Anticancer Drugs Practice Questions

Q: What is the main side effect of Imatinib mesylate?

Fluid retention. Imatinib mesylate is a selective Tyrosine Kinase Inhibitor (TKI) that targets the BCR-ABL protein (Philadelphia chromosome), as well as c-KIT and PDGFR [1]. It is the first-line treatment for Chronic Myeloid Leukemia (CML) [1] and Gastrointestinal Stromal Tumors (GIST) [2]. 1. Why Fluid Retention is Correct: The most characteristic and common side effect of Imatinib is fluid retention, which typically manifests as periorbital edema (puffiness around the eyes) and peripheral edema. In severe cases, it can lead to pleural effusion or ascites. This occurs due to the inhibition of the Platelet-Derived Growth Factor Receptor (PDGFR) [1], which regulates interstitial fluid pressure. 2. Analysis of Incorrect Options: * A. Leg ulcers: These are classically associated with Hydroxyurea, often used in myeloproliferative disorders. * C. Flagellate hyperpigmentation: This is a pathognomonic side effect of Bleomycin [3]. It presents as linear, whip-like streaks on the trunk. * D. Irreversible myelosuppression: While Imatinib can cause myelosuppression (neutropenia/thrombocytopenia), it is usually reversible upon dose adjustment. Irreversible bone marrow suppression is more characteristic of Busulfan or high-dose radiation. High-Yield Clinical Pearls for NEET-PG: * Mechanism: Inhibits the ATP-binding site of the BCR-ABL tyrosine kinase [1]. * Drug of Choice (DOC): Chronic Myeloid Leukemia (CML) [1]. * Other Side Effects: Muscle cramps, GI upset, and skin rashes. * Metabolism: Metabolized by CYP3A4; therefore, grapefruit juice should be avoided as it increases drug toxicity [2].

Q: What is the most common side effect of cisplatin in a patient being treated for esophageal carcinoma?

Acute tubular necrosis. **Explanation:** **Cisplatin** is a potent platinum-based alkylating agent used extensively in solid tumors like esophageal, lung, and germ cell carcinomas. **1. Why Acute Tubular Necrosis (ATN) is correct:** The dose-limiting toxicity of Cisplatin is **nephrotoxicity**. Cisplatin accumulates in the proximal convoluted tubule (PCT) and the S3 segment of the straight tubule, leading to oxidative stress and apoptosis of tubular cells. This manifests clinically as **Acute Tubular Necrosis**, characterized by a decrease in GFR and an increase in serum creatinine. To mitigate this, patients are typically managed with aggressive **pre-treatment hydration** (saline diuresis) and the administration of **Amifostine** (a cytoprotective free-radical scavenger). **2. Why the other options are incorrect:** * **Thrombocytopenia:** While Cisplatin causes mild bone marrow suppression, it is notably **less myelosuppressive** than most other anticancer drugs (like Carboplatin). * **Hepatic failure:** Cisplatin is not typically associated with significant hepatotoxicity; its primary elimination is renal. * **Cardiomyopathy:** This is a classic side effect of **Anthracyclines** (e.g., Doxorubicin), not Cisplatin. **High-Yield Clinical Pearls for NEET-PG:** * **Mnemonic for Cisplatin Toxicity:** "3 N's" — **N**ephrotoxicity (ATN), **N**eurotoxicity (Peripheral neuropathy), and **N**eusea/Vomiting (it is highly emetogenic). * **Ototoxicity:** Cisplatin causes high-frequency hearing loss (tinnitus/deafness) which is often irreversible. * **Electrolyte Imbalance:** It frequently causes **hypomagnesemia** due to renal wasting. * **Amifostine:** Specifically used to reduce Cisplatin-induced nephrotoxicity.

Q: Which of the following agents is NOT anti-VEGF?

