Anticancer Drugs — MCQs

Anticancer Drugs Indian Medical PG Practice Questions and MCQs

Question 141: The combination of meclorethamine, vincristine, prednisolone, and procarbazine is used for the treatment of patients with which condition?

A. Acute lymphocytic leukemia
B. Chronic lymphocytic leukemia
C. Hodgkin's disease (Correct Answer)
D. Acute myelocytic leukemia

Explanation: **Explanation:** The combination of **Meclorethamine, Oncovin (Vincristine), Procarbazine, and Prednisolone** is known as the **MOPP regimen**. This was the first chemotherapy combination to achieve a high cure rate in advanced **Hodgkin’s disease (HD)**. * **Mechanism:** Each drug in this regimen targets the cell cycle differently to maximize cytotoxicity while minimizing overlapping toxicities. Meclorethamine is an alkylating agent (nitrogen mustard), Vincristine is a microtubule inhibitor, Procarbazine is a unique alkylating agent that also inhibits DNA/RNA synthesis, and Prednisolone provides lympholytic effects. * **Clinical Note:** While MOPP was the gold standard, it has largely been replaced by the **ABVD regimen** (Adriamycin, Bleomycin, Vinblastine, and Dacarbazine) because ABVD is less leukemogenic and does not cause the permanent sterility associated with the MOPP regimen. **Analysis of Incorrect Options:** * **A. Acute Lymphocytic Leukemia (ALL):** The standard induction regimen typically involves Vincristine, Prednisolone, L-Asparaginase, and an Anthracycline (e.g., Daunorubicin). * **B. Chronic Lymphocytic Leukemia (CLL):** Treatment usually involves targeted therapies like Ibrutinib or Fludarabine-based regimens (FCR: Fludarabine, Cyclophosphamide, Rituximab). * **D. Acute Myelocytic Leukemia (AML):** The classic treatment is the **"7+3" regimen**, consisting of Cytarabine (7 days) and an Anthracycline like Daunorubicin (3 days). **High-Yield Clinical Pearls for NEET-PG:** * **MOPP side effect:** High risk of **secondary leukemia** (AML) and **sterility** (azoospermia). * **ABVD side effect:** Pulmonary fibrosis (Bleomycin) and Cardiotoxicity (Adriamycin/Doxorubicin). * **Procarbazine:** Known for causing a **Disulfiram-like reaction** with alcohol and hypertensive crises with tyramine-rich foods (MAO inhibition).

Question 142: Which of the following antineoplastic drugs should not be administered to a chronic alcoholic patient due to the risk of developing a disulfiram-like reaction?

A. Dacarbazine
B. Procarbazine (Correct Answer)
C. Melphalan
D. Hydroxyurea

Explanation: **Explanation:** **Procarbazine** is the correct answer because it is a methylhydrazine derivative that possesses unique biochemical properties, including the inhibition of several enzymes. Most notably, it inhibits **aldehyde dehydrogenase (ALDH)**, the enzyme responsible for metabolizing acetaldehyde into acetic acid. When a patient taking procarbazine consumes alcohol, acetaldehyde accumulates in the blood, leading to a **disulfiram-like reaction** characterized by flushing, tachycardia, nausea, vomiting, and hypotension. **Analysis of Options:** * **Procarbazine (Correct):** In addition to ALDH inhibition, it is a weak **Monoamine Oxidase (MAO) inhibitor**. Patients must avoid tyramine-rich foods (cheese, wine) to prevent hypertensive crises. It is primarily used in the MOPP regimen for Hodgkin’s Lymphoma. * **Dacarbazine:** An alkylating agent used in melanoma and Hodgkin’s (ABVD regimen). Its main side effect is severe emesis, but it does not cause disulfiram-like reactions. * **Melphalan:** A nitrogen mustard alkylating agent used primarily in Multiple Myeloma. Its toxicity is mainly hematological (bone marrow suppression). * **Hydroxyurea:** An S-phase specific inhibitor of ribonucleotide reductase used in CML and Sickle Cell Anemia. It does not interfere with alcohol metabolism. **High-Yield Clinical Pearls for NEET-PG:** * **Other drugs causing Disulfiram-like reactions:** Metronidazole (most common), Tinidazole, Cefotetan, Cefoperazone, Chlorpropamide, and Griseofulvin. * **Procarbazine Toxicity:** It is highly leukemogenic and carries a high risk of causing secondary acute leukemia. * **Mnemonic:** Remember **"P"** for Procarbazine, **"P"** for Pro-drug, and **"P"** for Psychosis (as it can cross the BBB and cause CNS effects).

