Anticancer Drugs — MCQs

Anticancer Drugs Indian Medical PG Practice Questions and MCQs

Question 81: Which of the following is an alkylating agent used in chemotherapy?

A. Mechlorethamine
B. Procarbazine
C. Cyclophosphamide
D. All of the above (Correct Answer)

Explanation: **Explanation:** Alkylating agents are a major class of cytotoxic drugs that act by forming covalent bonds with DNA, specifically by attaching an alkyl group to the **N7 position of guanine**. This results in DNA cross-linking, strand breakage, and inhibition of DNA replication, ultimately leading to apoptosis. * **Mechlorethamine (Option A):** This is the prototype **Nitrogen Mustard**. It is highly reactive and was historically the first non-hormonal drug used in cancer (specifically for Hodgkin’s lymphoma in the MOPP regimen). * **Procarbazine (Option B):** This is a **Methylhydrazine derivative**. Although it requires metabolic activation, it functions as an alkylating agent by producing free radicals and methylating DNA. It is a key component of the BEACOPP and MOPP regimens. * **Cyclophosphamide (Option C):** This is the most widely used alkylating agent. It is a **prodrug** activated by hepatic cytochrome P450 (CYP2B) into active metabolites (phosphoramide mustard and acrolein). Since all three drugs belong to the alkylating agent category, **Option D** is the correct answer. **High-Yield Clinical Pearls for NEET-PG:** 1. **Cyclophosphamide Toxicity:** The metabolite **Acrolein** causes Hemorrhagic Cystitis. This is prevented by vigorous hydration and **MESNA** (a sulfhydryl compound that neutralizes acrolein in the bladder). 2. **Procarbazine Side Effects:** It is a weak MAO inhibitor (risk of hypertensive crisis with tyramine-rich foods) and can cause a **Disulfiram-like reaction** with alcohol. 3. **Resistance:** Increased production of **Glutathione** or enhanced DNA repair mechanisms (like MGMT) are common ways tumors develop resistance to alkylating agents.

Question 82: What is the mechanism of action of tamoxifen?

A. Androgenic receptor blocking action
B. Inhibition of enzyme 5α-reductase
C. Partial agonist and antagonist action on estrogen receptors (Correct Answer)
D. Inhibition of FSH and LH release from the pituitary

Explanation: **Explanation:** **Mechanism of Action:** Tamoxifen is the prototype **Selective Estrogen Receptor Modulator (SERM)**. Its unique mechanism involves binding to estrogen receptors (ER), but its effect is tissue-specific due to the recruitment of different co-activators or co-repressors. It acts as a **competitive antagonist** in the breast (inhibiting tumor growth) but functions as a **partial agonist** in other tissues like the bone, liver, and endometrium. **Analysis of Options:** * **Option A (Incorrect):** Androgen receptor blockers (e.g., Flutamide, Bicalutamide) are used in the management of prostate cancer, not breast cancer. * **Option B (Incorrect):** 5α-reductase inhibitors (e.g., Finasteride, Dutasteride) prevent the conversion of testosterone to dihydrotestosterone (DHT) and are used for BPH and male pattern baldness. * **Option D (Incorrect):** Inhibition of FSH/LH release is the mechanism of GnRH agonists (e.g., Leuprolide) when given continuously, or GnRH antagonists (e.g., Degarelix). **High-Yield Clinical Pearls for NEET-PG:** * **Indications:** Drug of choice for ER-positive breast cancer in both pre- and post-menopausal women. It is also used for primary prevention in high-risk females. * **Side Effects (Agonist effects):** Increased risk of **endometrial carcinoma** (due to uterine stimulation) and **thromboembolism** (DVT/PE). * **Beneficial Agonist effect:** It prevents post-menopausal bone loss (decreases osteoporosis risk) and improves lipid profiles. * **Metabolism:** It is a prodrug converted to its active metabolite, **Endoxifen**, by the enzyme **CYP2D6**.

Question 83: What is the most preferred acute emetic for emesis induced by anticancer drugs?

