Anticancer Drugs — MCQs

Anticancer Drugs Indian Medical PG Practice Questions and MCQs

Question 481: All of the following anticancer drugs are cell cycle non-specific except?

A. Cisplatin
B. Vincristine (Correct Answer)
C. Mitomycin-C
D. Cyclophosphamide

Explanation: ### Explanation The classification of anticancer drugs based on cell cycle kinetics is a high-yield topic for NEET-PG. Drugs are categorized into **Cell Cycle Specific (CCS)** agents, which act on specific phases (e.g., M or S phase), and **Cell Cycle Non-Specific (CCNS)** agents, which act on both resting and dividing cells. **Why Vincristine is the Correct Answer:** Vincristine is a **Vinca alkaloid** that acts specifically during the **M-phase (Mitosis)**. It binds to tubulin and inhibits its polymerization into microtubules, preventing the formation of the mitotic spindle. This leads to mitotic arrest in metaphase. Since it targets a specific phase, it is a **Cell Cycle Specific (CCS)** drug. **Analysis of Incorrect Options:** * **Cisplatin (Option A):** A platinum coordination complex that cross-links DNA. It is **CCNS**, although it shows maximum toxicity during the G1 and S phases. * **Mitomycin-C (Option C):** An antitumor antibiotic that acts as an alkylating agent. It is **CCNS** and is particularly effective against hypoxic tumor cells. * **Cyclophosphamide (Option D):** An alkylating agent (nitrogen mustard) that causes DNA cross-linking. Alkylating agents are the classic examples of **CCNS** drugs because they damage DNA regardless of the cell cycle stage. **High-Yield Clinical Pearls for NEET-PG:** * **CCS Drugs:** Remember the mnemonic **"M-S-G"**: **M**-phase (Vincas, Taxanes), **S**-phase (Antimetabolites like Methotrexate, 5-FU), and **G2**-phase (Bleomycin). * **CCNS Drugs:** Alkylating agents, Platinum compounds, and Anthracyclines (Doxorubicin). * **Vincristine Side Effect:** Distinctive for **peripheral neuropathy** (paresthesia, loss of reflexes) and **constipation** (paralytic ileus), but notably **bone marrow sparing**.

Question 482: What is the characteristic toxicity of doxorubicin?

A. Pulmonary fibrosis
B. Cardiotoxicity (Correct Answer)
C. Peripheral neuropathy
D. Hemorrhagic cystitis

Explanation: **Explanation:** **Doxorubicin** is an anthracycline antibiotic used widely in chemotherapy. Its primary mechanism involves DNA intercalation and inhibition of Topoisomerase II. **Why Cardiotoxicity is the Correct Answer:** The hallmark toxicity of doxorubicin is **cardiotoxicity**, which occurs via two mechanisms: 1. **Acute:** Transient ECG changes (arrhythmias, ST-T wave changes). 2. **Chronic (Dose-dependent):** Dilated cardiomyopathy leading to congestive heart failure (CHF). This is mediated by the generation of **iron-dependent free radicals** (reactive oxygen species) that cause lipid peroxidation of the myocardial membranes. The heart is particularly vulnerable because it lacks sufficient **catalase** to neutralize these radicals. **Analysis of Incorrect Options:** * **A. Pulmonary Fibrosis:** This is the classic dose-limiting toxicity of **Bleomycin** and **Busulfan**. * **C. Peripheral Neuropathy:** This is characteristic of microtubule inhibitors like **Vinca alkaloids** (Vincristine) and **Taxanes** (Paclitaxel). * **D. Hemorrhagic Cystitis:** This is caused by **Cyclophosphamide** and **Ifosfamide** due to the accumulation of the toxic metabolite **Acrolein**. **High-Yield Clinical Pearls for NEET-PG:** * **Dexrazoxane:** An iron-chelating agent administered to prevent/reduce doxorubicin-induced cardiotoxicity. * **Lifetime Cumulative Dose:** Risk of CHF increases significantly when the cumulative dose exceeds **550 mg/m²**. * **Monitoring:** Periodic **Echocardiography** or MUGA scans to monitor Left Ventricular Ejection Fraction (LVEF) are mandatory. * **Red Urine:** Doxorubicin can cause harmless reddish discoloration of urine (not to be confused with hematuria).