Question 143: What is the drug of choice for surgically unresectable renal cell carcinoma?

A. Sorafenib
B. Sunitinib (Correct Answer)
C. Imatinib
D. Cetuximab

Explanation: **Explanation:** **Sunitinib** is the drug of choice for surgically unresectable or metastatic **Renal Cell Carcinoma (RCC)**. The underlying medical concept involves the pathophysiology of RCC, which is a highly vascular tumor often associated with the loss of the VHL (von Hippel-Lindau) gene. This loss leads to an overproduction of **Vascular Endothelial Growth Factor (VEGF)**. Sunitinib is an oral multi-kinase inhibitor that targets VEGF receptors (VEGFR-1, 2, and 3) and Platelet-Derived Growth Factor receptors (PDGFR), effectively inhibiting angiogenesis and tumor cell proliferation. **Analysis of Incorrect Options:** * **Sorafenib (Option A):** While also a multi-kinase inhibitor used in RCC, it is generally considered a second-line agent or used when sunitinib is not tolerated. It is the drug of choice for **Hepatocellular Carcinoma (HCC)**. * **Imatinib (Option B):** This is a selective BCR-ABL tyrosine kinase inhibitor. It is the drug of choice for **Chronic Myeloid Leukemia (CML)** and Gastrointestinal Stromal Tumors (GIST). * **Cetuximab (Option D):** This is a monoclonal antibody against the **Epidermal Growth Factor Receptor (EGFR)**. It is primarily used in the treatment of metastatic colorectal cancer and head and neck squamous cell carcinoma. **High-Yield Clinical Pearls for NEET-PG:** * **Pazopanib** is an alternative first-line agent for RCC with a similar mechanism to Sunitinib but a different side-effect profile. * **Side Effect Highlight:** Sunitinib is notorious for causing **Hand-Foot Syndrome** (palmar-plantar erythrodysesthesia) and potential cardiotoxicity (decreased LVEF). * **Temsirolimus/Everolimus:** These are mTOR inhibitors used specifically in high-risk/poor-prognosis RCC.

Question 144: What is the mechanism of action of vincristine?

A. Tubulin inhibitor (Correct Answer)
B. Antimetabolite
C. Adenylate cyclase inhibitor
D. Anti folate

Explanation: **Explanation:** **Mechanism of Action (Option A):** Vincristine is a **Vinca alkaloid** derived from the periwinkle plant (*Catharanthus roseus*). Its primary mechanism involves binding to **β-tubulin**, which inhibits its polymerization into microtubules. This prevents the formation of the mitotic spindle, leading to **cell cycle arrest in the M-phase (Metaphase)**. Without a functional spindle, the cell cannot segregate its chromosomes and eventually undergoes apoptosis. **Analysis of Incorrect Options:** * **Option B (Antimetabolite):** These drugs (e.g., Methotrexate, 5-Fluorouracil) interfere with DNA/RNA synthesis and typically act on the **S-phase** of the cell cycle, not the M-phase. * **Option C (Adenylate cyclase inhibitor):** This is not a standard mechanism for cytotoxic anticancer drugs. Adenylate cyclase is involved in intracellular signaling (cAMP production). * **Option D (Anti-folate):** This specifically refers to drugs like **Methotrexate**, which inhibit dihydrofolate reductase (DHFR), depleting the folate pool required for thymidylate synthesis. **High-Yield Clinical Pearls for NEET-PG:** * **Dose-Limiting Toxicity:** Unlike many chemotherapy drugs, Vincristine is **bone marrow sparing** (minimal myelosuppression). Its dose-limiting toxicity is **Peripheral Neuropathy** (paresthesia, loss of deep tendon reflexes, and "foot drop"). * **Autonomic Toxicity:** Can cause paralytic ileus and constipation. * **Vinca vs. Taxanes:** Remember the distinction—Vincas (Vincristine/Vinblastine) **inhibit polymerization**, while Taxanes (Paclitaxel/Docetaxel) **inhibit depolymerization** (stabilize microtubules). * **Fatal Route:** Vincristine is **fatal if given intrathecally**; it must only be administered intravenously.

