Anticancer Drugs Practice Questions

Q: Cetuximab and rituximab are examples of which class of therapeutic agents?

Chimeric monoclonal antibodies. **Explanation:** Monoclonal antibodies (mAbs) are classified based on the percentage of human versus non-human (usually murine/mouse) protein sequences they contain. This classification is easily identified by the **suffix/infix** of the drug name. 1. **Why Chimeric (Option C) is correct:** **Chimeric monoclonal antibodies** contain approximately 65% human and 35% murine protein (specifically, the variable region is murine while the constant region is human). They are identified by the infix **"-xi-"**. * **Cetuximab:** An EGFR inhibitor used in colorectal and head/neck cancers. * **Rituximab:** A CD20 inhibitor used in Non-Hodgkin Lymphoma and CLL. Both contain the "-xi-" infix, confirming their chimeric nature. 2. **Analysis of Incorrect Options:** * **Humanized (Option A):** These contain >90% human protein (only the CDRs are murine). They use the infix **"-zu-"** (e.g., Trastu**zu**mab, Bevacizu**zu**mab). * **Murine (Option B):** These are 100% mouse-derived and use the suffix **"-omab"** (e.g., Ibritumomab). They have a high risk of hypersensitivity (HAMA response). * **Antinuclear antibodies (Option D):** These are autoantibodies produced by the immune system that target the nucleus of one's own cells, used as diagnostic markers for autoimmune diseases (like SLE), not as therapeutic anticancer agents. **High-Yield NEET-PG Pearls:** * **Suffix Mnemonic:** * **-omab:** 100% Mouse (Murine) * **-ximab:** Chimeric (Mixed) * **-zumab:** Humani**z**ed * **-umab:** 100% **U**man (Human) * **Clinical Fact:** Chimeric antibodies like Rituximab carry a higher risk of infusion-related reactions compared to fully human antibodies due to the higher murine content. Pre-medication with paracetamol and antihistamines is often required.

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

Kaposi sarcoma. **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].

Q: 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?

Hypertrophic cardiomyopathy. **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).

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

Paclitaxel. **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.

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

Cisplatin. **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).

Q: Which of the following drugs can cause pancreatitis?

L-asparaginase. **Explanation:** **L-asparaginase** is a chemotherapy agent primarily used in the treatment of Acute Lymphoblastic Leukemia (ALL). It works by depleting extracellular asparagine, which leukemic cells require for protein synthesis. **Acute pancreatitis** is a well-documented and serious side effect of L-asparaginase, occurring in approximately 5–10% of patients. The mechanism is attributed to the inhibition of protein synthesis within pancreatic acinar cells, leading to cellular injury and the premature activation of digestive enzymes. **Analysis of Incorrect Options:** * **Colchicine (A):** Primarily used for gout, its dose-limiting toxicity is gastrointestinal distress (diarrhea, vomiting) and bone marrow suppression, but it is not a recognized cause of pancreatitis. * **Ciprofloxacin (C) & Nalidixic acid (D):** These fluoroquinolones/quinolones are more commonly associated with tendon rupture, QT prolongation, and CNS side effects (seizures). While many drugs are rare idiosyncratic causes of pancreatitis, they are not classic high-yield associations like L-asparaginase. **High-Yield Clinical Pearls for NEET-PG:** * **Common Drug-Induced Pancreatitis (DIP) Mnemonic:** "**F-A-S-T**" (**F**urosemide, **A**zathioprine/Asparaginase, **S**ulfonamides/Steroids, **T**etracyclines/Thiazides). * **Other notable causes:** Valproate, Estrogens, Didanosine (NRTI), and 6-Mercaptopurine. * **L-asparaginase** is also uniquely associated with **hypofibrinogenemia** and **thrombosis** due to decreased synthesis of clotting factors and Antithrombin III.

Q: Sclerosing cholangitis is a known side effect caused by which of the following drugs?

Floxuridine. **Explanation:** **Floxuridine (Option A)** is the correct answer. It is a pyrimidine analog (a prodrug of 5-Fluorouracil) primarily used for the treatment of gastrointestinal cancers and hepatic metastases. When administered via **hepatic arterial infusion (HAI)** to achieve high local drug concentrations, it can cause chemical-induced biliary injury. This leads to **Sclerosing Cholangitis**, characterized by strictures of the biliary tree that mimic Primary Sclerosing Cholangitis (PSC). The mechanism involves ischemic injury to the bile ducts, as they receive their blood supply solely from the hepatic artery. **Analysis of Incorrect Options:** * **Carbamazepine (Option B):** Primarily associated with anticonvulsant hypersensitivity syndrome, Stevens-Johnson Syndrome (SJS/TEN), and idiosyncratic **cholestatic hepatitis**, but not sclerosing cholangitis. * **Sulfonamides (Option C):** These drugs typically cause hypersensitivity reactions, crystalluria, or **mixed hepatocellular-cholestatic injury**, but do not cause the structural biliary scarring seen with Floxuridine. * **Indinavir (Option D):** A protease inhibitor used in HIV treatment, it is classic for causing **nephrolithiasis** (kidney stones) due to drug crystallization in the urine, not biliary sclerosis. **High-Yield Clinical Pearls for NEET-PG:** * **Floxuridine:** Always associate "Hepatic Arterial Infusion" and "Biliary Sclerosis/Sclerosing Cholangitis" with this drug. * **Drug-Induced Liver Injury (DILI):** * *Pure Cholestasis:* Anabolic steroids, Oral Contraceptive Pills. * *Cholestatic Hepatitis:* Chlorpromazine, Erythromycin estolate. * *Sclerosing Cholangitis:* Floxuridine, Formaldehyde (if injected into hydatid cysts). * **Monitoring:** Patients on HAI Floxuridine require regular monitoring of Alkaline Phosphatase (ALP) and Bilirubin to detect early biliary toxicity.

