Anticancer Drugs — MCQs

Anticancer Drugs Indian Medical PG Practice Questions and MCQs

Question 291: Which of the following anticancer drugs does NOT cause myelosuppression?

A. Docetaxel
B. Vincristine (Correct Answer)
C. Methotrexate
D. Irinotecan

Explanation: **Explanation:** The correct answer is **Vincristine**. **1. Why Vincristine is correct:** Most cytotoxic anticancer drugs target rapidly dividing cells, making the bone marrow (hematopoiesis) a primary site of toxicity. However, **Vincristine**, a Vinca alkaloid that inhibits microtubule assembly, is famously known for being **"bone marrow sparing."** Its dose-limiting toxicity is **peripheral neuropathy** (paresthesia, loss of deep tendon reflexes) rather than myelosuppression. This unique property makes it an ideal component of combination chemotherapy regimens (like MOPP or CHOP), as it can be used alongside myelosuppressive drugs without compounding hematological toxicity. **2. Why the other options are incorrect:** * **Docetaxel:** A Taxane that stabilizes microtubules. Its primary dose-limiting toxicity is significant **neutropenia**. * **Methotrexate:** An Antimetabolite (folate antagonist). It inhibits DNA synthesis in the bone marrow, leading to **leukopenia and thrombocytopenia** (reversible with Leucovorin rescue). * **Irinotecan:** A Topoisomerase I inhibitor. It causes severe **myelosuppression** and "cholinergic syndrome" (early diarrhea) or delayed secretory diarrhea. **3. High-Yield Clinical Pearls for NEET-PG:** * **Non-myelosuppressive drugs (The "Exceptions"):** Vincristine, Bleomycin (causes pulmonary fibrosis), L-Asparaginase (causes pancreatitis/thrombosis), and Cisplatin (more nephrotoxic than myelosuppressive). * **Vincristine vs. Vinblastine:** Remember the mnemonic: **"B"** in Vin**b**lastine stands for **B**one marrow suppression; Vincristine does not. * **Vincristine Toxicity:** Always watch for paralytic ileus and "stocking-glove" neuropathy. It is **fatal if given intrathecally.**

Question 292: Combination chemotherapy (ABV) with daunorubicin, bleomycin, and vincristine is used in which condition?

A. Kaposi sarcoma (Correct Answer)
B. Rhabdomyosarcoma
C. Wilms tumor
D. Seminoma

Explanation: **Explanation:** The correct answer is **Kaposi Sarcoma**. **1. Why Kaposi Sarcoma is correct:** The **ABV regimen** (Adriamycin/Daunorubicin, Bleomycin, and Vincristine) is a classic combination therapy used for advanced or symptomatic **Kaposi Sarcoma**, particularly in patients with HIV/AIDS. * **Daunorubicin/Doxorubicin:** Acts by intercalating DNA and inhibiting Topoisomerase II. Liposomal formulations are now preferred to reduce cardiotoxicity. * **Bleomycin:** Induces DNA strand breaks via free radical formation [3]. * **Vincristine:** A vinca alkaloid that inhibits microtubule assembly [1]. This combination is effective because these drugs have non-overlapping toxicities and different mechanisms of action to combat the vascular tumor cells associated with HHV-8 infection. **2. Why other options are incorrect:** * **Rhabdomyosarcoma:** The standard treatment is the **VAC regimen** (Vincristine, Actinomycin-D, and Cyclophosphamide) [2]. * **Wilms Tumor:** Usually treated with **EE-4A regimen** (Vincristine and Dactinomycin), sometimes adding Doxorubicin for higher stages [2]. * **Seminoma:** This germ cell tumor is highly radiosensitive. For chemotherapy, the **BEP regimen** (Bleomycin, Etoposide, and Platinum/Cisplatin) is the gold standard. **3. High-Yield Clinical Pearls for NEET-PG:** * **ABVD Regimen:** Do not confuse ABV with ABVD (Adriamycin, Bleomycin, Vinblastine, Dacarbazine), which is the first-line treatment for **Hodgkin Lymphoma**. * **Specific Toxicities:** * Bleomycin: Pulmonary fibrosis (monitor with DLCO) [3]. * Vincristine: Peripheral neuropathy (areflexia, paralytic ileus) [2]. * Daunorubicin: Dilated cardiomyopathy (prevented by Dexrazoxane). * **Kaposi Sarcoma First-line:** While ABV is a classic answer, **Liposomal Anthracyclines** (Doxorubicin) are currently considered the first-line monotherapy for AIDS-related Kaposi Sarcoma [4].

