Anticancer Drugs — MCQs
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Which of the following is an anti-VEGF drug?
Which of the following is not an alkylating agent?
Which of the following is an anti-CD25 antibody?
A patient with tumor lysis syndrome (TLS) is taking allopurinol. Which laboratory value should the nurse monitor to determine the effectiveness of the medication?
Ifosfamide belongs to which class of drugs?
Which is the most commonly used cardiotoxic anticancer drug?
Which of the following statements is true about Biclutamide?
Which of the following drugs is cell cycle phase specific?
Sustained neutropenia is seen with which of the following chemotherapeutic agents?
Herceptin is used for which cancer?
Anticancer Drugs Indian Medical PG Practice Questions and MCQs
Question 51: Which of the following is an anti-VEGF drug?
- A. Adalimumab
- B. Bevacizumab (Correct Answer)
- C. Cetuximab
- D. Daclizumab
Explanation: **Explanation:** **Bevacizumab** is a recombinant humanized monoclonal antibody that acts as a potent **anti-VEGF (Vascular Endothelial Growth Factor)** agent. It binds directly 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 required for growth and metastasis. It is clinically used in the treatment of metastatic colorectal cancer, renal cell carcinoma, and age-related macular degeneration (AMD). **Analysis of Incorrect Options:** * **Adalimumab:** A monoclonal antibody against **TNF-α** (Tumor Necrosis Factor-alpha). It is primarily used in chronic inflammatory conditions like Rheumatoid Arthritis, Psoriasis, and Crohn’s disease. * **Cetuximab:** A monoclonal antibody that targets the **EGFR** (Epidermal Growth Factor Receptor). It is used in the treatment of KRAS wild-type colorectal cancer and head and neck cancers. * **Daclizumab:** An antibody against the **IL-2 receptor (CD25)**. It was historically used to prevent renal transplant rejection and in multiple sclerosis (though largely withdrawn due to hepatic toxicity). **High-Yield Clinical Pearls for NEET-PG:** * **Adverse Effects of Bevacizumab:** The most characteristic side effects are **hypertension**, impaired wound healing, and gastrointestinal perforation. * **Suffix Trick:** Monoclonal antibodies ending in **"-umab"** are fully human, while **"-ximab"** are chimeric. * **Other Anti-VEGF agents:** **Ranibizumab** (fragment used for AMD) and **Aflibercept** (a "VEGF trap" fusion protein).
Question 52: Which of the following is not an alkylating agent?
- A. Cyclophosphamide
- B. Methotrexate (Correct Answer)
- C. Mechlorethamine
- D. Busulfan
Explanation: **Explanation:** The core concept tested here is the classification of anticancer drugs based on their mechanism of action. **Why Methotrexate is the correct answer:** **Methotrexate** is an **Antimetabolite**, specifically a **Folate Antagonist**. It works by competitively inhibiting the enzyme **Dihydrofolate Reductase (DHFR)**. This prevents the conversion of dihydrofolate to tetrahydrofolate, thereby inhibiting the synthesis of DNA, RNA, and proteins. It does not act by alkylating DNA strands. **Why the other options are incorrect:** * **Cyclophosphamide:** A nitrogen mustard and a classic **alkylating agent**. It is a pro-drug activated by cytochrome P450 in the liver to form phosphoramide mustard, which creates cross-links in DNA. * **Mechlorethamine:** The first nitrogen mustard used clinically; it is a bifunctional **alkylating agent** that causes DNA interstrand cross-linking. * **Busulfan:** An alkyl sulfonate and a cell-cycle non-specific **alkylating agent** primarily used in chronic myeloid leukemia (CML) and bone marrow ablation. **High-Yield Clinical Pearls for NEET-PG:** * **Cyclophosphamide:** Associated with **Hemorrhagic Cystitis** due to the metabolite **Acrolein**. This is prevented by aggressive hydration and **MESNA** (2-Mercaptoethane sulfonate). * **Methotrexate Toxicity:** Managed with **Leucovorin (Folinic acid) rescue**, which bypasses the inhibited DHFR enzyme. * **Busulfan:** Classically associated with **Pulmonary Fibrosis** ("Busulfan Lung") and hyperpigmentation. * **Alkylating Agents** are generally **Cell Cycle Non-Specific (CCNS)**, whereas Antimetabolites like Methotrexate are **S-phase specific**.