Q: What is the anti-CD25 monoclonal antibody used in the prophylaxis of acute organ rejection in adult patients?

Basiliximab. **Explanation:** **Basiliximab** is a chimeric monoclonal antibody that acts as an **IL-2 receptor antagonist**. It specifically binds to the **α-chain (CD25)** of the IL-2 receptor expressed on the surface of activated T-lymphocytes. By blocking this receptor, it inhibits IL-2-mediated T-cell proliferation, which is a critical step in the immune response leading to graft rejection. It is primarily used for the **prophylaxis of acute organ rejection** in renal transplantation, often as part of an induction regimen. **Analysis of Incorrect Options:** * **Muromonab (OKT3):** This is a murine monoclonal antibody against the **CD3** receptor on T-cells. While used for transplant rejection, it is associated with "cytokine release syndrome" and has largely been replaced by newer agents. * **Efalizumab:** This is an anti-**CD11a** antibody (targeting LFA-1) formerly used for plaque psoriasis. It was withdrawn from the market due to the risk of progressive multifocal leukoencephalopathy (PML). * **Eculizumab:** This is a monoclonal antibody against the **C5 complement protein**. It is used in the treatment of Paroxysmal Nocturnal Hemoglobinuria (PNH) and Atypical Hemolytic Uremic Syndrome (aHUS). **High-Yield Pearls for NEET-PG:** * **Daclizumab** is another anti-CD25 antibody (humanized), though it was primarily used for Multiple Sclerosis before being withdrawn. * **Basiliximab** is "chimeric" (suffix **-ximab**), meaning it is ~75% human and 25% murine, which reduces its immunogenicity compared to Muromonab. * Unlike general immunosuppressants, Basiliximab does not cause significant myelosuppression, making it ideal for induction therapy.

Question 1

Which LHRH analogue is used in the treatment of breast cancer?

Accepted Answer

Leuprolide

Answer

Cetrorelix

Answer

Anastrozole

Answer

Tamoxifen

Question 2

Cetuximab and rituximab are examples of which class of therapeutic agents?

Accepted Answer

Chimeric monoclonal antibodies

Answer

Humanized monoclonal antibodies

Answer

Murine monoclonal antibodies

Answer

Antinuclear antibodies

Question 3

A 64-year-old man receiving chemotherapy for squamous cell cancer of the lung develops erythema, induration, thickening, and eventual peeling of the skin on his fingers, palms, and soles of his feet. What is the most likely chemotherapeutic agent causing this adverse reaction?

Accepted Answer

bleomycin

Answer

methotrexate

Answer

cytarabine

Answer

5-fluorouracil (5-FU)

Question 4

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

Accepted Answer

Kaposi sarcoma

Answer

Rhabdomyosarcoma

Answer

Wilms tumor

Answer

Seminoma

Question 5

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?

Accepted Answer

Hypertrophic cardiomyopathy

Answer

Dilated cardiomyopathy

Answer

Pericardial effusion

Answer

Restrictive cardiomyopathy

Question 6

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

Accepted Answer

Paclitaxel

Answer

Vinblastine

Answer

Etoposide

Answer

Mitoxantrone

Question 7

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

Accepted Answer

Cisplatin

Answer

Cyclophosphamide

Answer

Busulfan

Answer

Procarbazine

Question 8

Which of the following drugs can cause pancreatitis?

Accepted Answer

L-asparaginase

Answer

Colchicine

Answer

Ciprofloxacin

Answer

Nalidixic acid

Question 9

Sclerosing cholangitis is a known side effect caused by which of the following drugs?

Accepted Answer

Floxuridine

Answer

Carbamazepine

Answer

Sulfonamides

Answer

Indinavir

Question 10

What is the anti-CD25 monoclonal antibody used in the prophylaxis of acute organ rejection in adult patients?

Accepted Answer

Basiliximab

Answer

Muromonab

Answer

Efalizumab

Answer

Eculizumab

Anticancer Drugs — MCQs

Anticancer Drugs — MCQs

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