A. Ondansetron (Correct Answer)
B. Metoclopramide
C. Chlorpromazine
D. Dicyclomine

Explanation: **Explanation:** **1. Why Ondansetron is Correct:** Ondansetron is a selective **5-HT₃ receptor antagonist**. [2] Cytotoxic chemotherapy triggers the release of serotonin (5-HT) from enterochromaffin cells in the GI tract, which stimulates vagal afferents to the vomiting center. [1] By blocking these receptors both peripherally (vagus nerve) and centrally (Chemoreceptor Trigger Zone - CTZ), 5-HT₃ antagonists have become the **first-line agents** for preventing acute emesis (occurring within 24 hours) induced by highly and moderately emetogenic chemotherapy (e.g., Cisplatin). [1][2] **2. Why Other Options are Incorrect:** * **Metoclopramide:** A D₂ receptor antagonist. While used for mild emesis or prokinesis, it is less effective than 5-HT₃ antagonists for chemotherapy and carries a risk of extrapyramidal side effects (EPS). [2] * **Chlorpromazine:** A dopamine antagonist (antipsychotic). It is rarely used as a primary agent for chemo-induced nausea due to significant sedation and alpha-blocking side effects. [2] * **Dicyclomine:** An anticholinergic used primarily as an antispasmodic for IBS. It has no significant role in managing chemotherapy-induced emesis. [3] **3. High-Yield NEET-PG Pearls:** * **Drug of Choice (DOC):** For *Acute* emesis = Ondansetron/Palonosetron. For *Delayed* emesis (e.g., Cisplatin) = **Aprepitant** (NK₁ receptor antagonist). [1][2] * **Longest Acting 5-HT₃ Antagonist:** Palonosetron (often preferred for its longer half-life). [2] * **Common Side Effects:** Headache and constipation are the most frequent; **QT interval prolongation** is a critical cardiac concern. [2] * **Synergy:** The efficacy of 5-HT₃ antagonists is significantly enhanced when combined with **Dexamethasone**. [2]

Question 84: Allopurinol potentiates the action of which of the following drugs?

A. Azathioprine (Correct Answer)
B. Busulfan
C. Actinomycin
D. Procarbazine

Explanation: **Explanation:** **1. Why Azathioprine is Correct:** Azathioprine is a prodrug that is converted into **6-Mercaptopurine (6-MP)**. The primary metabolic pathway for the inactivation of 6-MP involves the enzyme **Xanthine Oxidase (XO)**, which converts it into 6-thiouric acid. **Allopurinol** is a potent inhibitor of Xanthine Oxidase. When administered concurrently, Allopurinol prevents the degradation of 6-MP, leading to toxic accumulation and increased bone marrow suppression. Therefore, if these drugs are used together, the dose of Azathioprine/6-MP must be reduced by **50-75%**. **2. Why Other Options are Incorrect:** * **B. Busulfan:** An alkylating agent (alkyl sulfonate) primarily used in CML. Its metabolism is independent of Xanthine Oxidase; it is mainly conjugated with glutathione. * **C. Actinomycin (Dactinomycin):** An antitumor antibiotic that intercalates into DNA. It is excreted primarily unchanged in the bile and urine, not metabolized by XO. * **D. Procarbazine:** A methylhydrazine derivative used in Hodgkin’s lymphoma. It is metabolized by hepatic CYP450 enzymes and acts as a weak MAO inhibitor, but it does not interact with the XO pathway. **3. High-Yield Clinical Pearls for NEET-PG:** * **Tumor Lysis Syndrome (TLS):** Allopurinol is often co-administered with chemotherapy to prevent hyperuricemia resulting from rapid cell death. This makes the interaction with 6-MP/Azathioprine a common clinical scenario. * **TPMT Deficiency:** Thiopurine Methyltransferase (TPMT) is another enzyme that metabolizes 6-MP. Patients with genetic TPMT deficiency are at extreme risk of toxicity, similar to the effect of Allopurinol. * **Febuxostat:** Like Allopurinol, Febuxostat is a non-purine selective inhibitor of XO and carries the same interaction warning.