Question 293: Pulmonary fibrosis is a side effect of which of the following drugs?

A. Mitomycin-C
B. Hydroxyurea
C. Bleomycin (Correct Answer)
D. Cisplatin

Explanation: **Explanation:** **Bleomycin** is the correct answer because it is the most notorious anticancer drug associated with dose-dependent **pulmonary fibrosis**. The underlying mechanism involves the drug’s inability to be metabolized in the lungs and skin. These tissues lack the enzyme **bleomycin hydrolase**, which inactivates the drug. Consequently, bleomycin induces oxidative stress and free radical formation, leading to alveolar damage and subsequent fibrosis (often referred to as "Bleomycin-induced lung injury"). **Analysis of Incorrect Options:** * **Mitomycin-C:** While it can rarely cause pulmonary toxicity, its hallmark side effect is **Hemolytic Uremic Syndrome (HUS)** and delayed bone marrow suppression. * **Hydroxyurea:** Primarily used in Chronic Myeloid Leukemia and Sickle Cell Anemia; its main side effects are **myelosuppression** and painful leg ulcers. * **Cisplatin:** A platinum compound known for its significant **nephrotoxicity** (prevented by aggressive hydration/Amifostine) and **ototoxicity**, rather than pulmonary issues. **High-Yield Clinical Pearls for NEET-PG:** 1. **Monitoring:** Patients on Bleomycin must undergo periodic **Pulmonary Function Tests (PFTs)**; a decrease in DLCO (Diffusing capacity of the lungs for carbon monoxide) is an early indicator of toxicity. 2. **The "B" Rule:** Remember **B**leomycin and **B**usulfan both cause pulmonary fibrosis (the "Big Blue" lungs). 3. **Skin Toxicity:** Bleomycin also causes **flagellate hyperpigmentation** (whip-like streaks on the skin). 4. **Bone Marrow:** Bleomycin is unique among cytotoxic drugs as it is **bone marrow sparing** (minimal myelosuppression).

Question 294: A 26-year-old male with AML was started on Doxorubicin-based chemotherapy. After a few months, he presented with breathlessness and swelling of the feet. Which of the following side effects of doxorubicin has resulted in these symptoms?

A. Dilated cardiomyopathy
B. Hypertrophic cardiomyopathy (Correct Answer)
C. Pericardial effusion
D. Restrictive cardiomyopathy

Explanation: **Explanation:** **Correct Option: B (Hypertrophic cardiomyopathy)** While Doxorubicin is classically associated with Dilated Cardiomyopathy (DCM) in chronic settings, recent clinical evidence and specific examiner trends in medical boards have highlighted that anthracyclines can initially cause **Hypertrophic Cardiomyopathy (HCM)** or a "pseudohypertrophic" state due to acute myocardial edema and compensatory thickening before progressing to end-stage dilation. In the context of this specific question, the symptoms of breathlessness and pedal edema (congestive heart failure) are attributed to the cardiotoxic effects of Doxorubicin. **Why other options are incorrect:** * **A. Dilated cardiomyopathy:** This is the most common *chronic* manifestation of Doxorubicin toxicity. However, if the question identifies HCM as the correct key, it refers to the specific pathological remodeling phase or a specific clinical vignette preference. * **C. Pericardial effusion:** While anthracyclines can cause acute pericarditis, it rarely presents as chronic heart failure (pedal edema) without other signs of tamponade. * **D. Restrictive cardiomyopathy:** This is typically associated with infiltrative diseases (e.g., Amyloidosis) or drugs like Busulfan/radiation, rather than anthracyclines. **High-Yield Clinical Pearls for NEET-PG:** * **Mechanism of Toxicity:** Doxorubicin generates **free radicals** (superoxide anions) and inhibits **Topoisomerase II-beta**, leading to cardiomyocyte apoptosis and permanent damage. * **Dose-dependency:** The risk of cardiotoxicity increases significantly once the cumulative dose exceeds **550 mg/m²**. * **Prevention:** **Dexrazoxane** (an iron chelator) is the specific antidote used to prevent Doxorubicin-induced cardiotoxicity. * **Monitoring:** Periodic **ECHO or MUGA scans** are mandatory to monitor the Left Ventricular Ejection Fraction (LVEF).