Question 145: Vinca alkaloids act on:

A. G phase
B. S phase
C. Mitotic spindle (Correct Answer)
D. M phase

Explanation: ### Explanation **Mechanism of Action (Why C is correct):** Vinca alkaloids (e.g., Vincristine, Vinblastine, Vinorelbine) are **cell-cycle specific** agents that act primarily during the **M phase** of the cell cycle. Their specific molecular target is **tubulin**. They bind to $\beta$-tubulin and **inhibit its polymerization** into microtubules. This prevents the formation of the **mitotic spindle**, leading to "mitotic arrest" in metaphase and subsequent apoptosis. **Analysis of Incorrect Options:** * **A & B (G and S phases):** Vinca alkaloids do not directly interfere with protein synthesis (G1/G2) or DNA replication (S phase). Antimetabolites like Methotrexate and 5-Fluorouracil are the classic drugs acting on the S phase. * **D (M phase):** While Vinca alkaloids act *during* the M phase, the question asks for the specific structure they act *on*. In pharmacology entrance exams, if both the phase (M phase) and the specific target (Mitotic spindle/Tubulin) are provided, the **molecular target** is the more precise and preferred answer. **High-Yield Clinical Pearls for NEET-PG:** * **Vincristine:** Notable for **Peripheral Neuropathy** (microtubules are essential for axonal transport) and **SIADH**. It is relatively bone marrow sparing. * **Vinblastine:** Notable for **Bone Marrow Suppression** ("Blast" blasts the bone marrow). * **Taxanes (Paclitaxel):** These also act on the mitotic spindle but have the *opposite* mechanism—they **prevent depolymerization** (stabilize microtubules), creating "frozen" spindles. * **Fatal Route:** Vinca alkaloids are **fatal if given intrathecally**; they must only be administered intravenously.

Question 146: Which of the following statements about Ifosfamide is INCORRECT?

A. It is a nitrogen mustard.
B. It is metabolized by CYP3A4 to form an active metabolite.
C. Chloracetaldehyde is an active metabolite.
D. It is less neurotoxic than cyclophosphamide. (Correct Answer)

Explanation: ### Explanation **Why Option D is the correct (Incorrect) statement:** Ifosfamide is actually **more neurotoxic** than cyclophosphamide. This is because the metabolism of ifosfamide produces significantly higher levels of **chloroacetaldehyde**, a byproduct that crosses the blood-brain barrier and causes encephalopathy (confusion, seizures, or coma). In contrast, cyclophosphamide produces very little chloroacetaldehyde, making its neurotoxic profile much lower. **Analysis of other options:** * **Option A (Correct):** Ifosfamide is a structural isomer of cyclophosphamide and belongs to the **Nitrogen Mustard** class of alkylating agents. * **Option B (Correct):** It is a prodrug that requires hepatic activation. It is metabolized primarily by **CYP3A4** (and CYP2B6) to form the active alkylating species, **ifosfamide mustard**. * **Option C (Correct):** While ifosfamide mustard is the "active" cytotoxic metabolite for DNA cross-linking, **chloroacetaldehyde** is also a metabolite formed during the dechloroethylation pathway. It is clinically significant as it is responsible for the drug's characteristic neurotoxicity. **High-Yield Clinical Pearls for NEET-PG:** 1. **Hemorrhagic Cystitis:** Both ifosfamide and cyclophosphamide produce **Acrolein**, which causes bladder toxicity. However, the risk is higher with ifosfamide; therefore, **MESNA** (Mercaptoethane sulfonate) and aggressive hydration are mandatory. 2. **Fanconi Syndrome:** Ifosfamide is specifically associated with proximal renal tubular acidosis (Fanconi-like syndrome) due to chloroacetaldehyde-induced damage. 3. **Metabolism:** Unlike cyclophosphamide (primarily CYP2B6), ifosfamide relies heavily on **CYP3A4**, making it more prone to drug-drug interactions.