Question 483: Bevacizumab is used for the treatment of which carcinoma?

A. Breast (Correct Answer)
B. Stomach
C. Lung
D. None of the above

Explanation: **Explanation:** **Bevacizumab** is a recombinant humanized monoclonal antibody that acts as a potent **VEGF (Vascular Endothelial Growth Factor) inhibitor**. It binds to circulating VEGF-A, preventing it from interacting with its receptors (VEGFR-1 and VEGFR-2) on the surface of endothelial cells. This inhibits **angiogenesis** (the formation of new blood vessels), thereby "starving" the tumor of the blood supply necessary for growth and metastasis. 1. **Why Breast Carcinoma is correct:** Bevacizumab is FDA-approved and widely used in the management of **metastatic HER2-negative breast cancer**, typically in combination with chemotherapy (like paclitaxel). It helps in delaying disease progression by limiting the tumor's vascular network. 2. **Why other options are incorrect:** While Bevacizumab is used in several solid tumors (Colorectal, Renal Cell, and Non-Small Cell Lung Cancer), in the context of this specific question and standard NEET-PG patterns, **Breast Cancer** is a primary indication. While it is used in Lung cancer, it is specifically for *non-squamous* NSCLC; however, Breast cancer remains a classic textbook association for this drug's clinical utility. It is not a standard first-line treatment for Gastric (Stomach) carcinoma (where Trastuzumab or Ramucirumab are more commonly discussed). **High-Yield Clinical Pearls for NEET-PG:** * **Mechanism:** Angiogenesis inhibitor (Anti-VEGF). * **Adverse Effects:** The most characteristic side effects are **Hypertension**, **Proteinuria**, impaired wound healing, and increased risk of gastrointestinal perforation/hemorrhage. * **Other Indications:** Metastatic colorectal cancer (first-line), Glioblastoma multiforme, and Age-related Macular Degeneration (off-label/intravitreal). * **Contraindication:** It should be avoided for at least 28 days before or after elective surgery due to wound healing complications.

Question 484: A 56-year-old female presented with breast carcinoma and was prescribed herceptin (trastuzumab). Which of the following statements regarding this drug is true?

A. It is an antibody produced entirely from mice, containing no human component.
B. It is a monoclonal antibody produced by injecting the HER2 antigen. (Correct Answer)
C. Injection of herceptin increases the antibody response.
D. The protein HER2/Neu is expressed in increased amounts by breast cancer cells.

Explanation: **Explanation:** **Trastuzumab (Herceptin)** is a recombinant DNA-derived humanized monoclonal antibody that selectively binds to the extracellular domain of the **Human Epidermal Growth Factor Receptor 2 (HER2/neu)**. 1. **Why the correct answer is right:** Monoclonal antibodies are produced using hybridoma technology. To create Trastuzumab, the HER2 antigen is injected into a host (typically a mouse) to stimulate B-cells to produce specific antibodies. these are then fused with immortal myeloma cells. While the final drug is "humanized" (to reduce immunogenicity), its origin lies in the immune response triggered by the HER2 antigen. 2. **Analysis of incorrect options:** * **Option A:** Trastuzumab is a **humanized** antibody (indicated by the suffix *-zumab*), meaning it is ~95% human and only ~5% murine. Antibodies entirely from mice end in *-omab*. * **Option C:** Trastuzumab does not "increase the antibody response" in the patient; rather, it acts via **Antibody-Dependent Cellular Cytotoxicity (ADCC)** and by inhibiting downstream signaling pathways that lead to cell proliferation. * **Option D:** While HER2 is overexpressed in about 20-30% of breast cancers, it is **not** expressed by *all* breast cancer cells. Testing for HER2 overexpression (via IHC or FISH) is a mandatory prerequisite before starting therapy. **High-Yield Clinical Pearls for NEET-PG:** * **Mechanism:** Binds HER2 $\rightarrow$ inhibits MAPK and PI3K/Akt pathways $\rightarrow$ G1 cell cycle arrest. * **Major Side Effect:** **Cardiotoxicity** (decreased LVEF/Heart Failure). Unlike anthracyclines (Doxorubicin), Trastuzumab-induced cardiotoxicity is **not** dose-dependent and is usually **reversible**. * **Contraindication:** Avoid concurrent use with Anthracyclines due to synergistic cardiotoxicity. * **Nomenclature Tip:** *-umab* (Human), *-zumab* (Humanized), *-ximab* (Chimeric), *-omab* (Mouse).