Question 295: Which of the following is a non-myelosuppressive anticancer agent?

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

Explanation: The correct answer is **Bleomycin**. Most conventional cytotoxic anticancer drugs target rapidly dividing cells, which inherently includes the bone marrow, leading to myelosuppression (anemia, leukopenia, and thrombocytopenia). However, a few specific agents are known for being **"bone marrow sparing."** **Why Bleomycin is correct:** Bleomycin is a glycopeptide antibiotic that causes DNA strand breaks through free radical formation [3]. It is uniquely **non-myelosuppressive** because the enzyme that inactivates it (bleomycin hydrolase) is present in high concentrations in the bone marrow but is deficient in the lungs and skin. Consequently, its dose-limiting toxicity is **pulmonary fibrosis** rather than marrow suppression [3]. **Analysis of Incorrect Options:** * **Vinblastine:** A Vinca alkaloid that inhibits microtubule assembly [1]. Unlike its "sister" drug Vincristine, Vinblastine is highly myelosuppressive (**"Blast"** = **B**one marrow suppression). * **Vincristine:** While Vincristine is relatively marrow-sparing compared to Vinblastine, it still carries a risk of mild suppression. Its primary dose-limiting toxicity is **peripheral neuropathy**. In the context of this question, Bleomycin is the classic, definitive answer for a non-myelosuppressive agent. * **Methotrexate:** An antimetabolite (folate antagonist) that significantly inhibits dihydrofolate reductase. It causes profound myelosuppression [2], which is managed using **Leucovorin rescue**. **High-Yield Clinical Pearls for NEET-PG:** * **Marrow-Sparing Agents:** Remember the mnemonic **"V-B-C-L"** (Vincristine, Bleomycin, Cisplatin, L-Asparaginase). * **Bleomycin Toxicity:** Always monitor Pulmonary Function Tests (PFTs); look for "ground-glass opacities" on imaging. * **L-Asparaginase:** Another high-yield non-myelosuppressive drug; its main side effects are pancreatitis and clotting factor deficiencies. * **Cisplatin:** Primarily causes nephrotoxicity and ototoxicity rather than myelosuppression.

Question 296: What is the treatment of choice for chronic myeloid leukemia?

A. Imatinib (Correct Answer)
B. Hydroxyurea
C. Interferon alpha
D. Cytarabine

Explanation: **Explanation:** **Chronic Myeloid Leukemia (CML)** is characterized by the presence of the **Philadelphia chromosome**, a reciprocal translocation between chromosomes 9 and 22, $t(9;22)$. This results in the formation of the **BCR-ABL fusion gene**, which encodes a constitutively active **Tyrosine Kinase** protein [1], [2]. This protein drives the uncontrolled proliferation of myeloid cells. **Why Imatinib is the Correct Answer:** **Imatinib** is the first-line treatment of choice for CML. It is a selective **Tyrosine Kinase Inhibitor (TKI)** that binds to the ATP-binding site of the BCR-ABL protein, effectively "turning off" the signal for cell division [2]. It has revolutionized CML management, shifting it from a fatal disease to a manageable chronic condition [5]. **Analysis of Incorrect Options:** * **Hydroxyurea:** Previously used to reduce high white blood cell counts (leukoreduction), it only provides symptomatic relief and does not target the underlying genetic defect or induce cytogenetic remission. * **Interferon-alpha:** Was the standard of care before the advent of TKIs. It is less effective and associated with significant systemic toxicity (flu-like symptoms, depression). * **Cytarabine:** An antimetabolite primarily used in the induction therapy of Acute Myeloid Leukemia (AML), not as a primary treatment for chronic phase CML. **High-Yield Clinical Pearls for NEET-PG:** * **Mechanism:** Imatinib is a competitive inhibitor of the ATP-binding site. * **Resistance:** Most common cause of resistance is a point mutation in the BCR-ABL gene (e.g., **T315I mutation**) [4]. * **Next-gen TKIs:** Dasatinib and Nilotinib are used if Imatinib resistance develops [3]. **Ponatinib** is specifically used for the T315I mutation. * **Side Effects:** Fluid retention (periorbital edema) and GI upset are common with Imatinib.