Question 147: A 30-year-old male diagnosed with Hodgkin's lymphoma was started on Bleomycin. Which of the following is false regarding Bleomycin?

A. It can cause pulmonary fibrosis
B. It can cause flagellate pigmentation of skin
C. It is metabolized by hydrolase enzyme
D. It has a high risk of causing bone marrow suppression (Correct Answer)

Explanation: Bleomycin is a unique glycopeptide antibiotic used in the treatment of Hodgkin’s lymphoma and testicular tumors. Its primary mechanism involves binding to DNA and iron, leading to the formation of free radicals that cause single- and double-strand DNA breaks [1]. **1. Why Option D is correct (The False Statement):** Bleomycin is famously known as a **"bone marrow-sparing"** drug. Unlike most cytotoxic agents, it causes minimal to no myelosuppression. This makes it a vital component of combination regimens like ABVD (Adriamycin, Bleomycin, Vinblastine, Dacarbazine), as it does not add to the hematological toxicity of other drugs. **2. Why other options are incorrect (True Statements):** * **Option A:** Pulmonary fibrosis is the most serious dose-limiting toxicity of Bleomycin [2]. It occurs because the lungs lack the inactivating enzyme (hydrolase), leading to oxidative damage. * **Option B:** Flagellate pigmentation (linear, whip-like hyperpigmented streaks on the trunk) is a pathognomonic cutaneous side effect of Bleomycin [2]. * **Option C:** Bleomycin is inactivated by the enzyme **Bleomycin hydrolase**. This enzyme is found in high concentrations in most tissues but is notably deficient in the **lungs and skin**, explaining why toxicity is localized to these organs. **High-Yield Clinical Pearls for NEET-PG:** * **Cell Cycle Specificity:** Bleomycin acts specifically on the **G2 phase** [1]. * **Monitoring:** Pulmonary Function Tests (PFTs), specifically **DLCO** (Diffusion Capacity of Carbon Monoxide), are used to monitor early lung toxicity. * **Maximum Cumulative Dose:** To prevent irreversible fibrosis, the lifetime dose is usually capped at **400 units**.

Question 148: Trastuzumab is directed against which of the following targets?

A. Human epidermal growth factor receptor 2 (Correct Answer)
B. Vascular endothelial growth factor A
C. Platelet derived growth factor
D. Fibroblast growth factor 23

Explanation: **Explanation:** **Trastuzumab** is a recombinant humanized monoclonal antibody specifically designed to target the **Human Epidermal Growth Factor Receptor 2 (HER2/neu)**, a proto-oncogene. In about 20–30% of breast cancer cases, HER2 is overexpressed, leading to uncontrolled cell proliferation. Trastuzumab binds to the extracellular domain of this receptor, inhibiting downstream signaling pathways (like MAPK and PI3K/Akt) and inducing antibody-dependent cellular cytotoxicity (ADCC). **Analysis of Options:** * **Option A (Correct):** Trastuzumab targets **HER2**. It is the first-line treatment for HER2-positive breast cancer and is also used in HER2-positive metastatic gastric adenocarcinoma. * **Option B (Incorrect):** **Bevacizumab** is the monoclonal antibody directed against Vascular Endothelial Growth Factor A (VEGF-A), used to inhibit angiogenesis. * **Option C (Incorrect):** Platelet-derived growth factor (PDGF) receptors are typically targeted by small molecule tyrosine kinase inhibitors like **Imatinib** or **Dasatinib**, rather than Trastuzumab. * **Option D (Incorrect):** FGF-23 is involved in phosphate metabolism. **Burosumab** is the monoclonal antibody that targets FGF-23, used in X-linked hypophosphatemia. **High-Yield Clinical Pearls for NEET-PG:** 1. **Cardiotoxicity:** The most significant side effect of Trastuzumab is **cardiac dysfunction** (decreased LVEF/heart failure). Unlike anthracyclines, this toxicity is usually **reversible** and not dose-dependent. 2. **Drug-Drug Interaction:** Never co-administer Trastuzumab with **Doxorubicin** due to a synergistic increase in the risk of heart failure. 3. **Resistance:** If resistance to Trastuzumab develops, **Lapatinib** (a dual EGFR/HER2 tyrosine kinase inhibitor) or **Ado-trastuzumab emtansine** (an antibody-drug conjugate) can be used.