Question 485: Which of the following anticancer drugs can result in a "disulfiram reaction"?

A. Lomustine
B. L-Asparginase
C. Procarbazine (Correct Answer)
D. Busulfan

Explanation: **Explanation:** **Procarbazine** is a methylhydrazine derivative used primarily in the treatment of Hodgkin’s lymphoma (as part of the MOPP regimen). The correct answer is **Procarbazine** because it possesses unique biochemical properties that lead to several drug interactions: 1. **Disulfiram-like Reaction:** Procarbazine inhibits the enzyme **aldehyde dehydrogenase**. If a patient consumes alcohol while on this drug, acetaldehyde accumulates, leading to flushing, tachycardia, nausea, and hypotension (the disulfiram reaction). 2. **MAO Inhibition:** Procarbazine is also a weak **Monoamine Oxidase (MAO) inhibitor**. Patients must avoid tyramine-rich foods (like aged cheese) to prevent a hypertensive crisis. **Analysis of Incorrect Options:** * **Lomustine (A):** A nitrosourea that is highly lipid-soluble and crosses the blood-brain barrier. Its primary toxicity is delayed and prolonged myelosuppression, not disulfiram reactions. * **L-Asparaginase (B):** An enzyme used in Acute Lymphoblastic Leukemia (ALL). Its major side effects include acute pancreatitis, thrombosis, and hypersensitivity reactions. * **Busulfan (D):** An alkyl sulfonate used in CML and bone marrow ablation. Its classic "high-yield" toxicities are pulmonary fibrosis ("Busulfan lung") and generalized skin hyperpigmentation ("Busulfan tan"). **Clinical Pearls for NEET-PG:** * **Other drugs causing Disulfiram-like reactions:** Metronidazole (most common), Cefotetan/Cefoperazone, Tinidazole, and Sulfonylureas (Chlorpropamide). * **Procarbazine Toxicity:** It is highly leukemogenic; it carries a significant risk of causing secondary cancers, particularly Acute Myeloid Leukemia (AML).

Question 486: Which drug is given for delayed vomiting after chemotherapy?

A. Metoclopramide
B. Hyoscine
C. Domperidone
D. Aprepitant (Correct Answer)

Explanation: ### Explanation **Correct Option: D. Aprepitant** Chemotherapy-Induced Nausea and Vomiting (CINV) is classified into two phases: **Acute** (within 24 hours) and **Delayed** (after 24 hours, peaking at 48–72 hours). * **Mechanism:** Delayed vomiting is primarily mediated by **Substance P** acting on **Neurokinin-1 (NK1) receptors** in the area postrema. * **Aprepitant** is a selective NK1 receptor antagonist. It is the drug of choice for delayed emesis, especially when used in combination with dexamethasone and 5-HT3 antagonists (like Ondansetron) for highly emetogenic chemotherapy (e.g., Cisplatin). **Why Other Options are Incorrect:** * **A. Metoclopramide:** A D2 receptor antagonist with prokinetic properties. While it has some antiemetic effect, it is not the preferred agent for delayed CINV and carries a risk of extrapyramidal side effects. * **B. Hyoscine:** An anticholinergic used primarily for **motion sickness**, not for chemotherapy-induced emesis. * **C. Domperidone:** A peripheral D2 antagonist. It is used for general nausea or drug-induced dyspepsia but is ineffective against the potent emetogenic triggers of chemotherapy. **High-Yield Clinical Pearls for NEET-PG:** * **Acute Vomiting:** Mediated by Serotonin (5-HT3). Drug of choice: **Ondansetron**. * **Delayed Vomiting:** Mediated by Substance P (NK1). Drug of choice: **Aprepitant/Rolapitant**. * **Anticipatory Vomiting:** (Psychogenic trigger before chemo). Drug of choice: **Benzodiazepines (Lorazepam)**. * **Cisplatin:** The most common chemotherapy agent associated with severe delayed emesis. * **Aprepitant Interaction:** It is a CYP3A4 inhibitor; dose adjustment of dexamethasone is required when co-administered.

