to platinum compounds [3]. * **Dacarbazine:** Primarily used for **Malignant Melanoma** and **Hodgkin’s Lymphoma** (as part of the ABVD regimen). It has negligible roles in lung or ovarian carcinoma. **High-Yield Clinical Pearls for NEET-PG:** * **Toxicity Profile:** Cisplatin is notorious for **nephrotoxicity** (prevented by aggressive hydration and Amifostine) and is the **most emetogenic** anticancer drug [3]. * **Ototoxicity:** It can cause high-frequency hearing loss [3]. * **Carboplatin vs. Cisplatin:** Carboplatin is often preferred in ovarian cancer due to a better side-effect profile (less vomiting/nephrotoxicity) but causes more **myelosuppression** (thrombocytopenia) [3].

Q: Bleomycin toxicity is characterized by destruction of?

Type I pneumocytes. **Explanation:** Bleomycin is a glycopeptide antibiotic used as a chemotherapeutic agent. Its most serious dose-limiting toxicity is **pulmonary fibrosis**. **Why Type I Pneumocytes are the correct answer:** Bleomycin acts by producing reactive oxygen species (free radicals) that cause DNA strand breaks. The lung is particularly susceptible because it lacks the enzyme **bleomycin hydrolase**, which normally inactivates the drug. The primary site of injury is the **Type I pneumocyte**. Destruction of these cells leads to an inflammatory response, recruitment of fibroblasts, and subsequent collagen deposition, resulting in irreversible interstitial pulmonary fibrosis. **Analysis of Incorrect Options:** * **A. Endothelial cells:** While bleomycin can cause some initial microvascular damage, the hallmark of its toxicity is the specific destruction of the alveolar epithelium (Type I cells). * **C. Type II pneumocytes:** These cells actually undergo **hyperplasia** and proliferation in an attempt to repair the alveolar basement membrane after Type I cells are destroyed. They do not undergo primary destruction. * **D. Alveolar macrophages:** These cells remain functional and are involved in the inflammatory cascade by releasing cytokines (like TGF-beta) that promote fibrosis, rather than being the primary target of destruction. **High-Yield Clinical Pearls for NEET-PG:** * **Dose-limiting toxicity:** Pulmonary fibrosis occurs typically when the cumulative dose exceeds **400 units**. * **Monitoring:** Serial **DLCO (Diffusion Capacity of the Lung for Carbon Monoxide)** is the most sensitive test to detect early toxicity. * **Risk Factor:** Administration of high concentrations of **supplemental oxygen** (e.g., during surgery) can exacerbate bleomycin-induced lung injury due to increased free radical formation. * **Other Side Effect:** Flagellate hyperpigmentation of the skin.

Q: Which of the following conditions is treated with tyrosine kinase inhibitors?

Gastrointestinal stromal tumors (GIST). **Correct Option: A. Gastrointestinal stromal tumors (GIST)** Gastrointestinal stromal tumors (GIST) are characterized by the overexpression of the **c-KIT (CD117)** proto-oncogene, which encodes a transmembrane receptor tyrosine kinase. **Imatinib**, a first-generation tyrosine kinase inhibitor (TKI), specifically inhibits the BCR-ABL, c-KIT, and PDGF-R kinases. By blocking the ATP-binding site of the c-KIT enzyme, Imatinib inhibits the constitutive signaling that drives tumor cell proliferation. It is the first-line targeted therapy for unresectable or metastatic GIST [3]. **Analysis of Incorrect Options:** * **B. Acute myeloid leukemia (AML):** While some subtypes (like FLT3-mutated AML) use TKIs, the standard "7+3" induction regimen consists of Cytarabine and Anthracylines (Daunorubicin). TKIs are more classically associated with Chronic Myeloid Leukemia (CML) [2, 3]. * **C. Neurofibromatosis:** This is a genetic disorder caused by mutations in the NF1 or NF2 genes. While MEK inhibitors (like Selumetinib) are now used for plexiform neurofibromas, standard TKIs are not the primary treatment modality for the condition itself. * **D. Small cell carcinoma of the lung (SCLC):** SCLC is highly aggressive and primarily treated with chemotherapy (Etoposide + Cisplatin). TKIs (like Erlotinib or Gefitinib) are used for **Non-Small Cell Lung Cancer (NSCLC)** with EGFR mutations, not SCLC [1]. **High-Yield Clinical Pearls for NEET-PG:** * **Imatinib** is the drug of choice for **CML** (targeting BCR-ABL/Philadelphia chromosome t(9;22)) [2, 3]. * **Adverse Effect:** A characteristic side effect of Imatinib is **periorbital edema**. * **Resistance:** Resistance to Imatinib in CML often occurs due to the **T315I mutation**, which is treated with **Ponatinib**. * **Sunitinib** is an alternative TKI used for Imatinib-resistant GIST.

Q: Which of the following statements about cyclophosphamide is incorrect?