Question 85: Sodium 2-mercaptoethane sulfonate is used as a protective agent in:

A. Radiotherapy
B. Cancer chemotherapy (Correct Answer)
C. Lithotripsy
D. Hepatic encephalopathy

Explanation: **Explanation:** **Sodium 2-mercaptoethane sulfonate**, commonly known as **MESNA**, is a cytoprotective adjuvant used specifically in **cancer chemotherapy** to prevent hemorrhagic cystitis. **Why the correct answer is right:** Certain oxazaphosphorine alkylating agents, namely **Cyclophosphamide** and **Ifosfamide**, are metabolized into a toxic byproduct called **Acrolein**. Acrolein accumulates in the urinary bladder, causing severe irritation and sloughing of the bladder mucosa, leading to **hemorrhagic cystitis** [1]. MESNA works by: 1. Concentrating in the urine. 2. Using its free sulfhydryl (-SH) group to bind and neutralize acrolein into a non-toxic thioether. 3. Increasing the excretion of the neutralized complex, thereby protecting the urothelium. **Why the other options are wrong:** * **Radiotherapy:** While radioprotectors like *Amifostine* (a free radical scavenger) are used to protect salivary glands and lungs during radiation, MESNA has no role here. * **Lithotripsy:** This is a procedure to break kidney stones using shock waves; it does not involve chemical toxicity requiring a sulfhydryl donor. * **Hepatic encephalopathy:** This condition is managed with ammonia-lowering agents like *Lactulose, Rifaximin,* or *L-ornithine L-aspartate (LOLA)*. **High-Yield Clinical Pearls for NEET-PG:** * **Drug of Choice:** MESNA is the mandatory co-administration drug for **Ifosfamide** (due to higher acrolein production) and high-dose **Cyclophosphamide** [1]. * **Alternative Management:** Vigorous hydration and frequent voiding are also essential to reduce the contact time of acrolein with the bladder wall. * **Amifostine:** Often confused with MESNA; it is used to prevent **Cisplatin-induced nephrotoxicity** and radiation-induced xerostomia. * **Dexrazoxane:** Another high-yield protector used to prevent **Doxorubicin-induced cardiotoxicity**.

Question 86: Methotrexate, a medication used for rheumatologic and psoriatic diseases, can cause side effects that mimic vitamin deficiencies. Which of the following vitamin deficiencies is most closely mimicked by methotrexate usage?

A. Pyridoxine (B6)
B. Biotin (B7)
C. Niacin (B2)
D. Folate (B9) (Correct Answer)

Explanation: **Explanation:** **1. Why Folate (B9) is Correct:** Methotrexate (MTX) is a structural analogue of folic acid. Its primary mechanism of action involves the **competitive inhibition of the enzyme Dihydrofolate Reductase (DHFR)** [5]. This enzyme is responsible for converting dihydrofolate into its active form, tetrahydrofolate (THF). THF is a crucial co-factor for the synthesis of thymidylate and purines, which are essential for DNA synthesis and cell division [1]. By depleting the pool of active folate, MTX causes side effects that mirror folate deficiency, such as **megaloblastic anemia, mucositis, and myelosuppression.** [4] **2. Why Other Options are Incorrect:** * **Pyridoxine (B6):** Deficiency is commonly associated with **Isoniazid (INH)** therapy, leading to peripheral neuropathy and sideroblastic anemia. * **Biotin (B7):** Deficiency is rare but can occur with excessive consumption of raw egg whites (avidin binding). It is not related to MTX. * **Niacin (B3):** Deficiency causes Pellagra (3Ds: Dermatitis, Diarrhea, Dementia). While MTX causes skin issues, the mechanism is unrelated to Niacin metabolism. **3. Clinical Pearls for NEET-PG:** * **Leucovorin Rescue:** To mitigate MTX toxicity, **Folinic acid (Leucovorin)** is administered [3]. It bypasses the inhibited DHFR enzyme to provide a source of active reduced folate [5]. * **Monitoring:** Patients on long-term MTX (e.g., for Rheumatoid Arthritis) require regular **Complete Blood Counts (CBC)** and **Liver Function Tests (LFTs)** due to risks of bone marrow suppression and hepatic fibrosis [4]. * **Contraindication:** MTX is highly **teratogenic** (Neural Tube Defects) and is contraindicated in pregnancy [2].

