Anticancer Drugs — MCQs

Anticancer Drugs Indian Medical PG Practice Questions and MCQs

Question 131: Which of the following statements about rituximab is FALSE?

A. It is a chimeric monoclonal antibody against CD-20.
B. It has dose-dependent kinetics. (Correct Answer)
C. It is used for the treatment of non-Hodgkin lymphoma.
D. Its most common adverse effect is infusion-related reactions.

Explanation: **Explanation** **Rituximab** is a cornerstone of immunotherapy in hematological malignancies and autoimmune disorders. Understanding its pharmacology is high-yield for NEET-PG. **1. Why Option B is the correct (False) statement:** Rituximab follows **non-linear (target-mediated) pharmacokinetics**, but it does **not** follow simple dose-dependent kinetics in the traditional sense. Its clearance decreases with repeated dosing because as the tumor burden (CD20+ cells) decreases, there are fewer targets for the drug to bind to, leading to a longer half-life over time. Therefore, its elimination is more dependent on the **target burden** rather than just the dose administered. **2. Analysis of Incorrect Options:** * **Option A (True):** Rituximab is a **chimeric** monoclonal antibody (indicated by the suffix *-ximab*). It specifically targets the **CD20 antigen** found on the surface of normal and malignant B-lymphocytes. * **Option C (True):** It is a first-line agent for **Non-Hodgkin Lymphoma (NHL)**, particularly Diffuse Large B-Cell Lymphoma (DLBCL) and Follicular Lymphoma. It is also used in Chronic Lymphocytic Leukemia (CLL) and Rheumatoid Arthritis. * **Option D (True):** The **most common adverse effect** is **infusion-related reactions** (fever, chills, rigors), occurring typically during the first infusion due to cytokine release. **Clinical Pearls for NEET-PG:** * **Mechanism:** Causes B-cell lysis via Antibody-Dependent Cellular Cytotoxicity (ADCC) and Complement-Dependent Cytotoxicity (CDC). * **Black Box Warning:** Reactivation of **Hepatitis B virus (HBV)**; screening is mandatory before starting therapy. * **Rare Side Effect:** Progressive Multifocal Leukoencephalopathy (PML) due to JC virus reactivation. * **Target:** CD20 is expressed on pre-B and mature B cells but **not** on hematopoietic stem cells or plasma cells.

Question 132: Which one of the following alkaloids is used as an anti-cancer agent?

A. Vincristine (Correct Answer)
B. Papaverine
C. Ephedrine
D. Atropine

Explanation: **Explanation:** **Vincristine (Option A)** is the correct answer. It is a natural alkaloid derived from the periwinkle plant (*Vinca rosea*). In oncology, it belongs to the class of **Vinca Alkaloids**, which act as **M-phase specific** cell cycle agents. Their mechanism of action involves binding to tubulin and inhibiting its polymerization into microtubules, thereby preventing the formation of the mitotic spindle and causing mitotic arrest. **Analysis of Incorrect Options:** * **Papaverine (Option B):** An opium alkaloid used as a smooth muscle relaxant and vasodilator (primarily for erectile dysfunction or peripheral vascular disease), not for cancer. * **Ephedrine (Option C):** A sympathomimetic alkaloid used as a bronchodilator and decongestant; it acts by releasing stored norepinephrine. * **Atropine (Option D):** A belladonna alkaloid that acts as a competitive muscarinic antagonist. It is used to treat bradycardia and organophosphate poisoning. **High-Yield Clinical Pearls for NEET-PG:** 1. **Dose-Limiting Toxicity:** Unlike most anticancer drugs, Vincristine is **bone marrow sparing**. Its major dose-limiting toxicity is **Peripheral Neuropathy** (presents as "stocking-glove" numbness or foot drop). 2. **Vinblastine vs. Vincristine:** While Vincristine causes neurotoxicity, its sister drug **Vinblastine** is notorious for **Bone marrow suppression** ("Blast" = Bone marrow). 3. **Contraindication:** Vincristine must **NEVER** be administered intrathecally, as it is fatal (causes ascending myeloencephalopathy). 4. **Other Plant-Derived Alkaloids:** * **Taxanes (Paclitaxel):** Prevent microtubule *depolymerization* (stabilize spindles). * **Camptothecins (Irinotecan):** Inhibit Topoisomerase I. * **Epipodophyllotoxins (Etoposide):** Inhibit Topoisomerase II.