Question 487: Which antifungal agent is also used as a cancer chemotherapeutic agent?

A. Flucytosine (Correct Answer)
B. Nystatin
C. Voriconazole
D. Terbinafine

Explanation: **Explanation:** **Flucytosine (5-Fluorocytosine)** is the correct answer because it acts as a prodrug that is converted into **5-Fluorouracil (5-FU)**, a well-known antimetabolite used in cancer chemotherapy [1]. 1. **Mechanism of Action:** In fungal cells, the enzyme **cytosine deaminase** converts flucytosine into 5-FU. 5-FU is then metabolized into 5-FdUMP, which inhibits **thymidylate synthase**, thereby halting DNA synthesis [1]. While humans lack cytosine deaminase (minimizing systemic toxicity), 5-FU itself is a cornerstone treatment for colorectal, breast, and head and neck cancers. 2. **Why other options are incorrect:** * **Nystatin:** A polyene antifungal used topically for candidiasis; it works by binding to ergosterol to form pores in the fungal membrane. It is too toxic for systemic use and has no role in oncology. * **Voriconazole:** A second-generation triazole that inhibits ergosterol synthesis. It is the drug of choice for invasive aspergillosis but lacks cytotoxic properties [2]. * **Terbinafine:** An allylamine that inhibits squalene epoxidase. It is used primarily for dermatophytoses (onychomycosis) and has no chemotherapeutic application [2]. **High-Yield Clinical Pearls for NEET-PG:** * **Synergy:** Flucytosine is almost always used in combination with **Amphotericin B** (especially for Cryptococcal meningitis) to prevent the rapid development of resistance and to take advantage of increased cell permeability [2], [3]. * **Toxicity:** The most significant side effect of Flucytosine is **bone marrow suppression** (anemia, leukopenia, thrombocytopenia), which is a classic side effect shared with many anticancer agents. * **Conversion:** Remember: Flucytosine $\xrightarrow{Cytosine\ Deaminase}$ 5-Fluorouracil.

Question 488: Rituximab is used in all of the following conditions except:

A. NHL
B. PNH (Correct Answer)
C. RA
D. SLE

Explanation: **Explanation:** **Rituximab** is a chimeric monoclonal antibody directed against the **CD20 antigen**, which is primarily expressed on the surface of mature B-lymphocytes [1]. By binding to CD20, it mediates B-cell lysis through complement-dependent cytotoxicity and antibody-dependent cellular cytotoxicity [1]. * **Why PNH is the correct answer:** Paroxysmal Nocturnal Hemoglobinuria (PNH) is a stem cell disorder characterized by a deficiency of GPI-anchored proteins (like CD55 and CD59), leading to complement-mediated hemolysis of RBCs. Rituximab has no role here because the pathology involves the complement system attacking red blood cells, not B-cells. The drug of choice for PNH is **Eculizumab** (a C5 complement inhibitor). * **Why other options are incorrect:** * **NHL (Non-Hodgkin Lymphoma):** Rituximab is a cornerstone of therapy for B-cell NHLs (e.g., Diffuse Large B-cell Lymphoma) because these malignant cells overexpress CD20 [1]. * **RA (Rheumatoid Arthritis):** It is used in refractory RA to deplete the B-cells responsible for producing autoantibodies and presenting antigens to T-cells. * **SLE (Systemic Lupus Erythematosus):** While often used off-label, Rituximab is a recognized treatment for severe or refractory SLE to reduce the B-cell population. **Clinical Pearls for NEET-PG:** 1. **Infusion Reaction:** The most common side effect; managed by pre-medicating with antihistamines and acetaminophen [1]. 2. **HBV Reactivation:** Always screen for Hepatitis B before starting Rituximab, as it can cause fatal viral reactivation [1]. 3. **PML:** It is associated with Progressive Multifocal Leukoencephalopathy (JC virus reactivation) [1]. 4. **Other Indications:** ITP, Pemphigus vulgaris, and Wegener’s Granulomatosis (GPA).