Question 87: Etoposide acts by which mechanism?

A. Inhibition of dihydrofolate
B. Inhibition of topoisomerase (Correct Answer)
C. Inhibition of purine synthesis
D. Inhibition of protein synthesis

Explanation: **Explanation:** **Mechanism of Action:** Etoposide (and its analog Teniposide) is a semi-synthetic derivative of podophyllotoxin. It acts specifically by inhibiting **Topoisomerase II**. This enzyme is responsible for creating transient double-stranded breaks in DNA to manage supercoiling during replication. Etoposide binds to the DNA-topoisomerase II complex, preventing the re-ligation of these strands. This leads to the accumulation of DNA breaks, eventually triggering apoptosis (cell death). It is **cell-cycle specific**, acting primarily in the **S and G2 phases**. **Analysis of Incorrect Options:** * **Option A (Dihydrofolate inhibition):** This is the mechanism of **Methotrexate**, which inhibits dihydrofolate reductase (DHFR), depleting tetrahydrofolate required for thymidylate synthesis. * **Option C (Purine synthesis inhibition):** This describes antimetabolites like **6-Mercaptopurine** and **6-Thioguanine**, which act as purine analogs to disrupt DNA synthesis. * **Option D (Protein synthesis inhibition):** While common in antibiotics (e.g., Macrolides), in oncology, drugs like **L-Asparaginase** deplete amino acids to inhibit protein synthesis, but this is not the mechanism of podophyllotoxins. **NEET-PG High-Yield Pearls:** * **Topoisomerase I vs. II:** Remember **"ET"** (Etoposide/Teniposide) for Topoisomerase **II**, and **"Irino/Topo"** (Irinotecan/Topotecan) for Topoisomerase **I**. * **Clinical Use:** Etoposide is a cornerstone in treating **Small Cell Lung Cancer (SCLC)** and **Testicular tumors** (often part of the BEP regimen). * **Side Effects:** A unique high-yield toxicity is **alopecia** and the potential for **secondary leukemia** (specifically AML with 11q23 translocation) with long-term use.

Question 88: Which of the following is a non-cell cycle specific anticancer drug?

A. Methotrexate
B. Paclitaxel
C. Etoposide
D. Cyclophosphamide (Correct Answer)

Explanation: **Explanation:** Anticancer drugs are broadly classified into **Cell Cycle-Specific (CCS)** agents, which act on specific phases of the cell cycle, and **Cell Cycle-Non-Specific (CCNS)** agents, which act on cells regardless of their phase (including the resting G0 phase). **Why Cyclophosphamide is the correct answer:** Cyclophosphamide is an **Alkylating Agent**. These drugs work by covalently bonding alkyl groups to DNA (specifically the N7 position of guanine), leading to DNA cross-linking and strand breakage. Because this chemical reaction can occur at any time and does not require the cell to be actively synthesizing DNA or dividing, it is classified as **Cell Cycle-Non-Specific (CCNS)**. **Why the other options are incorrect:** * **Methotrexate:** An Antimetabolite that inhibits Dihydrofolate Reductase (DHFR). It is specific to the **S-phase** (DNA synthesis). * **Paclitaxel:** A Taxane that stabilizes microtubules, preventing their disassembly. It is specific to the **M-phase** (Mitosis). * **Etoposide:** A Topoisomerase II inhibitor that causes DNA strand breaks. It is specific to the **S and G2 phases**. **High-Yield Clinical Pearls for NEET-PG:** * **CCNS Drugs:** Include Alkylating agents (Cyclophosphamide, Cisplatin), Antitumor Antibiotics (Dactinomycin, Mitomycin C), and Nitrosoureas. * **Cyclophosphamide Toxicity:** Characterized by **Hemorrhagic Cystitis** due to the metabolite **Acrolein**. This is prevented by aggressive hydration and **MESNA** (Mercaptoethane sulfonate). * **Memory Aid:** "Antimetabolites are S-phase specific; Microtubule inhibitors (Vincas/Taxanes) are M-phase specific."