Question 133: Which monoclonal antibody targets CD20 and is used in treating Non-Hodgkin Lymphoma (NHL)?

A. Cyclophosphamide
B. Trastuzumab
C. Denosumab
D. Rituximab (Correct Answer)

Explanation: **Explanation:** **Rituximab** is the correct answer. It is a chimeric monoclonal antibody that specifically targets the **CD20 antigen**, which is expressed on the surface of normal and malignant B-lymphocytes. By binding to CD20, Rituximab induces B-cell lysis through antibody-dependent cellular cytotoxicity (ADCC), complement-dependent cytotoxicity (CDC), and apoptosis. It is a cornerstone therapy for **B-cell Non-Hodgkin Lymphomas (NHL)**, such as Diffuse Large B-cell Lymphoma (DLBCL) and Follicular Lymphoma, as well as Chronic Lymphocytic Leukemia (CLL). **Analysis of Incorrect Options:** * **A. Cyclophosphamide:** This is an **alkylating agent** (nitrogen mustard), not a monoclonal antibody. It works by cross-linking DNA. While used in NHL (as part of the CHOP regimen), it does not target CD20. * **B. Trastuzumab:** This monoclonal antibody targets the **HER2/neu (ErbB2) receptor**. It is primarily used in the treatment of HER2-positive breast cancer and gastric cancer. * **C. Denosumab:** This is a monoclonal antibody against **RANKL** (Receptor Activator of Nuclear Factor kappa-B Ligand). It is used to treat osteoporosis and giant cell tumor of bone by inhibiting osteoclast activity. **High-Yield Clinical Pearls for NEET-PG:** * **Infusion Reaction:** The most common side effect of Rituximab is an infusion-related reaction (fever, chills, rash); premedication with paracetamol and antihistamines is standard. * **HBV Reactivation:** Always screen for Hepatitis B before starting Rituximab, as it can cause fatal viral reactivation. * **PML:** Rituximab is associated with a rare risk of Progressive Multifocal Leukoencephalopathy (PML) due to JC virus reactivation. * **Other CD20 Inhibitors:** Newer agents include **Ofatumumab** and **Obinutuzumab**.

Question 134: What is the mechanism of action of vincristine in the treatment of cancers?

A. Inhibition of topoisomerase II to cause breaks in DNA strands
B. Alkylation and cross-linking DNA strands
C. Inhibition of DNA-mediated RNA synthesis
D. Inhibition of polymerization of tubulin to form microtubules (Correct Answer)

Explanation: **Explanation:** **Vincristine** is a member of the **Vinca Alkaloids** class, derived from the periwinkle plant (*Vinca rosea*). Its primary mechanism of action involves binding to **β-tubulin**. This binding inhibits the **polymerization** of tubulin dimers into microtubules. Since microtubules are essential for the formation of the mitotic spindle, their absence leads to **mitotic arrest in the M-phase** (specifically metaphase), eventually triggering apoptosis. **Analysis of Incorrect Options:** * **Option A:** This describes **Etoposide** or **Teniposide**. These drugs stabilize the DNA-topoisomerase II complex, preventing the religation of DNA strands. * **Option B:** This is the mechanism of **Alkylating Agents** (e.g., Cyclophosphamide, Cisplatin). they form covalent bonds with DNA, leading to cross-linking and strand breakage. * **Option C:** This describes **Dactinomycin** (Actinomycin D), which intercalates into DNA and inhibits RNA polymerase. **High-Yield Clinical Pearls for NEET-PG:** * **Cell Cycle Specificity:** Vincristine is **M-phase specific**. * **Dose-Limiting Toxicity:** Unlike most anticancer drugs, Vincristine is **bone marrow sparing** (minimal myelosuppression). Its major side effect is **peripheral neuropathy** (stocking-glove pattern) and paralytic ileus. * **Vinca vs. Taxanes:** While Vinca alkaloids (Vincristine/Vinblastine) inhibit **polymerization**, Taxanes (Paclitaxel/Docetaxel) inhibit **depolymerization** (stabilizing microtubules). * **Contraindication:** Vincristine is **fatal if given intrathecally**; it must only be administered intravenously.