Causes local irritation. **Explanation:** **Cyclophosphamide** is a nitrogen mustard derivative and a prototype **alkylating agent**. The key to understanding this question lies in its pharmacokinetics: it is a **prodrug**. **Why "Causes local irritation" is Incorrect (The Correct Answer):** Unlike many other alkylating agents (like Mechlorethamine), cyclophosphamide is **not a vesicant**. It is inactive in its original form and must be activated in the liver by cytochrome P450 enzymes (specifically CYP2B6) into active metabolites like phosphoramide mustard and acrolein. Because it is inactive at the site of administration, it does **not cause local tissue irritation** or cellulitis if extravasation occurs. **Analysis of Other Options:** * **A. Causes immunosuppression:** Cyclophosphamide is a potent immunosuppressant. It suppresses both B-cell and T-cell functions and is frequently used in autoimmune diseases like SLE and Wegener’s granulomatosis. * **C. Well absorbed orally:** It has high oral bioavailability (nearly 100%), making it one of the few anticancer drugs that can be administered both orally and intravenously. * **D. Alkylating agent:** It acts by attaching an alkyl group to the guanine base of DNA (at the N-7 position), leading to cross-linking and inhibition of DNA replication. **High-Yield Clinical Pearls for NEET-PG:** * **Dose-limiting toxicity:** Bone marrow suppression. * **Specific Toxicity:** **Hemorrhagic Cystitis**, caused by the metabolite **Acrolein**. * **Prevention:** Aggressive hydration and administration of **MESNA** (2-Mercaptoethane sulfonate Na), which neutralizes acrolein in the bladder. * **Other Side Effects:** SIADH (dilutional hyponatremia), alopecia, and secondary malignancies (bladder cancer).

Q: Which of the following drugs can cause non-ischaemic chest pain?

Bleomycin. **Explanation:** **Bleomycin** is a glycopeptide antibiotic used in cancer chemotherapy (e.g., Hodgkin lymphoma, germ cell tumors). While its most notorious side effect is pulmonary fibrosis, it is also uniquely associated with **acute chest pain syndrome**. This is a **non-ischaemic** phenomenon, often occurring during or shortly after infusion. It is characterized by retrosternal pain that mimics pleurisy or pericarditis but occurs without evidence of myocardial ischemia or EKG changes. The exact mechanism is thought to be related to acute inflammation or irritation of the pleura or mediastinal structures. **Analysis of Incorrect Options:** * **Vincristine:** Primarily known for **peripheral neuropathy** (stocking-glove pattern) and autonomic dysfunction (paralytic ileus). While it can rarely cause vasospastic angina, it is not the classic cause of non-ischaemic chest pain. * **Cyclophosphamide:** Its dose-limiting toxicity is **hemorrhagic cystitis** (prevented by Mesna). At very high doses, it can cause acute cardiotoxicity (myocarditis), but this is typically ischaemic or congestive in nature, not simple non-ischaemic chest pain. * **Cisplatin:** Highly **nephrotoxic** and **emetogenic**. It is associated with electrolyte imbalances and ototoxicity, but not specifically with non-ischaemic chest pain. **High-Yield Clinical Pearls for NEET-PG:** * **Bleomycin:** Remember the "Pulmonary-Skin-Pain" triad: Pulmonary fibrosis, skin hyperpigmentation (flagellate dermatosis), and non-ischaemic chest pain. * **Oxygen Caution:** Patients previously treated with Bleomycin are at high risk of fatal pulmonary toxicity if given high concentrations of inspired oxygen (FiO2) during surgery. * **Cell Cycle:** Bleomycin acts on the **G2 phase** by inducing free radical-mediated DNA strand breaks.

Q: A young man with leukemia is treated with methotrexate. What is the mechanism of action of this drug?

Inhibiting dihydrofolate reductase. **Explanation:** **Mechanism of Action:** Methotrexate (MTX) is a folate antagonist and a cell cycle-specific antimetabolite (acting in the **S-phase**). It works by competitively and irreversibly inhibiting the enzyme **Dihydrofolate Reductase (DHFR)** [1]. Under normal conditions, DHFR converts dihydrofolate into tetrahydrofolate (THF), which is a critical one-carbon carrier required for the synthesis of thymidylate and purine nucleotides [2]. By blocking DHFR, MTX leads to a depletion of THF, thereby inhibiting DNA synthesis and cell replication [1]. **Analysis of Incorrect Options:** * **Option A:** MTX does not interfere with the intestinal absorption of dietary folic acid; it interferes with its intracellular metabolism. * **Option C:** While DNA synthesis is the primary target, MTX does not directly prevent the formation of mRNA (which is the mechanism of drugs like Actinomycin D or certain RNA polymerase inhibitors). * **Option D:** This describes drugs like 6-Mercaptopurine or 5-Fluorouracil, which are prodrugs converted into active cytotoxic metabolites [2]. MTX is active in its parent form, though it undergoes intracellular polyglutamation which enhances its potency. **High-Yield Clinical Pearls for NEET-PG:** * **Rescue Therapy:** **Leucovorin (Folinic acid)** is used to "rescue" normal cells from MTX toxicity by bypassing the inhibited DHFR enzyme. * **Resistance:** Most commonly occurs due to decreased drug uptake or an increase in DHFR enzyme levels within the cell. * **Adverse Effects:** Nephrotoxicity (prevented by hydration and urinary alkalinization), hepatotoxicity (cirrhosis), and pulmonary fibrosis. * **Antidote:** **Glucarpidase** can be used in cases of toxic plasma MTX concentrations in patients with delayed clearance.