5-Fluorouracil. **Explanation:** The correct answer is **5-Fluorouracil (5-FU)**. **Why 5-Fluorouracil is the correct answer:** 5-Fluorouracil is an **antimetabolite** (pyrimidine analogue) that inhibits the enzyme thymidylate synthase, thereby interfering with DNA synthesis. In ophthalmology, it is primarily used as an **anti-fibrotic agent** during glaucoma filtration surgery (trabeculectomy) to prevent subconjunctival scarring and bleb failure. It does not target Vascular Endothelial Growth Factor (VEGF). **Analysis of Incorrect Options (Anti-VEGF Agents):** * **Pegaptanib:** This was the first FDA-approved anti-VEGF for neovascular AMD. It is an RNA aptamer that specifically binds to the VEGF-165 isoform. * **Bevacizumab:** A recombinant humanized monoclonal antibody that binds to all isoforms of VEGF-A. While used "off-label" in ophthalmology, it is widely utilized for conditions like diabetic retinopathy and wet AMD due to its cost-effectiveness. * **Ranibizumab:** A humanized monoclonal antibody fragment (Fab) designed specifically for ocular use. It has a high affinity for all active isoforms of VEGF-A. **High-Yield Clinical Pearls for NEET-PG:** * **Mechanism of Anti-VEGF:** These agents inhibit angiogenesis and reduce vascular permeability by blocking VEGF, a key mediator in neovascularization. * **Common Indications:** Wet Age-Related Macular Degeneration (AMD), Diabetic Macular Edema (DME), and Central Retinal Vein Occlusion (CRVO). * **Other Anti-VEGFs to remember:** **Aflibercept** (a "VEGF Trap" that binds VEGF-A, VEGF-B, and Placental Growth Factor) and **Brolucizumab**. * **5-FU vs. Mitomycin-C:** Both are used in trabeculectomy, but Mitomycin-C is a more potent alkylating agent often preferred for high-risk cases.

Q: Which alkylating agent is known to cause a disulfiram-like reaction?

Procarbazine. **Procarbazine** is the correct answer because it is a methylhydrazine derivative alkylating agent [1] that possesses unique biochemical properties. It inhibits several enzymes, most notably **aldehyde dehydrogenase (ALDH)**. When a patient consumes alcohol while taking Procarbazine, acetaldehyde accumulates in the blood, leading to a **disulfiram-like reaction** characterized by flushing, tachycardia, nausea, and hypotension. **Analysis of Options:** * **Procarbazine (Correct):** Beyond its alkylating action, it is a weak **Monoamine Oxidase Inhibitor (MAOI)**. Therefore, it can also cause hypertensive crises if taken with tyramine-rich foods (cheese reaction) or certain antidepressants. * **Melphalan:** A nitrogen mustard primarily used in Multiple Myeloma. Its chief toxicity is bone marrow suppression; it does not interfere with alcohol metabolism. * **Carmustine (BCNU):** A nitrosourea known for its high lipid solubility, allowing it to cross the blood-brain barrier (used for brain tumors). Its dose-limiting toxicity is delayed myelosuppression and pulmonary fibrosis. * **Ifosfamide:** An analogue of cyclophosphamide. While it causes significant urotoxicity (hemorrhagic cystitis) and neurotoxicity (due to chloroacetaldehyde), it does not cause a disulfiram-like reaction. **High-Yield Clinical Pearls for NEET-PG:** * **Procarbazine Dual Toxicity:** Remember the "Two A's" — **A**lcohol (disulfiram-like) and **A**mines (MAO inhibition). * **Leukemogenic Potential:** Procarbazine has a high risk of causing secondary leukemia (especially AML) compared to other alkylating agents. * **Other drugs causing Disulfiram-like reactions:** Metronidazole (classic), Cefotetan/Cefoperazone, Griseofulvin, and Sulfonylureas (Tolbutamide).

Q: Cardiotoxicity induced by Doxorubicin can be reduced by:

Dexrazoxane. ### Explanation **Correct Option: A. Dexrazoxane** Doxorubicin (an Anthracycline) causes dose-dependent cardiotoxicity primarily through the generation of **iron-mediated free radicals** (reactive oxygen species) [1]. These radicals damage the myocardium, which is particularly vulnerable due to low levels of catalase. **Dexrazoxane** is an iron-chelating agent that binds to intracellular iron, preventing the formation of the iron-anthracycline complex and subsequent oxidative stress [1]. It is FDA-approved specifically to reduce the incidence and severity of cardiomyopathy associated with doxorubicin administration. **Analysis of Incorrect Options:** * **B. Amifostine:** A cytoprotective agent (free radical scavenger) used primarily to reduce **nephrotoxicity** associated with Cisplatin and to prevent xerostomia during radiation therapy. * **C. Leucovorin (Folinic Acid):** Used as a "rescue" therapy to prevent bone marrow toxicity after high-dose **Methotrexate** or to enhance the efficacy of 5-Fluorouracil (5-FU) in colorectal cancer. * **D. Bisphosphonates:** Used in oncology to manage **hypercalcemia of malignancy** and to prevent skeletal-related events (fractures) in patients with bone metastases. **High-Yield Clinical Pearls for NEET-PG:** * **Doxorubicin Toxicity:** Look for "dilated cardiomyopathy" or "congestive heart failure" in clinical vignettes [1]. * **Cumulative Dose:** The risk of cardiotoxicity increases significantly when the cumulative dose of Doxorubicin exceeds **450–550 mg/m²** [1]. * **Monitoring:** Baseline and periodic evaluation of **LVEF (Left Ventricular Ejection Fraction)** via ECHO or MUGA scan is mandatory [1]. * **Other Protective Agents:** Mesna is used to prevent hemorrhagic cystitis caused by Cyclophosphamide/Ifosfamide.

Q: Which of the following is a radioactive anti-cancer monoclonal antibody?

Ibritumomab. **Explanation:** **Correct Answer: C. Ibritumomab** Ibritumomab tiuxetan is a murine monoclonal antibody directed against the **CD20 antigen** found on the surface of B-lymphocytes. It is unique because it acts as a carrier for a radioisotope (Radioimmunotherapy). In clinical practice, it is conjugated with **Yttrium-90** ($^{90}$Y). The antibody targets the B-cells, and the attached radioisotope delivers targeted radiation, causing DNA damage and cell death to both the target cell and neighboring tumor cells (the "bystander effect"). It is primarily used in the treatment of relapsed or refractory follicular B-cell non-Hodgkin lymphoma. **Analysis of Incorrect Options:** * **A. Basiliximab:** This is a chimeric monoclonal antibody that binds to the **IL-2 receptor (CD25)** on T-cells. It is used as an immunosuppressant to prevent acute organ rejection in renal transplants, not as a radioactive anticancer agent. * **B. Bevacizumab:** This is a humanized monoclonal antibody that targets **VEGF** (Vascular Endothelial Growth Factor). It acts as an angiogenesis inhibitor used in various cancers (colorectal, lung, renal), but it does not carry a radioisotope. * **D. Rituximab:** While Rituximab also targets the **CD20 antigen** (like Ibritumomab), it is a "naked" monoclonal antibody. It works via antibody-dependent cellular cytotoxicity (ADCC) and complement-mediated lysis rather than radiation. **High-Yield Clinical Pearls for NEET-PG:** * **Radioimmunotherapy (RIT) Examples:** Ibritumomab ($^{90}$Y) and Tositumomab ($^{131}$I). * **Suffix "–mab":** Monoclonal Antibody. * **Suffix "–ximab":** Chimeric (e.g., Rituximab). * **Suffix "–zumab":** Humanized (e.g., Bevacizumab). * **Suffix "–umab":** Fully Human (e.g., Panitumumab). * **Common Target:** CD20 is the most common target for B-cell lymphomas (Rituximab, Ibritumomab, Ofatumumab).

Q: Which of the following is not an antineoplastic antibiotic?

Spiramycin. **Explanation:** The correct answer is **Spiramycin** because it is a **Macrolide antibiotic**, not an antineoplastic (anticancer) agent. It is primarily used to treat toxoplasmosis and various bacterial infections by inhibiting protein synthesis (binding to the 50S ribosomal subunit). **Why the other options are incorrect:** * **Actinomycin D (Dactinomycin):** An antineoplastic antibiotic derived from *Streptomyces*. It acts by intercalating between DNA base pairs and inhibiting RNA polymerase, primarily used in pediatric tumors like Wilms' tumor and Ewing’s sarcoma. * **Doxorubicin:** An **Anthracycline** antibiotic. It works via DNA intercalation, inhibition of Topoisomerase II, and the generation of free radicals. It is a broad-spectrum anticancer drug but is notorious for cardiotoxicity. * **Bleomycin:** A glycopeptide antibiotic that causes DNA strand scission by generating free radicals. It is unique because it is "cell cycle specific" (G2 phase) and lacks significant bone marrow toxicity. **High-Yield Clinical Pearls for NEET-PG:** * **Bleomycin:** Most significant side effect is **Pulmonary Fibrosis**. It is "bone marrow sparing." * **Doxorubicin:** Dose-limiting toxicity is **Dilated Cardiomyopathy**. **Dexrazoxane** is used to prevent this cardiotoxicity. * **Actinomycin D:** Highly effective against gestational choriocarcinoma and Wilms' tumor. * **Spiramycin:** The drug of choice for **Toxoplasmosis in pregnancy** to prevent vertical transmission to the fetus.

