Anticancer Drugs Practice Questions

Q: Which of the following statements about rituximab is FALSE?

It has dose-dependent kinetics.. **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.

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

Vincristine. **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.

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

Rituximab. **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**.

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

Pulmonary fibrosis. **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.

Q: 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?

dTMP. 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.

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

N-acetylcysteine. 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.

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

Vomiting. **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].

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

Cutaneous T-cell lymphoma. **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 1

Which of the following statements about rituximab is FALSE?

Accepted Answer

It has dose-dependent kinetics.

Answer

It is a chimeric monoclonal antibody against CD-20.

Answer

It is used for the treatment of non-Hodgkin lymphoma.

Answer

Its most common adverse effect is infusion-related reactions.

Question 2

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

Accepted Answer

Vincristine

Answer

Papaverine

Answer

Ephedrine

Answer

Atropine

Question 3

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

Accepted Answer

Rituximab

Answer

Cyclophosphamide

Answer

Trastuzumab

Answer

Denosumab

Question 4

What is the mechanism of action of vincristine in the treatment of cancers?

Accepted Answer

Inhibition of polymerization of tubulin to form microtubules

Answer

Inhibition of topoisomerase II to cause breaks in DNA strands

Answer

Alkylation and cross-linking DNA strands

Answer

Inhibition of DNA-mediated RNA synthesis

Question 5

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

Accepted Answer

Pulmonary fibrosis

Answer

Cystitis

Answer

Loss of hair

Answer

Peripheral neuropathy

Question 6

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?

Accepted Answer

dTMP

Answer

FH4

Answer

UMP

Answer

Methylcobalamin

Question 7

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

Accepted Answer

N-acetylcysteine

Answer

Slow rate of infusion

Answer

Chloride diuresis

Answer

Amifostine

Question 8

Which of the following is a common side effect of cisplatin?

Accepted Answer

Vomiting

Answer

Diarrhea

Answer

Pulmonary fibrosis

Answer

Alopecia

Question 9

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

Accepted Answer

Cutaneous T-cell lymphoma

Answer

Bladder

Answer

Stomach

Answer

Liver

Question 10

Methotrexate resistance is due to?

Accepted Answer

Increased concentrations of intracellular dihydrofolate reductase (DHFR) through gene amplification

Answer

Failure of efflux pumps

Answer

Bacterial modification

Answer

Increased synthesis of polyglutamates

Anticancer Drugs — MCQs

Anticancer Drugs — MCQs

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