Question 489: Which of the following is an IL-2 receptor inhibitor?

A. Basiliximab
B. Daclizumab
C. Both Basiliximab and Daclizumab (Correct Answer)
D. None of the above

Explanation: **Explanation:** **Mechanism of Action:** Basiliximab and Daclizumab are monoclonal antibodies that function as **IL-2 receptor antagonists**. Specifically, they bind to the **alpha subunit (CD25)** of the IL-2 receptor expressed on the surface of activated T-lymphocytes. By blocking this receptor, they inhibit IL-2 mediated T-cell proliferation, which is a critical step in the cellular immune response. **Analysis of Options:** * **Basiliximab:** A chimeric (murine-human) monoclonal antibody. It has a high affinity for the CD25 receptor and is currently the most commonly used IL-2 receptor antagonist in clinical practice. * **Daclizumab:** A humanized monoclonal antibody. While it also targets the CD25 receptor, it was primarily used for multiple sclerosis but has been largely withdrawn from the market due to safety concerns (hepatic injury). However, pharmacologically, it remains classified as an IL-2 receptor inhibitor. * **Conclusion:** Since both drugs share the same mechanism of inhibiting the IL-2 receptor, **Option C** is the correct answer. **NEET-PG High-Yield Pearls:** 1. **Clinical Use:** These drugs are primarily used for the **prophylaxis of acute organ rejection** in renal transplant patients (induction therapy). 2. **Side Effects:** Generally well-tolerated; however, they can cause hypersensitivity reactions and increased susceptibility to infections. 3. **Mnemonic:** Remember **"BD"** (Basiliximab/Daclizumab) for **"Blocking CD25"**. 4. **Distinction:** Unlike Cyclosporine or Tacrolimus (which inhibit IL-2 *production* via calcineurin inhibition), these drugs inhibit the IL-2 *receptor* directly.

Question 490: Which anticancer drug, also used in Rheumatoid Arthritis, produces acrolein in urine that leads to hemorrhagic cystitis?

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

Explanation: ### Explanation **Correct Answer: A. Cyclophosphamide** **Mechanism and Pathophysiology:** Cyclophosphamide is an **alkylating agent** (nitrogen mustard) that acts as a prodrug. It is activated in the liver by cytochrome P450 enzymes into 4-hydroxycyclophosphamide, which eventually breaks down into two active metabolites: **phosphoramide mustard** (the cytotoxic component) and **acrolein**. Acrolein is a toxic byproduct excreted in the urine. It causes direct irritation and sloughing of the bladder mucosal lining, leading to **hemorrhagic cystitis**. Clinically, this presents as gross hematuria and dysuria. Beyond oncology, it is widely used as a Disease-Modifying Antirheumatic Drug (DMARD) for severe Rheumatoid Arthritis and systemic vasculitis. **Analysis of Incorrect Options:** * **B. Busulfan:** An alkylating agent primarily used in Chronic Myeloid Leukemia (CML) and bone marrow ablation. Its classic side effects include **pulmonary fibrosis** ("Busulfan lung"), adrenal insufficiency-like syndrome, and skin hyperpigmentation. * **C. Procarbazine:** A methylating agent used in Hodgkin’s lymphoma. It is known for causing **disulfiram-like reactions** with alcohol and hypertensive crises when taken with tyramine-rich foods (MAO inhibition). * **D. Mesna:** This is not an anticancer drug but a **cytoprotective agent**. It is the specific antidote used to *prevent* hemorrhagic cystitis by neutralizing acrolein in the bladder. **NEET-PG High-Yield Pearls:** * **Prevention of Hemorrhagic Cystitis:** Managed by aggressive hydration and administration of **Mesna** (2-MercaptoEthane Sulfonate Na). * **Other Side Effects:** Cyclophosphamide is also associated with SIADH and infertility (premature ovarian failure/azoospermia). * **Ifosfamide:** A related drug that produces even higher levels of acrolein and *always* requires Mesna co-administration.

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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