Q: What medication should be administered prophylactically to individuals at high risk for developing breast cancer?

Tamoxifen. **Explanation:** **Tamoxifen** is the drug of choice for the chemoprevention of breast cancer in high-risk individuals (e.g., those with a strong family history or biopsy-confirmed atypical hyperplasia) [1]. It is a **Selective Estrogen Receptor Modulator (SERM)** that acts as a competitive antagonist at estrogen receptors in breast tissue, thereby inhibiting the proliferation of estrogen-dependent cancer cells [1]. Large clinical trials (like NSABP P-1) demonstrated that Tamoxifen reduces the incidence of invasive breast cancer by approximately 50% in high-risk pre- and post-menopausal women. **Analysis of Incorrect Options:** * **Aminoglutethimide:** This is a first-generation aromatase inhibitor and adrenal steroid synthesis inhibitor. While it was used in advanced breast cancer, it is not used for prophylaxis due to its significant side-effect profile (adrenal suppression). * **Diethylstilbestrol (DES):** A synthetic non-steroidal estrogen. It is actually associated with an *increased* risk of clear cell adenocarcinoma of the vagina in daughters of women who took it during pregnancy; it is never used for cancer prophylaxis. * **Flutamide:** A non-steroidal anti-androgen used primarily in the management of prostate cancer. It has no role in breast cancer prevention. **High-Yield Clinical Pearls for NEET-PG:** * **Dual Action:** Tamoxifen is an **antagonist in the breast** but an **agonist in the endometrium and bone**. * **Side Effects:** Increased risk of **endometrial carcinoma** and **thromboembolism** (DVT/PE) [1]. It also causes "hot flashes." * **Alternative:** **Raloxifene** is also used for prophylaxis in post-menopausal women and carries a lower risk of endometrial cancer compared to Tamoxifen [1]. * **Drug Interaction:** Tamoxifen is a prodrug activated by **CYP2D6**. Potent inhibitors like Fluoxetine or Paroxetine can decrease its efficacy.

Q: Which of the following is NOT used in the treatment protocol of Hodgkin's lymphoma?

Vincristine. To answer this question correctly, one must distinguish between the two primary chemotherapy regimens used for Hodgkin’s Lymphoma (HL): the historical **MOPP** regimen and the current gold standard **ABVD** regimen. ### 1. Why Vincristine is the Correct Answer While **Vincristine** is a mainstay in the treatment of Non-Hodgkin Lymphoma (as part of the CHOP regimen) and Pediatric Hodgkin’s (in the OEPA/COPP protocols), it is **not** part of the standard **ABVD** regimen, which is the first-line treatment for adult Hodgkin’s Lymphoma. Historically, Vincristine was used in the MOPP regimen (Mustine, Oncovin/Vincristine, Procarbazine, Prednisolone), but this has been largely phased out due to high toxicity and secondary malignancy risks. ### 2. Analysis of Incorrect Options (Components of ABVD) * **B. Vinblastine:** This is the "V" in ABVD. Unlike Vincristine, which causes significant neurotoxicity, Vinblastine is more associated with bone marrow suppression. * **C. Bleomycin:** The "B" in ABVD. It is an antitumor antibiotic known for causing pulmonary fibrosis but is unique because it lacks significant myelosuppression. * **D. Adriamycin (Doxorubicin):** The "A" in ABVD. It is an anthracycline that works via topoisomerase II inhibition and DNA intercalation. Its dose-limiting toxicity is cardiotoxicity. ### 3. High-Yield Clinical Pearls for NEET-PG * **ABVD Regimen:** **A**driamycin, **B**leomycin, **V**inblastine, **D**acarbazine. * **Vincristine vs. Vinblastine:** Remember the mnemonic: **"Vincristine blasts the nerves (Neurotoxicity), Vinblastine blasts the marrow (Bone marrow suppression)."** * **Dacarbazine:** An alkylating agent that is the "D" in ABVD. * **Drug of Choice:** ABVD is preferred over MOPP because it does not cause sterility and has a lower risk of inducing secondary leukemias.