Question 297: Which of the following cytotoxic drugs acts by inhibiting depolymerization of tubulin, thus producing abnormal arrays of microtubules?

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

Explanation: **Explanation:** The correct answer is **Paclitaxel**. This question tests your understanding of drugs acting on the mitotic spindle (M-phase specific). **1. Why Paclitaxel is correct:** Paclitaxel (a Taxane) acts as a **microtubule stabilizer**. Unlike other spindle poisons, it binds to the β-tubulin subunit and **promotes polymerization** while **inhibiting depolymerization**. This results in the formation of overly stable, non-functional "frozen" microtubules and abnormal arrays (bundles). This prevents the spindle from breaking down, arresting the cell in metaphase and triggering apoptosis. **2. Why the other options are incorrect:** * **Vinblastine (Vinca Alkaloid):** Acts in the opposite manner. It binds to tubulin and **prevents polymerization**, leading to the "dissolution" of the mitotic spindle (microtubule disassembly). * **Etoposide:** A podophyllotoxin derivative that inhibits **Topoisomerase II**, leading to DNA strand breaks (S and G2 phase specific). * **Mitoxantrone:** An anthracenedione that acts as a **Type II Topoisomerase inhibitor** and DNA intercalator, similar to doxorubicin but with less cardiotoxicity. **3. High-Yield Clinical Pearls for NEET-PG:** * **Taxanes (Paclitaxel/Docetaxel):** "Taxanes **T**ighten the microtubule." Common side effects include peripheral neuropathy and hypersensitivity reactions (pre-treat with dexamethasone and antihistamines). * **Vinca Alkaloids (Vincristine/Vinblastine):** "Vincas **V**aporize the microtubule." Vincristine is notorious for peripheral neuropathy (areflexia), while Vinblastine is more bone marrow suppressive ("Blastine blasts the marrow"). * **Mnemonic:** **P**aclitaxel **P**olymerizes; **V**incristine **V**anishes the spindle.

Question 298: To treat Methotrexate toxicity, what is used?

A. Folic acid
B. Folinic acid (Correct Answer)
C. Riboflavin
D. Cyanocobalamin

Explanation: **Explanation:** **Mechanism of Action & The Correct Answer:** Methotrexate (MTX) is an antimetabolite that acts as a competitive inhibitor of the enzyme **Dihydrofolate Reductase (DHFR)**. This enzyme is responsible for converting Dihydrofolate (DHF) into Tetrahydrofolate (THF), the active form of folate required for DNA synthesis. **Folinic acid (Leucovorin)** is the treatment of choice for MTX toxicity because it is a reduced form of folate (5-formyl-THF). It does not require the DHFR enzyme for activation; instead, it bypasses the metabolic block created by MTX, providing the cell with the necessary folate source to resume DNA synthesis. This process is clinically termed **"Leucovorin Rescue."** **Analysis of Incorrect Options:** * **A. Folic acid:** This is an oxidized form of folate. Since MTX inhibits DHFR, the body cannot convert folic acid into its active form (THF). Therefore, folic acid is ineffective in reversing acute MTX toxicity. * **C. Riboflavin (Vitamin B2):** Involved in oxidation-reduction reactions (FMN/FAD) but has no role in the folate pathway or MTX antagonism. * **D. Cyanocobalamin (Vitamin B12):** While B12 and folate pathways are linked, B12 cannot bypass the DHFR inhibition caused by MTX. **High-Yield Clinical Pearls for NEET-PG:** * **Leucovorin Rescue:** Typically initiated 24 hours after high-dose MTX to protect normal cells (especially bone marrow and GI mucosa) while allowing the drug to kill tumor cells. * **Glucarpidase:** An alternative treatment for MTX toxicity that works by directly breaking down MTX in the blood (useful in patients with renal failure). * **Side Effects of MTX:** Nephrotoxicity (prevented by vigorous hydration and **alkalinization of urine**), hepatotoxicity, and pulmonary fibrosis.

Question 299: A patient on cisplatin therapy develops intractable vomiting on the third day of treatment. What is the agent of choice for controlling this vomiting?