Question 53: Which of the following is an anti-CD25 antibody?
- A. Muromonab
- B. Daclizumab (Correct Answer)
- C. Adalimumab
- D. Transtuzumab
Explanation: **Explanation:** **Correct Answer: B. Daclizumab** **Mechanism of Action:** Daclizumab (and Basiliximab) are recombinant monoclonal antibodies that act as **IL-2 receptor antagonists**. Specifically, they bind to the **α-subunit (CD25)** of the IL-2 receptor expressed on the surface of activated T-lymphocytes. By blocking this receptor, they inhibit T-cell proliferation and the subsequent immune response. They are primarily used to prevent acute organ rejection in renal transplant patients. **Analysis of Incorrect Options:** * **A. Muromonab (OKT3):** This is a murine monoclonal antibody directed against the **CD3** receptor on T-cells. It was the first monoclonal antibody used in clinical practice but has largely been replaced due to "cytokine release syndrome." * **C. Adalimumab:** This is a fully human monoclonal antibody directed against **TNF-α**. It is widely used in the management of rheumatoid arthritis, psoriasis, and inflammatory bowel disease. * **D. Trastuzumab:** This is a humanized monoclonal antibody directed against the **HER2/neu (ErbB2)** receptor. It is a cornerstone therapy for HER2-positive breast cancer and gastric cancer. **High-Yield Clinical Pearls for NEET-PG:** * **CD25 Blockers:** Remember the mnemonic **"BD"** (Basiliximab, Daclizumab) for CD25. * **Chimeric vs. Humanized:** Basiliximab is *chimeric* (-ximab), while Daclizumab is *humanized* (-zumab). * **Rituximab:** Targets **CD20** (used in Non-Hodgkin Lymphoma). * **Alemtuzumab:** Targets **CD52** (used in CLL and Multiple Sclerosis). * **Infliximab:** Another TNF-α inhibitor, but unlike Adalimumab, it is a *chimeric* antibody.
Question 54: A patient with tumor lysis syndrome (TLS) is taking allopurinol. Which laboratory value should the nurse monitor to determine the effectiveness of the medication?
- A. Blood urea nitrogen (BUN)
- B. Serum phosphate
- C. Serum potassium
- D. Uric acid level (Correct Answer)
Explanation: ### Explanation **Correct Answer: D. Uric acid level** **Mechanism and Rationale:** Tumor Lysis Syndrome (TLS) occurs due to the rapid breakdown of malignant cells, leading to the release of intracellular contents into the bloodstream. This results in hyperuricemia, hyperkalemia, hyperphosphatemia, and hypocalcemia. **Allopurinol** is a **xanthine oxidase inhibitor**; it prevents the conversion of hypoxanthine and xanthine into uric acid. Since the primary therapeutic goal of allopurinol in TLS is to prevent and reduce the formation of uric acid to avoid urate nephropathy, monitoring the **serum uric acid level** is the direct way to assess the drug's effectiveness. **Analysis of Incorrect Options:** * **A. Blood urea nitrogen (BUN):** While BUN monitors renal function (which can be impaired by uric acid crystals), it is a non-specific marker and does not directly reflect the pharmacological action of allopurinol. * **B. Serum phosphate:** Hyperphosphatemia is a feature of TLS, but allopurinol has no effect on phosphate metabolism. Phosphate levels are managed via phosphate binders or hydration. * **C. Serum potassium:** Hyperkalemia is the most dangerous electrolyte abnormality in TLS. However, allopurinol does not lower potassium levels; this requires insulin/dextrose, calcium gluconate, or ion-exchange resins. **NEET-PG High-Yield Pearls:** * **Drug of Choice for Prophylaxis:** Allopurinol is used for the *prevention* of hyperuricemia in TLS. * **Rasburicase:** For *established* hyperuricemia or high-risk patients, Rasburicase (recombinant urate oxidase) is preferred as it metabolizes existing uric acid into highly soluble **allantoin**. * **Drug Interaction:** Allopurinol inhibits the metabolism of **6-Mercaptopurine (6-MP)** and **Azathioprine**. If co-administered, the dose of these cytotoxic drugs must be reduced by 50–75% to prevent toxicity.