Q: Peripheral neuropathy may occur with the use of all the following anticancer agents except?

L-Asparaginase. **Explanation:** The correct answer is **L-Asparaginase**. **1. Why L-Asparaginase is the correct answer:** L-Asparaginase is an enzyme used primarily in Acute Lymphoblastic Leukemia (ALL). Its mechanism involves depleting circulating asparagine, which leukemic cells cannot synthesize. Unlike many other chemotherapeutic agents, it does not interfere with microtubule function or cause direct axonal damage. Its hallmark toxicities are related to protein synthesis inhibition, leading to **hypoalbuminemia, pancreatitis, and clotting factor deficiencies** (causing both thrombosis and hemorrhage). It is notably **not** associated with peripheral neuropathy. **2. Why the other options are incorrect:** * **Vincristine:** A microtubule inhibitor (Vinca alkaloid) that disrupts axonal transport. It is the most notorious cause of peripheral neuropathy among anticancer drugs, often presenting as "glove and stocking" anesthesia and foot drop. * **Cisplatin:** A platinum compound known for causing significant sensory neurotoxicity (ototoxicity and peripheral neuropathy) due to accumulation in the dorsal root ganglia. * **Procarbazine:** An alkylating agent that can cause a variety of CNS effects and peripheral neuropathy, especially when used in combination regimens like MOPP. **Clinical Pearls for NEET-PG:** * **Microtubule Inhibitors:** Both Vincas (Vincristine) and Taxanes (Paclitaxel) are high-yield causes of neuropathy. * **Cisplatin Toxicity Triad:** Nephrotoxicity, Ototoxicity, and Peripheral Neuropathy. (Amifostine is used to reduce nephrotoxicity). * **L-Asparaginase Unique Fact:** It is the only anticancer drug that acts as an enzyme and is known for causing **Acute Pancreatitis**. * **Thalidomide & Bortezomib:** Other important non-cytotoxic agents frequently tested for causing peripheral neuropathy.

Question 1

Pulmonary fibrosis is a complication of which of the following drugs?

Accepted Answer

Busulfan

Answer

Methotrexate

Answer

Doxorubicin

Answer

Cisplatin

Question 2

Chemotherapy can be successful during the treatment of which of the following conditions?

Accepted Answer

Leukemia

Answer

Anneloblastoma

Answer

Fibrosarcoma

Answer

Basal cell carcinoma

Question 3

Which of the following drugs used in the treatment of lung cancer is also used in the treatment of ovarian carcinoma?

Accepted Answer

Cisplatin

Answer

Methotrexate

Answer

Cyclophosphamide

Answer

Dacarbazine

Question 4

Bleomycin toxicity is characterized by destruction of?

Accepted Answer

Type I pneumocytes

Answer

Endothelial cells

Answer

Type II pneumocytes

Answer

Alveolar macrophages

Question 5

Which of the following conditions is treated with tyrosine kinase inhibitors?

Accepted Answer

Gastrointestinal stromal tumors (GIST)

Answer

Acute myeloid leukemia

Answer

Neurofibromatosis

Answer

Small cell carcinoma of the lung

Question 6

Which of the following statements about cyclophosphamide is incorrect?

Accepted Answer

Causes local irritation

Answer

Causes immunosuppression

Answer

Well absorbed orally

Answer

Alkylating agent

Question 7

Bortezomib is used for the treatment of which cancer?

Accepted Answer

Multiple myeloma

Answer

Breast cancer

Answer

Tyrosine kinase inhibitor

Answer

Janus kinase inhibitor

Question 8

Which of the following drugs can cause non-ischaemic chest pain?

Accepted Answer

Bleomycin

Answer

Vincristine

Answer

Cyclophosphamide

Answer

Cisplatin

Question 9

A young man with leukemia is treated with methotrexate. What is the mechanism of action of this drug?

Accepted Answer

Inhibiting dihydrofolate reductase

Answer

Preventing absorption of folic acid

Answer

Preventing formation of messenger ribonucleic acid (mRNA)

Answer

Forming a cytotoxic metabolite

Question 10

Peripheral neuropathy may occur with the use of all the following anticancer agents except?

Accepted Answer

L-Asparaginase

Answer

Vincristine

Answer

Cisplatin

Answer

Procarbazine

Anticancer Drugs — MCQs

Anticancer Drugs — MCQs

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