Q: L–asparaginase is particularly used in which type of leukemia?

Acute Lymphoblastic Leukemia (ALL). **Explanation:** **Mechanism of Action & Rationale for ALL:** L-asparaginase is an enzyme that catalyzes the hydrolysis of circulating **L-asparagine** into aspartic acid and ammonia. Normal cells can synthesize their own asparagine using the enzyme *asparagine synthetase*. However, **Acute Lymphoblastic Leukemia (ALL)** cells lack this enzyme and are entirely dependent on exogenous (blood-derived) asparagine for protein synthesis. By depleting the systemic supply of asparagine, L-asparaginase selectively induces metabolic stress and apoptosis in lymphoblasts while sparing most normal tissues. **Analysis of Options:** * **Acute Lymphoblastic Leukemia (ALL):** This is the primary indication. It is a cornerstone of induction therapy, especially in pediatric populations. * **AML, CML, and CLL:** These myeloid and chronic lymphoid malignancies typically possess sufficient levels of asparagine synthetase. Therefore, they are not "asparagine-dependent" and do not respond significantly to L-asparaginase therapy. **High-Yield Clinical Pearls for NEET-PG:** * **Unique Toxicity Profile:** Unlike most cytotoxic drugs, L-asparaginase is **not bone marrow suppressive** (it is "bone marrow sparing"). * **Key Side Effects:** 1. **Hypersensitivity Reactions:** Being a foreign bacterial protein (derived from *E. coli*), it frequently causes anaphylaxis. 2. **Acute Pancreatitis:** A classic, high-yield association. 3. **Clotting Abnormalities:** It decreases the synthesis of clotting factors and Antithrombin III, leading to both thrombosis and hemorrhage. 4. **Hyperammonemia:** Due to the byproduct of asparagine breakdown.

Question 1

What is the main side effect of Imatinib mesylate?

Accepted Answer

Fluid retention

Answer

Leg ulcers

Answer

Flagellate hyperpigmentation

Answer

Irreversible myelosuppression

Question 2

What is the most common side effect of cisplatin in a patient being treated for esophageal carcinoma?

Accepted Answer

Acute tubular necrosis

Answer

Thrombocytopenia

Answer

Hepatic failure

Answer

Cardiomyopathy

Question 3

Which of the following agents is NOT anti-VEGF?

Accepted Answer

5-Fluorouracil

Answer

Pegaptanib

Answer

Bevacizumab

Answer

Ranibizumab

Question 4

Which alkylating agent is known to cause a disulfiram-like reaction?

Accepted Answer

Procarbazine

Answer

Melphalan

Answer

Carmustine

Answer

Ifosfamide

Question 5

Cardiotoxicity induced by Doxorubicin can be reduced by:

Accepted Answer

Dexrazoxane

Answer

Amifostine

Answer

Leucovorin

Answer

Bisphosphonates

Question 6

Which of the following is a radioactive anti-cancer monoclonal antibody?

Accepted Answer

Ibritumomab

Answer

Basiliximab

Answer

Bevacizumab

Answer

Rituximab

Question 7

Which of the following is not an antineoplastic antibiotic?

Accepted Answer

Spiramycin

Answer

Actinomycin D

Answer

Doxorubicin

Answer

Bleomycin

Question 8

What medication should be administered prophylactically to individuals at high risk for developing breast cancer?

Accepted Answer

Tamoxifen

Answer

Aminoglutethimide

Answer

Diethylstilbestrol

Answer

Flutamide

Question 9

Which of the following is NOT used in the treatment protocol of Hodgkin's lymphoma?

Accepted Answer

Vincristine

Answer

Vinblastine

Answer

Bleomycin

Answer

Adriamycin

Question 10

L–asparaginase is particularly used in which type of leukemia?

Accepted Answer

Acute Lymphoblastic Leukemia (ALL)

Answer

Acute Myeloid Leukemia (AML)

Answer

Chronic Myeloid Leukemia (CML)

Answer

Chronic Lymphocytic Leukemia (CLL)

Anticancer Drugs — MCQs

Anticancer Drugs — MCQs

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