Question 135: Which of the following adverse effects may be caused by Busulfan?

A. Cystitis
B. Pulmonary fibrosis (Correct Answer)
C. Loss of hair
D. Peripheral neuropathy

Explanation: **Explanation:** **Busulfan** is an alkylating agent (specifically an alkyl sulfonate) used primarily in the treatment of Chronic Myeloid Leukemia (CML) and as a conditioning agent before bone marrow transplantation. **Why Pulmonary Fibrosis is correct:** Busulfan is notorious for causing dose-dependent interstitial pulmonary fibrosis, often referred to as **"Busulfan Lung."** This occurs due to the drug’s ability to cause oxidative stress and damage to alveolar epithelial cells, leading to fibroblast proliferation. Patients typically present with dyspnea and cough months to years after starting therapy. **Analysis of Incorrect Options:** * **A. Cystitis:** Hemorrhagic cystitis is a classic side effect of **Cyclophosphamide** and **Ifosfamide** due to the metabolite **Acrolein**. It is managed with Mesna and aggressive hydration. * **C. Loss of hair (Alopecia):** While many cytotoxic drugs cause alopecia, Busulfan is unique because it causes minimal to no hair loss at standard doses, making this an unlikely primary answer compared to the specific lung toxicity. * **D. Peripheral neuropathy:** This is the dose-limiting toxicity of **Vinca alkaloids** (Vincristine) and **Taxanes** (Paclitaxel), caused by interference with microtubule function. **High-Yield Clinical Pearls for NEET-PG:** * **Adrenal-like insufficiency:** Busulfan can cause a syndrome characterized by hyperpigmentation, wasting, and hypotension (Addisonian-like syndrome), but without actual biochemical adrenal failure. * **Mnemonic:** "B" for **B**usulfan, **B**one marrow suppression (prolonged), and **B**ig lung (fibrosis). * **Seizures:** At high doses (pre-transplant), Busulfan can cross the blood-brain barrier and cause seizures; prophylactic anticonvulsants (like Phenytoin) are often used.

Question 136: A 42-year-old woman has been diagnosed with liver cancer and is being treated with 5-FU. 5-FU is successful in destroying the tumor cells because it blocks the production of which one of the following?

A. FH4
B. dTMP (Correct Answer)
C. UMP
D. Methylcobalamin

Explanation: Explanation:Mechanism of Action (Why dTMP is correct):5-Fluorouracil (5-FU) is a pyrimidine analog and a cycle-specific antimetabolite. Inside the cell, it is converted into its active metabolite, **5-FdUMP** (5-fluorodeoxyuridine monophosphate) [1, 2]. This metabolite acts as a suicide inhibitor of the enzyme **Thymidylate Synthase** [1, 2]. Normally, this enzyme converts dUMP to **dTMP** (deoxythymidine monophosphate) by adding a methyl group [2]. By inhibiting this step, 5-FU causes a "thymineless death" of the cell, as dTMP is essential for DNA synthesis and repair [1].Analysis of Incorrect Options:* **A. FH4 (Tetrahydrofolate):** 5-FU does not block the production of FH4. However, it requires N5,N10-methylene FH4 as a co-factor to form a stable ternary complex with Thymidylate Synthase [1].* **C. UMP (Uridine Monophosphate):** 5-FU is a fluorinated analog of uracil; it mimics the precursors but does not block the initial synthesis of UMP itself.* **D. Methylcobalamin:** This is a form of Vitamin B12 involved in the conversion of homocysteine to methionine. 5-FU has no direct inhibitory effect on B12 metabolism.NEET-PG High-Yield Pearls:* **Leucovorin Rescue vs. Potentiation:** Unlike in Methotrexate toxicity (where Leucovorin is used as a "rescue"), Leucovorin is given with 5-FU to **potentiate** its action by stabilizing the binding of 5-FdUMP to Thymidylate Synthase.* **Adverse Effects:** Hand-foot syndrome (palmar-plantar erythrodysesthesia) and GI toxicity (mucositis) are characteristic.* **Dihydropyrimidine Dehydrogenase (DPD) Deficiency:** Patients with this genetic deficiency are at high risk of severe, life-threatening toxicity when given 5-FU.