Question 55: Ifosfamide belongs to which class of drugs?
- A. Alkylating agent (Correct Answer)
- B. Antimetabolite
- C. Taxanes
- D. Antibiotics
Explanation: **Explanation:** **Ifosfamide** is a nitrogen mustard derivative and a structural isomer of cyclophosphamide. It belongs to the **Alkylating Agents** class of anticancer drugs. These agents work by attaching alkyl groups to DNA (specifically at the N7 position of guanine), leading to DNA cross-linking, strand breakage, and inhibition of DNA synthesis, which ultimately triggers apoptosis. **Why the other options are incorrect:** * **Antimetabolites (e.g., Methotrexate, 5-FU):** These drugs interfere with the synthesis of nucleic acids by mimicking normal metabolites (S-phase specific). * **Taxanes (e.g., Paclitaxel, Docetaxel):** These are microtubule stabilizers that inhibit mitosis by preventing the disassembly of the mitotic spindle (M-phase specific). * **Antibiotics (e.g., Doxorubicin, Bleomycin):** These are derived from microbial sources and act via intercalation into DNA or by producing free radicals. **High-Yield Clinical Pearls for NEET-PG:** 1. **Metabolism:** Ifosfamide is a **prodrug** activated by hepatic CYP3A4. 2. **Specific Toxicity:** It produces **Acrolein**, a toxic metabolite that causes **Hemorrhagic Cystitis**. 3. **Prevention:** To prevent bladder toxicity, it is mandatory to co-administer **MESNA** (2-Mercaptoethane sulfonate Na) and ensure vigorous hydration. 4. **Neurotoxicity:** Unlike cyclophosphamide, Ifosfamide is more likely to cause **Encephalopathy** (due to the metabolite chloroacetaldehyde). This is managed with Methylene Blue. 5. **Fanconi Syndrome:** Ifosfamide is a known cause of drug-induced proximal renal tubular acidosis.
Question 56: Which is the most commonly used cardiotoxic anticancer drug?
- A. Doxorubicin (Correct Answer)
- B. Vincristine
- C. L-Asparginase
- D. Paclitaxol
Explanation: **Explanation:** **Doxorubicin** (an Anthracycline antibiotic) is the most notorious and commonly used anticancer drug associated with cardiotoxicity. The underlying mechanism involves the generation of **superoxide free radicals** and iron-dependent lipid peroxidation, which damages the myocardial cell membrane. Since the heart has low levels of protective enzymes like catalase and glutathione peroxidase, it is particularly vulnerable. Cardiotoxicity manifests in two forms: 1. **Acute:** Transient ECG changes (arrhythmias). 2. **Chronic:** Dose-dependent **Dilated Cardiomyopathy (DCM)** leading to Congestive Heart Failure (CHF). This risk increases significantly when the cumulative dose exceeds 550 mg/m². **Analysis of Incorrect Options:** * **Vincristine:** Primarily known for **Peripheral Neuropathy** (stocking-glove anesthesia) and paralytic ileus. It is a spindle poison that inhibits microtubule assembly. * **L-Asparaginase:** Most commonly associated with **Acute Pancreatitis**, hyperglycemia, and clotting factor deficiencies (hypofibrinogenemia). * **Paclitaxel:** Its dose-limiting toxicity is **Myelosuppression** and peripheral neuropathy. While it can cause transient bradycardia, it is not the "most common" cardiotoxic agent compared to Doxorubicin. **High-Yield Clinical Pearls for NEET-PG:** * **Dexrazoxane:** An iron chelator used to prevent/reduce Doxorubicin-induced cardiotoxicity. * **Monitoring:** Periodic **Echocardiography (MUGA scan)** to monitor Left Ventricular Ejection Fraction (LVEF) is mandatory for patients on Anthracyclines. * **Liposomal Doxorubicin:** A formulation developed to reduce cardiac uptake and decrease toxicity.
Question 57: Which of the following statements is true about Biclutamide?