Question 89: Side effects of cisplatin include all of the following EXCEPT:

A. Nausea and vomiting
B. Nephrotoxicity
C. Blindness (Correct Answer)
D. Ototoxicity

Explanation: **Explanation:** Cisplatin is a potent platinum-based alkylating agent used for various solid tumors. While it has a significant side-effect profile, **blindness** is not a characteristic or common side effect of the drug. **Why Blindness is the Correct Answer:** Ocular toxicity with cisplatin is rare and usually limited to optic neuritis or blurred vision at extremely high doses. It does not typically cause blindness. In contrast, the other options represent the "classic" triad of cisplatin toxicities. **Analysis of Incorrect Options:** * **Nausea and Vomiting (Option A):** Cisplatin is the **most highly emetogenic** chemotherapy drug. It triggers both central and peripheral pathways, often requiring aggressive antiemetic prophylaxis (e.g., Aprepitant + Ondansetron + Dexamethasone). * **Nephrotoxicity (Option B):** This is the **dose-limiting toxicity**. It causes acute tubular necrosis. To prevent this, patients are managed with **aggressive IV hydration** and **Amifostine** (a cytoprotective free-radical scavenger). * **Ototoxicity (Option C):** Cisplatin causes high-frequency hearing loss and tinnitus due to damage to the hair cells in the cochlea. This is often irreversible and more common in children. **High-Yield Clinical Pearls for NEET-PG:** * **Mnemonic for Cisplatin:** Remember the **"3 N's"** — **N**ephrotoxicity, **N**eurotoxicity (peripheral neuropathy), and **N**ausea/vomiting, plus **Ototoxicity**. * **Amifostine:** Specifically used to reduce cisplatin-induced nephrotoxicity. * **Electrolyte Imbalance:** Cisplatin frequently causes **hypomagnesemia** and hypokalemia due to renal tubular damage. * **Carboplatin:** A related drug that is less nephrotoxic and emetogenic but more **myelosuppressive** (causes thrombocytopenia).

Question 90: Ramucircumab is used in the treatment of:

A. Psoriasis
B. Non-small cell carcinoma of lungs (Correct Answer)
C. Ascites
D. Severe asthma

Explanation: **Explanation:** **Ramucircumab** is a fully human IgG1 monoclonal antibody that acts as a specific **VEGFR-2 (Vascular Endothelial Growth Factor Receptor 2) antagonist**. By binding to the extracellular domain of VEGFR-2, it prevents the binding of VEGF ligands (VEGF-A, VEGF-C, and VEGF-D), thereby inhibiting downstream signaling pathways involved in angiogenesis, tumor vascularization, and metastasis. **1. Why Option B is Correct:** Ramucircumab is FDA-approved for the treatment of metastatic **Non-Small Cell Lung Cancer (NSCLC)**, typically used in combination with Docetaxel after progression on platinum-based chemotherapy. It is also used in gastric/gastroesophageal junction adenocarcinoma, colorectal cancer, and hepatocellular carcinoma. **2. Why Other Options are Incorrect:** * **Option A (Psoriasis):** Psoriasis is treated with biologics targeting TNF-α (Infliximab), IL-17 (Secukinumab), or IL-23 (Ustekinumab). * **Option C (Ascites):** While VEGF inhibitors can sometimes reduce malignant effusions, Ramucircumab is not a standard treatment for ascites. Diuretics and paracentesis remain the mainstay. * **Option D (Severe Asthma):** This is managed with monoclonal antibodies targeting IgE (Omalizumab), IL-5 (Mepolizumab), or IL-4/IL-13 (Dupilumab). **Clinical Pearls for NEET-PG:** * **Mechanism:** Unlike Bevacizumab (which binds to the VEGF-A ligand), Ramucircumab binds directly to the **VEGFR-2 receptor**. * **Key Side Effects:** Hypertension, proteinuria, arterial thromboembolic events, and impaired wound healing (common to most VEGF inhibitors). * **High-Yield Association:** Always associate "mab" drugs ending in "-umab" with human origin and those targeting "VEGFR" with anti-angiogenesis.

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

Practice Questions

Immunotherapy

Practice Questions

Management of Chemotherapy Side Effects

Practice Questions

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