Question 137: All of the following are used to limit the toxicity of cisplatin except:

A. N-acetylcysteine (Correct Answer)
B. Slow rate of infusion
C. Chloride diuresis
D. Amifostine

Explanation: The primary dose-limiting toxicity of **Cisplatin** is **nephrotoxicity** (acute tubular necrosis). This occurs because cisplatin accumulates in the renal proximal tubules, leading to oxidative stress and DNA damage [1]. **1. Why N-acetylcysteine (NAC) is the correct answer:** While NAC is a potent antioxidant and the specific antidote for **Acetaminophen (Paracetamol) toxicity**, it is **not** a standard clinical intervention used to prevent cisplatin-induced nephrotoxicity. Its role in this context remains experimental and is not part of established oncology protocols. **2. Why the other options are incorrect (Standard Preventive Measures):** * **Chloride Diuresis:** This is the most critical preventive step. Administering Cisplatin in **Normal Saline (0.9% NaCl)** maintains a high chloride concentration in the renal tubules [1]. High chloride levels suppress the conversion of cisplatin into its highly reactive (and toxic) aquated form, thereby protecting the kidneys. * **Slow Rate of Infusion:** Rapid bolus doses increase peak plasma concentrations, significantly raising the risk of renal damage. Infusing the drug slowly over several hours reduces the peak concentration reaching the kidneys. * **Amifostine:** This is a cytoprotective adjuvant (a prodrug) that is converted by alkaline phosphatase into a free thiol. It acts as a scavenger for reactive metabolites of cisplatin specifically in normal tissues, reducing nephrotoxicity without compromising antitumor efficacy [1]. **Clinical Pearls for NEET-PG:** * **Cisplatin Triad of Toxicity:** Nephrotoxicity, Ototoxicity (high-frequency hearing loss), and severe Emetogenicity (requires 5-HT3 antagonists + Dexamethasone + Aprepitant) [1]. * **Carboplatin:** A cisplatin analogue with less nephrotoxicity but significant **myelosuppression** (thrombocytopenia). * **Amifostine** is also used to reduce xerostomia (dry mouth) in patients undergoing radiotherapy.

Question 138: Which of the following is a common side effect of cisplatin?

A. Diarrhea
B. Vomiting (Correct Answer)
C. Pulmonary fibrosis
D. Alopecia

Explanation: **Explanation:** **Cisplatin** is a potent platinum-based alkylating agent used for various solid tumors [1]. It is classified as a **highly emetogenic** drug. 1. **Why Vomiting is Correct:** Cisplatin is the "gold standard" for inducing nausea and vomiting in clinical studies [2]. It triggers vomiting through two mechanisms: * **Acute phase:** Release of serotonin (5-HT) from enterochromaffin cells in the GI tract, stimulating the vagus nerve. * **Delayed phase:** Activation of neurokinin-1 (NK1) receptors by Substance P in the area postrema (Chemoreceptor Trigger Zone). Prophylaxis with 5-HT3 antagonists (Ondansetron), NK1 antagonists (Aprepitant), and Dexamethasone is mandatory [2]. 2. **Why Other Options are Incorrect:** * **Diarrhea:** While it can occur, it is not the hallmark toxicity. Drugs like **Irinotecan** (via cholinergic syndrome) or **5-Fluorouracil** are more classically associated with severe diarrhea. * **Pulmonary Fibrosis:** This is the classic dose-limiting toxicity of **Bleomycin** and **Busulfan**. * **Alopecia:** While many taxanes and anthracyclines cause severe hair loss, it is relatively less prominent with Cisplatin compared to its other toxicities. **High-Yield Clinical Pearls for NEET-PG:** * **Dose-limiting toxicity:** Nephrotoxicity (prevented by aggressive hydration and **Amifostine**, a cytoprotective agent) [2]. * **Ototoxicity:** High-frequency hearing loss and tinnitus (usually irreversible) [2]. * **Peripheral Neuropathy:** "Glove and stocking" distribution [2]. * **Electrolyte disturbances:** Characteristically causes **Hypomagnesemia** and hypokalemia. * **Carboplatin:** A related drug that is less emetogenic and nephrotoxic but causes significant **Myelosuppression** (Thrombocytopenia) [2].

