Anticancer Drugs Practice Questions

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.

Q: A 55-year-old male patient complains of an abnormal growth on his right cheek. The patient has a habit of tobacco chewing for 30 years. Radiologic findings reveal an 8x8 cm fungating mass invading the maxilla and mandible on the right side. The patient was advised palliative chemotherapy with cisplatin. Which of the following changes in DNA is NOT caused by this drug?

The changed structure cannot bind proteins. **Explanation:** **Cisplatin** is a platinum-based alkylating-like agent used extensively in ENT oncology for squamous cell carcinomas. Its mechanism of action involves the formation of **intra-strand cross-links** (primarily between adjacent Guanine bases). **Why Option D is Correct:** The core concept is that Cisplatin-induced DNA damage **does not prevent protein binding**; instead, it facilitates the binding of specific proteins. When Cisplatin creates DNA adducts, it causes significant structural distortion (bending). This distorted DNA is specifically recognized and bound by **High Mobility Group (HMG) domain proteins** and other DNA-repair proteins. These proteins "shield" the DNA from repair mechanisms, ultimately leading to programmed cell death (apoptosis). Therefore, saying the structure *cannot* bind proteins is factually incorrect. **Analysis of Incorrect Options:** * **Option A & B:** Cisplatin has a high affinity for specific sequences. It targets G-rich areas and can lead to the disruption of **A-tracts** (sequences of adenine). The resulting cross-links cause a structural **collapse of the DNA helix** into the minor groove, particularly affecting the geometry of A-tracts. * **Option C:** The hallmark of Cisplatin action is the **bending of the DNA duplex** (approximately 30-90 degrees). This bending is essential for its cytotoxic effect as it signals the cell's apoptotic machinery. **Clinical Pearls for NEET-PG:** * **Dose-limiting toxicity:** Nephrotoxicity (prevented by aggressive hydration and Amifostine). * **Other toxicities:** Ototoxicity (high-frequency hearing loss), peripheral neuropathy, and severe emesis (highly emetogenic). * **Mechanism:** Forms **1,2-intrastrand cross-links** (most common) rather than interstrand links.

Q: Which of the following drugs acts by inhibiting the tyrosine kinase activated by the EGF receptor as well as HER2?

Lapatinib. ### Explanation **Correct Option: D. Lapatinib** Lapatinib is a **dual tyrosine kinase inhibitor (TKI)**. It reversibly inhibits the intracellular kinase domains of both **EGFR (ErbB1)** and **HER2/neu (ErbB2)**. By blocking these receptors, it prevents the activation of downstream signaling pathways (like MAPK and PI3K) that promote cell proliferation and survival. It is primarily used in the treatment of HER2-positive advanced or metastatic breast cancer. **Analysis of Incorrect Options:** * **A. Imatinib:** This is the prototype TKI but it targets **BCR-ABL** (Philadelphia chromosome), **c-KIT**, and **PDGFR**. It is the first-line treatment for Chronic Myeloid Leukemia (CML) and Gastrointestinal Stromal Tumors (GIST). * **B. Gefitinib:** This is a selective **EGFR (ErbB1)** inhibitor. It does not have significant activity against HER2. It is primarily used in Non-Small Cell Lung Cancer (NSCLC) with EGFR mutations. * **C. Erlotinib:** Similar to Gefitinib, Erlotinib is a selective **EGFR** inhibitor used in NSCLC and pancreatic cancer. It lacks dual inhibition of HER2. **High-Yield Clinical Pearls for NEET-PG:** * **Trastuzumab vs. Lapatinib:** While both target HER2, Trastuzumab is a monoclonal antibody (extracellular), whereas Lapatinib is a small molecule inhibitor (intracellular). * **Afatinib:** Another drug to remember; it is an *irreversible* ErbB family blocker (inhibits EGFR, HER2, and HER4). * **Side Effects:** A common side effect of EGFR inhibitors (Gefitinib/Erlotinib) is an **acneiform skin rash**, the severity of which often correlates with a positive therapeutic response. Lapatinib is also associated with **diarrhea** and potential **hepatotoxicity**.