- A. Binds to androgen receptors
- B. Causes gynaecomastia
- C. Can be given as monotherapy in prostatic cancer
- D. All of the above (Correct Answer)
Explanation: **Explanation:** **Bicalutamide** is a potent, non-steroidal **competitive androgen receptor antagonist**. It is a key drug in the management of prostate cancer, and its pharmacological profile explains why all the given options are correct. 1. **Mechanism of Action (Option A):** Bicalutamide works by binding directly to the cytosolic androgen receptors in the prostate gland. By doing so, it competitively inhibits the binding of Dihydrotestosterone (DHT) and Testosterone, thereby preventing the growth of androgen-dependent malignant cells. 2. **Side Effects (Option B):** Unlike GnRH agonists, pure anti-androgens like Bicalutamide often cause **gynaecomastia** and breast pain. This occurs because the blockade of androgen receptors in the hypothalamus/pituitary leads to an increase in LH levels, which subsequently increases testicular testosterone production. This excess testosterone is peripherally aromatized into estrogen, leading to breast tissue enlargement. 3. **Clinical Use (Option C):** Bicalutamide has a long half-life and a favorable safety profile compared to older drugs like Flutamide. It can be used as **monotherapy** in patients with locally advanced prostate cancer or as part of **Combined Androgen Blockade (CAB)** alongside GnRH analogs to prevent the "testosterone flare" phenomenon. **High-Yield Clinical Pearls for NEET-PG:** * **Comparison with Flutamide:** Bicalutamide is preferred over Flutamide because it is **less hepatotoxic** and has a longer half-life (once-daily dosing). * **Enzalutamide:** A newer, "second-generation" anti-androgen that has a much higher affinity for the receptor and also inhibits nuclear translocation of the receptor. * **Drug of Choice:** For metastatic prostate cancer, the combination of a GnRH agonist (e.g., Leuprolide) + an anti-androgen (e.g., Bicalutamide) is a standard approach.
Question 58: Which of the following drugs is cell cycle phase specific?
- A. Ifosfamide
- B. Bleomycin (Correct Answer)
- C. Cisplatin
- D. Chlorambucil
Explanation: ### Explanation Anticancer drugs are broadly classified into **Cell Cycle Specific (CCS)** and **Cell Cycle Non-Specific (CCNS)** agents [1, 2]. **1. Why Bleomycin is Correct:** Bleomycin is a **Cell Cycle Specific (CCS)** antibiotic. It acts primarily by binding to DNA and producing free radicals (superoxide and hydroxyl radicals) that cause single- and double-strand breaks. Its activity is maximal in the **G2 phase** of the cell cycle, although it also shows some activity in the M phase. Because it targets cells at a specific stage of division, it is classified as CCS [3]. **2. Why the other options are Incorrect:** * **Ifosfamide & Chlorambucil (Options A & D):** These are **Alkylating Agents**. Alkylating agents work by forming covalent bonds with DNA, leading to cross-linking. This process occurs regardless of whether the cell is actively dividing or resting; hence, they are **Cell Cycle Non-Specific (CCNS)** [1]. * **Cisplatin (Option B):** This is a **Platinum Coordination Complex**. Like alkylating agents, it cross-links DNA strands (primarily intrastrand) and is effective throughout all phases of the cell cycle, making it **CCNS** [1]. **3. High-Yield NEET-PG Pearls:** * **CCS Drugs:** Think "Antimetabolites (S-phase), Bleomycin (G2), Vinca Alkaloids (M), and Taxanes (M)." * **CCNS Drugs:** Think "Alkylating agents, Platinum compounds, and most Antitumor Antibiotics (except Bleomycin)." * **Bleomycin Toxicity:** It is unique because it lacks significant bone marrow toxicity (**Marrow Sparing**). However, it is notorious for causing **Pulmonary Fibrosis** and hyperpigmentation of the skin. * **Elimination:** Bleomycin is primarily cleared by the kidneys; dose adjustment is required in renal failure.
Question 59: Sustained neutropenia is seen with which of the following chemotherapeutic agents?