Question 139: For which of the following cancers can retinoids be used for treatment?

A. Bladder
B. Cutaneous T-cell lymphoma (Correct Answer)
C. Stomach
D. Liver

Explanation: **Explanation:** Retinoids are natural and synthetic derivatives of Vitamin A that regulate cell growth, differentiation, and apoptosis by binding to specific nuclear receptors (RAR and RXR). **Why Cutaneous T-cell lymphoma (CTCL) is correct:** **Bexarotene**, a third-generation selective retinoid X receptor (RXR) agonist, is specifically FDA-approved for the treatment of refractory Cutaneous T-cell lymphoma (including Mycosis Fungoides). It induces apoptosis and inhibits the cell cycle progression of malignant T-cells. Additionally, **All-trans retinoic acid (ATRA)** is a cornerstone in treating Acute Promyelocytic Leukemia (APML) by inducing the differentiation of leukemic promyelocytes. **Why other options are incorrect:** * **Bladder, Stomach, and Liver Cancers:** While retinoids have been studied for their potential "chemopreventive" properties in various epithelial malignancies, they are not standard-of-care therapeutic agents for these solid tumors. These cancers are primarily managed with surgery, radiation, and conventional cytotoxic chemotherapy (e.g., Gemcitabine/Cisplatin for bladder, Fluorouracil for stomach). **High-Yield Clinical Pearls for NEET-PG:** * **APML (M3):** ATRA is the drug of choice. Watch for **"Differentiation Syndrome"** (fever, respiratory distress), treated with Dexamethasone. * **Acne & Psoriasis:** Isotretinoin (oral) and Tazarotene (topical) are common dermatological uses. * **Adverse Effects:** Hypertriglyceridemia, dry skin/mucosa, and **teratogenicity** (mandatory pregnancy testing is required before prescription). * **Alitretinoin:** Used topically for Kaposi Sarcoma lesions.

Question 140: Methotrexate resistance is due to?

A. Increased concentrations of intracellular dihydrofolate reductase (DHFR) through gene amplification (Correct Answer)
B. Failure of efflux pumps
C. Bacterial modification
D. Increased synthesis of polyglutamates

Explanation: **Explanation:** **Methotrexate (MTX)** is a folate antimetabolite that inhibits the enzyme **Dihydrofolate Reductase (DHFR)**. This inhibition prevents the conversion of dihydrofolate to tetrahydrofolate, halting DNA synthesis. **Why Option A is Correct:** The most common and clinically significant mechanism of resistance to Methotrexate is **gene amplification**, which leads to the **overproduction (increased concentration) of the target enzyme, DHFR**. When DHFR levels are excessively high, the standard doses of MTX are insufficient to inhibit all available enzyme sites, allowing the cancer cell to continue DNA synthesis. **Analysis of Incorrect Options:** * **Option B:** Resistance is actually associated with a **decrease in drug influx** (via reduced folate carriers) or an **increase in efflux** (via P-glycoprotein/multidrug resistance proteins), not a failure of efflux pumps. * **Option C:** Methotrexate is an anticancer/immunosuppressant drug, not an antibiotic; bacterial modification is a mechanism for antibiotic resistance (e.g., beta-lactamases). * **Option D:** MTX is converted to **polyglutamates** intracellularly, which increases its potency and duration of action. Resistance is caused by **decreased** synthesis of polyglutamates, not an increase. **High-Yield Clinical Pearls for NEET-PG:** * **Rescue Therapy:** **Leucovorin (Folinic acid)** is used to "rescue" normal cells from MTX toxicity by bypassing the inhibited DHFR enzyme. * **Adverse Effects:** Nephrotoxicity (prevented by hydration and urinary alkalinization), myelosuppression, and mucositis. * **Other Resistance Mechanisms:** Altered DHFR with reduced affinity for MTX and decreased expression of the Reduced Folate Carrier (RFC).

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

Practice Questions

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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