Anticancer Drugs Practice Questions

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.

Q: Which monoclonal antibody targets CD20 and is used in treating Non-Hodgkin Lymphoma (NHL)?

Rituximab. **Explanation:** **Rituximab** is the correct answer. It is a chimeric monoclonal antibody that specifically targets the **CD20 antigen**, which is expressed on the surface of normal and malignant B-lymphocytes. By binding to CD20, Rituximab induces B-cell lysis through antibody-dependent cellular cytotoxicity (ADCC), complement-dependent cytotoxicity (CDC), and apoptosis. It is a cornerstone therapy for **B-cell Non-Hodgkin Lymphomas (NHL)**, such as Diffuse Large B-cell Lymphoma (DLBCL) and Follicular Lymphoma, as well as Chronic Lymphocytic Leukemia (CLL). **Analysis of Incorrect Options:** * **A. Cyclophosphamide:** This is an **alkylating agent** (nitrogen mustard), not a monoclonal antibody. It works by cross-linking DNA. While used in NHL (as part of the CHOP regimen), it does not target CD20. * **B. Trastuzumab:** This monoclonal antibody targets the **HER2/neu (ErbB2) receptor**. It is primarily used in the treatment of HER2-positive breast cancer and gastric cancer. * **C. Denosumab:** This is a monoclonal antibody against **RANKL** (Receptor Activator of Nuclear Factor kappa-B Ligand). It is used to treat osteoporosis and giant cell tumor of bone by inhibiting osteoclast activity. **High-Yield Clinical Pearls for NEET-PG:** * **Infusion Reaction:** The most common side effect of Rituximab is an infusion-related reaction (fever, chills, rash); premedication with paracetamol and antihistamines is standard. * **HBV Reactivation:** Always screen for Hepatitis B before starting Rituximab, as it can cause fatal viral reactivation. * **PML:** Rituximab is associated with a rare risk of Progressive Multifocal Leukoencephalopathy (PML) due to JC virus reactivation. * **Other CD20 Inhibitors:** Newer agents include **Ofatumumab** and **Obinutuzumab**.

Q: Which of the following adverse effects may be caused by Busulfan?

Pulmonary fibrosis. **Explanation:** **Busulfan** is an alkylating agent (specifically an alkyl sulfonate) used primarily in the treatment of Chronic Myeloid Leukemia (CML) and as a conditioning agent before bone marrow transplantation. **Why Pulmonary Fibrosis is correct:** Busulfan is notorious for causing dose-dependent interstitial pulmonary fibrosis, often referred to as **"Busulfan Lung."** This occurs due to the drug’s ability to cause oxidative stress and damage to alveolar epithelial cells, leading to fibroblast proliferation. Patients typically present with dyspnea and cough months to years after starting therapy. **Analysis of Incorrect Options:** * **A. Cystitis:** Hemorrhagic cystitis is a classic side effect of **Cyclophosphamide** and **Ifosfamide** due to the metabolite **Acrolein**. It is managed with Mesna and aggressive hydration. * **C. Loss of hair (Alopecia):** While many cytotoxic drugs cause alopecia, Busulfan is unique because it causes minimal to no hair loss at standard doses, making this an unlikely primary answer compared to the specific lung toxicity. * **D. Peripheral neuropathy:** This is the dose-limiting toxicity of **Vinca alkaloids** (Vincristine) and **Taxanes** (Paclitaxel), caused by interference with microtubule function. **High-Yield Clinical Pearls for NEET-PG:** * **Adrenal-like insufficiency:** Busulfan can cause a syndrome characterized by hyperpigmentation, wasting, and hypotension (Addisonian-like syndrome), but without actual biochemical adrenal failure. * **Mnemonic:** "B" for **B**usulfan, **B**one marrow suppression (prolonged), and **B**ig lung (fibrosis). * **Seizures:** At high doses (pre-transplant), Busulfan can cross the blood-brain barrier and cause seizures; prophylactic anticonvulsants (like Phenytoin) are often used.

Q: A 42-year-old woman has been diagnosed with liver cancer and is being treated with 5-FU. 5-FU is successful in destroying the tumor cells because it blocks the production of which one of the following?

dTMP. Explanation:Mechanism of Action (Why dTMP is correct):5-Fluorouracil (5-FU) is a pyrimidine analog and a cycle-specific antimetabolite. Inside the cell, it is converted into its active metabolite, **5-FdUMP** (5-fluorodeoxyuridine monophosphate) [1, 2]. This metabolite acts as a suicide inhibitor of the enzyme **Thymidylate Synthase** [1, 2]. Normally, this enzyme converts dUMP to **dTMP** (deoxythymidine monophosphate) by adding a methyl group [2]. By inhibiting this step, 5-FU causes a "thymineless death" of the cell, as dTMP is essential for DNA synthesis and repair [1].Analysis of Incorrect Options:* **A. FH4 (Tetrahydrofolate):** 5-FU does not block the production of FH4. However, it requires N5,N10-methylene FH4 as a co-factor to form a stable ternary complex with Thymidylate Synthase [1].* **C. UMP (Uridine Monophosphate):** 5-FU is a fluorinated analog of uracil; it mimics the precursors but does not block the initial synthesis of UMP itself.* **D. Methylcobalamin:** This is a form of Vitamin B12 involved in the conversion of homocysteine to methionine. 5-FU has no direct inhibitory effect on B12 metabolism.NEET-PG High-Yield Pearls:* **Leucovorin Rescue vs. Potentiation:** Unlike in Methotrexate toxicity (where Leucovorin is used as a "rescue"), Leucovorin is given with 5-FU to **potentiate** its action by stabilizing the binding of 5-FdUMP to Thymidylate Synthase.* **Adverse Effects:** Hand-foot syndrome (palmar-plantar erythrodysesthesia) and GI toxicity (mucositis) are characteristic.* **Dihydropyrimidine Dehydrogenase (DPD) Deficiency:** Patients with this genetic deficiency are at high risk of severe, life-threatening toxicity when given 5-FU.

Question 1

Bleomycin toxicity is characterized by destruction of?

Accepted Answer

Type I pneumocytes

Answer

Endothelial cells

Answer

Type II pneumocytes

Answer

Alveolar macrophages

Question 2

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 3

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 4

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 5

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

Accepted Answer

Bleomycin

Answer

Vincristine

Answer

Cyclophosphamide

Answer

Cisplatin

Question 6

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 7

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

Accepted Answer

L-Asparaginase

Answer

Vincristine

Answer

Cisplatin

Answer

Procarbazine

Question 8

Which monoclonal antibody targets CD20 and is used in treating Non-Hodgkin Lymphoma (NHL)?

Accepted Answer

Rituximab

Answer

Cyclophosphamide

Answer

Trastuzumab

Answer

Denosumab

Question 9

Which of the following adverse effects may be caused by Busulfan?

Accepted Answer

Pulmonary fibrosis

Answer

Cystitis

Answer

Loss of hair

Answer

Peripheral neuropathy

Question 10

A 42-year-old woman has been diagnosed with liver cancer and is being treated with 5-FU. 5-FU is successful in destroying the tumor cells because it blocks the production of which one of the following?

Accepted Answer

dTMP

Answer

FH4

Answer

UMP

Answer

Methylcobalamin

Anticancer Drugs — MCQs

Anticancer Drugs — MCQs

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