- A. Vinblastine
- B. Cisplatin
- C. Carmustine (Correct Answer)
- D. Cyclophosphamide
Explanation: **Explanation:** The correct answer is **Carmustine (Option C)**. **1. Why Carmustine is correct:** Carmustine and Lomustine belong to the **Nitrosourea** class of alkylating agents. The hallmark of Nitrosoureas is **delayed and sustained bone marrow suppression**. While most cytotoxic drugs cause a "nadir" (lowest blood count) at 7–14 days with recovery by day 21, Nitrosoureas cause a nadir that occurs much later (4–6 weeks) and lasts significantly longer. This sustained neutropenia and thrombocytopenia often necessitate longer intervals between treatment cycles. **2. Why the other options are incorrect:** * **Vinblastine:** While "Blastine blasts the bone marrow" (unlike Vincristine, which is marrow-sparing), the neutropenia it causes is transient and follows the typical 7–10 day recovery pattern. * **Cisplatin:** Its primary dose-limiting toxicity is **nephrotoxicity** and ototoxicity. While it can cause mild myelosuppression, it is generally considered one of the less myelosuppressive conventional agents. * **Cyclophosphamide:** It causes significant neutropenia, but it is acute and recovers relatively quickly (usually within 14–21 days). Its unique dose-limiting toxicity is **hemorrhagic cystitis**. **3. NEET-PG High-Yield Pearls:** * **Nitrosoureas (Carmustine/Lomustine):** Highly lipid-soluble, cross the Blood-Brain Barrier (BBB); used primarily for **Glioblastoma Multiforme**. * **Marrow-Sparing Agents:** Remember the mnemonic **"V-C-B"** (Vincristine, Cisplatin, Bleomycin) – these drugs have minimal bone marrow toxicity compared to others. * **Busulfan:** Another alkylating agent known for prolonged marrow suppression and a specific side effect called "Busulfan Lung" (pulmonary fibrosis) and skin hyperpigmentation.
Question 60: Herceptin is used for which cancer?
- A. Breast (Correct Answer)
- B. Thyroid
- C. Cervical
- D. Ovarian
Explanation: **Explanation:** **Herceptin (Trastuzumab)** is a recombinant DNA-derived humanized monoclonal antibody specifically designed to target the **HER2/neu (ErbB2)** receptor. This receptor is a proto-oncogene encoding a transmembrane tyrosine kinase. 1. **Why Breast Cancer is Correct:** Approximately 20–30% of breast cancer patients overexpress the HER2 protein. Trastuzumab binds to the extracellular domain of this receptor, inhibiting cell proliferation and promoting antibody-dependent cellular cytotoxicity (ADCC). It is the standard of care for **HER2-positive breast cancer** (both early-stage and metastatic). It is also approved for HER2-positive metastatic gastric adenocarcinoma. 2. **Why Other Options are Incorrect:** * **Thyroid Cancer:** Treatment typically involves surgery, radioactive iodine, or kinase inhibitors like Sorafenib/Lenvatinib (for refractory cases), but not Trastuzumab. * **Cervical Cancer:** Primary treatments include surgery, radiotherapy, and chemotherapy (Cisplatin). Bevacizumab (anti-VEGF) is the primary monoclonal antibody used here. * **Ovarian Cancer:** Standard treatment involves platinum-based chemotherapy (Carboplatin/Paclitaxel) and Bevacizumab or PARP inhibitors (Olaparib). **High-Yield Clinical Pearls for NEET-PG:** * **Mechanism:** Binds HER2 receptor $\rightarrow$ inhibits MAPK and PI3K/Akt pathways $\rightarrow$ G1 cell cycle arrest. * **Major Side Effect:** **Cardiotoxicity** (manifests as a decrease in Left Ventricular Ejection Fraction). Unlike Anthracyclines (Doxorubicin), Trastuzumab-induced cardiotoxicity is **not dose-dependent** and is usually **reversible** upon discontinuation. * **Contraindication:** Avoid concurrent use with Anthracyclines due to synergistic cardiotoxicity. * **Companion Diagnostic:** HER2 status must be confirmed via IHC (Immunohistochemistry) or FISH (Fluorescence In Situ Hybridization) before starting therapy.
Practice by Chapter
Principles of Cancer Chemotherapy
Practice Questions
Alkylating Agents
Practice Questions
Antimetabolites
Practice Questions
Antitumor Antibiotics
Practice Questions
Plant Alkaloids
Practice Questions
Topoisomerase Inhibitors
Practice Questions
Hormonal Agents
Practice Questions
Targeted Therapy
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Immunotherapy
Practice Questions
Management of Chemotherapy Side Effects
Practice Questions
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