Q: Crizotinib is an inhibitor of which receptor?

Tyrosine kinase. **Explanation:** **Crizotinib** is a first-generation, orally active small-molecule inhibitor that primarily targets the **Tyrosine Kinase** domain. Specifically, it inhibits the **ALK (Anaplastic Lymphoma Kinase)** and **ROS1** tyrosine kinases. In certain cancers, chromosomal rearrangements (like the EML4-ALK fusion gene) lead to constitutive activation of tyrosine kinase signaling, driving uncontrolled cell proliferation. Crizotinib binds to the ATP-binding site of these receptors, blocking the downstream oncogenic signaling pathways. **Analysis of Options:** * **Option A (Correct):** Crizotinib is a multi-targeted receptor tyrosine kinase inhibitor (TKI). It is the standard treatment for patients with ALK-positive or ROS1-positive non-small cell lung cancer (NSCLC). * **Option B (Incorrect):** VEGF receptor inhibitors include drugs like **Bevacizumab** (monoclonal antibody) or **Sunitinib/Sorafenib** (TKIs with anti-angiogenic properties). While some TKIs overlap, Crizotinib’s primary clinical utility is not via VEGF inhibition. * **Option C (Incorrect):** TNF-alpha inhibitors are biological DMARDs used in autoimmune conditions (e.g., Rheumatoid Arthritis), such as **Infliximab, Adalimumab,** and **Etanercept**. * **Option D (Incorrect):** PDGF receptor inhibitors include **Imatinib** (which also targets BCR-ABL) and **Olaratumab**. **High-Yield Clinical Pearls for NEET-PG:** 1. **Indication:** First-line for **ALK-positive metastatic NSCLC**. 2. **Resistance:** Patients often develop resistance via the **L1196M "gatekeeper" mutation**; in such cases, second-generation inhibitors like **Ceritinib** or **Alectinib** are used. 3. **Side Effects:** Visual disturbances (flashes of light), hepatotoxicity, and QT interval prolongation. 4. **Diagnostic Marker:** ALK rearrangements are typically detected via **FISH** (Fluorescence In Situ Hybridization) or IHC.

Question 1

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 2

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 3

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 4

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

Accepted Answer

Cisplatin

Answer

Cyclophosphamide

Answer

Busulfan

Answer

Procarbazine

Question 5

Which of the following drugs can cause pancreatitis?

Accepted Answer

L-asparaginase

Answer

Colchicine

Answer

Ciprofloxacin

Answer

Nalidixic acid

Question 6

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

Accepted Answer

Floxuridine

Answer

Carbamazepine

Answer

Sulfonamides

Answer

Indinavir

Question 7

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

Question 8

A 55-year-old male patient complains of an abnormal growth on his right cheek. The patient has a habit of tobacco chewing for 30 years. Radiologic findings reveal an 8x8 cm fungating mass invading the maxilla and mandible on the right side. The patient was advised palliative chemotherapy with cisplatin. Which of the following changes in DNA is NOT caused by this drug?

Accepted Answer

The changed structure cannot bind proteins

Answer

A-tracts are replaced by other bases

Answer

Collapse of the helix into the minor groove of A-tract

Answer

Production of bent structures in DNA

Question 9

Which of the following drugs acts by inhibiting the tyrosine kinase activated by the EGF receptor as well as HER2?

Accepted Answer

Lapatinib

Answer

Imatinib

Answer

Gefitinib

Answer

Erlotinib

Question 10

Crizotinib is an inhibitor of which receptor?

Accepted Answer

Tyrosine kinase

Answer

VEGF receptor

Answer

TNF alpha receptor

Answer

PDGF receptor

Anticancer Drugs — MCQs

Anticancer Drugs — MCQs

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