Question 149: Which drug is useful in the treatment of breast cancer?

A. Tamoxifen (Correct Answer)
B. Cyproterone
C. Testosterone
D. Chlorambucil

Explanation: **Explanation:** **Tamoxifen** is the correct answer as it is a **Selective Estrogen Receptor Modulator (SERM)**. It acts as a competitive antagonist at estrogen receptors in breast tissue, thereby inhibiting the growth of estrogen-responsive breast cancer cells. It is considered the gold standard for hormonal therapy in premenopausal women with ER-positive breast cancer and is also used for chemoprophylaxis in high-risk individuals. **Analysis of Incorrect Options:** * **Cyproterone:** This is an anti-androgen with progestogenic activity. It is primarily used in the treatment of prostate cancer, hirsutism, and precocious puberty, rather than breast cancer. * **Testosterone:** As an androgen, it is generally not used to treat breast cancer today. In fact, in postmenopausal women, peripheral aromatization of androgens into estrogens could potentially stimulate tumor growth. * **Chlorambucil:** This is a nitrogen mustard alkylating agent. While it is a chemotherapy drug, its primary clinical utility is in Chronic Lymphocytic Leukemia (CLL) and certain lymphomas, not as a primary treatment for breast cancer. **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:** Due to its agonist effect on the uterus, it increases the risk of **endometrial carcinoma**. It also increases the risk of thromboembolism (DVT/PE). * **Bone Health:** Unlike Aromatase Inhibitors (e.g., Letrozole), Tamoxifen helps maintain bone mineral density in postmenopausal women. * **Drug of Choice:** For ER-positive breast cancer in **premenopausal** women, Tamoxifen is the drug of choice; for **postmenopausal** women, Aromatase Inhibitors are generally preferred.

Question 150: Which of the following anticancer drugs is known to be cardiotoxic?

A. Methotrexate
B. Cyclophosphamide
C. Adriamycin (Correct Answer)
D. Vincristine

Explanation: **Explanation:** **Adriamycin (Doxorubicin)**, an anthracycline antibiotic, is the correct answer. Its primary dose-limiting toxicity is **cardiotoxicity**. This occurs via two mechanisms: the generation of iron-dependent free radicals (superoxide anions) that cause lipid peroxidation of the myocardial membrane, and the inhibition of Topoisomerase IIβ in cardiomyocytes. This can manifest as acute arrhythmias or, more commonly, chronic **dilated cardiomyopathy** leading to congestive heart failure. **Analysis of Incorrect Options:** * **Methotrexate:** An antimetabolite (folate antagonist) primarily known for bone marrow suppression, mucositis, and hepatotoxicity. High doses can cause nephrotoxicity. * **Cyclophosphamide:** An alkylating agent. While very high doses (used in bone marrow transplants) can cause acute carditis, its "signature" high-yield side effect is **hemorrhagic cystitis** (prevented by Mesna). * **Vincristine:** A vinca alkaloid that inhibits microtubule assembly. Its hallmark toxicity is **peripheral neuropathy** (paresthesia, loss of deep tendon reflexes) and autonomic dysfunction (constipation). It is notably bone marrow-sparing. **High-Yield Clinical Pearls for NEET-PG:** 1. **Dexrazoxane:** An iron chelator used to prevent/reduce Adriamycin-induced cardiotoxicity. 2. **Monitoring:** Patients on Adriamycin should have regular **ECHO/MUGA scans** to monitor the Left Ventricular Ejection Fraction (LVEF). 3. **Lifetime Dose:** The risk of heart failure increases significantly once the cumulative dose of Doxorubicin exceeds **450–550 mg/m²**. 4. **Trastuzumab:** Another high-yield cardiotoxic drug (HER2 inhibitor), but unlike Adriamycin, its cardiotoxicity is usually reversible and not dose-dependent.

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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