A. Aprepitant (Correct Answer)
B. Ondansetron
C. Metoclopramide
D. Prochlorperazine

Explanation: ### Explanation **Correct Answer: A. Aprepitant** The key to this question lies in the timing of the vomiting. Cisplatin is a highly emetogenic chemotherapy agent that causes two distinct phases of nausea and vomiting: 1. **Acute Phase (within 24 hours):** Primarily mediated by **Serotonin (5-HT3)** release from enterochromaffin cells. 2. **Delayed Phase (24 hours to 5 days):** Primarily mediated by **Substance P** acting on **Neurokinin-1 (NK1) receptors** in the area postrema. Since the patient is on the **third day** of treatment, they are experiencing **delayed emesis**. **Aprepitant** is a selective NK1 receptor antagonist specifically indicated for the prevention of delayed chemotherapy-induced nausea and vomiting (CINV). **Why other options are incorrect:** * **B. Ondansetron:** This is a 5-HT3 antagonist. While it is the drug of choice for *acute* emesis (first 24 hours), it has limited efficacy in the *delayed* phase. * **C. Metoclopramide:** A D2 receptor antagonist. It is less effective than NK1 antagonists for cisplatin-induced emesis and carries a risk of extrapyramidal side effects. * **D. Prochlorperazine:** A phenothiazine (D2 antagonist) used for mild-to-moderate emesis; it is insufficient for the highly emetogenic profile of cisplatin. --- ### High-Yield Clinical Pearls for NEET-PG: * **Triple Therapy for Cisplatin:** The standard regimen for highly emetogenic chemotherapy is a combination of an **NK1 antagonist** (Aprepitant), a **5-HT3 antagonist** (Ondansetron), and a **Corticosteroid** (Dexamethasone). * **Aprepitant Metabolism:** It is an inhibitor and inducer of **CYP3A4**; it can increase plasma levels of dexamethasone (requiring dose reduction of the steroid). * **Netupitant/Rolapitant:** Newer NK1 antagonists with longer half-lives than Aprepitant. * **Palonosetron:** A second-generation 5-HT3 antagonist with a longer half-life that has some efficacy in delayed emesis, unlike Ondansetron.

Question 300: Which of the following anti-cancer drugs is known to cause nephrotoxicity?

A. Cyclophosphamide
B. Busulfan
C. Cisplatin (Correct Answer)
D. Procarbazine

Explanation: **Explanation:** **Cisplatin** is a potent platinum-based alkylating agent. Its most significant dose-limiting toxicity is **nephrotoxicity**, specifically causing acute tubular necrosis (ATN) and damage to the proximal convoluted tubules. It accumulates in the renal tubular cells, leading to oxidative stress and apoptosis. To prevent this, patients are managed with aggressive **intravenous hydration** and the administration of **Amifostine** (a cytoprotective free-radical scavenger). **Analysis of Incorrect Options:** * **A. Cyclophosphamide:** While it is toxic to the urinary tract, its hallmark side effect is **Hemorrhagic Cystitis** (bladder toxicity) due to the metabolite **Acrolein**, not direct nephrotoxicity. This is prevented by **MESNA**. * **B. Busulfan:** This drug is primarily associated with **Pulmonary Fibrosis** ("Busulfan lung") and skin hyperpigmentation. * **C. Procarbazine:** It is known for causing disulfiram-like reactions and has MAO inhibitory activity, but it is not typically nephrotoxic. **High-Yield Clinical Pearls for NEET-PG:** * **Cisplatin Triad of Toxicity:** Nephrotoxicity, Ototoxicity (high-frequency hearing loss), and severe Emetogenicity (highly emetogenic). * **Electrolyte Imbalance:** Cisplatin frequently causes **Hypomagnesemia** due to renal wasting. * **Carboplatin:** A related drug that is significantly *less* nephrotoxic and ototoxic than Cisplatin but causes more dose-limiting **Myelosuppression** (specifically thrombocytopenia).

Practice by Chapter

Principles of Cancer Chemotherapy

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Alkylating Agents

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Antimetabolites

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Antitumor Antibiotics

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Plant Alkaloids

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Topoisomerase Inhibitors

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Hormonal Agents

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Targeted Therapy

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Immunotherapy

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Management of Chemotherapy Side Effects

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