Anticancer Drugs Practice Questions

Q: Midostaurin is a new drug used for the treatment of which of the following conditions?

Acute Myeloid Leukemia (AML). **Explanation:** **Midostaurin** is a multi-targeted kinase inhibitor that primarily acts by inhibiting the **FLT3 (Fms-like tyrosine kinase 3)** receptor. FLT3 mutations (specifically internal tandem duplications, FLT3-ITD) are present in approximately 30% of patients with **Acute Myeloid Leukemia (AML)** and are associated with a poor prognosis. Midostaurin, when used in combination with standard induction (cytarabine and daunorubicin) and consolidation chemotherapy, significantly improves overall survival in FLT3-mutation-positive AML patients. **Analysis of Options:** * **A. Chronic Myeloid Leukemia (CML):** The mainstay of treatment for CML is BCR-ABL tyrosine kinase inhibitors like **Imatinib**, Dasatinib, or Nilotinib. Midostaurin does not target the Philadelphia chromosome. * **B. Acute Lymphoblastic Leukemia (ALL):** Treatment involves complex regimens (e.g., Vincristine, Steroids, L-Asparaginase). While some ALL cases are Ph+, they are treated with BCR-ABL inhibitors, not Midostaurin. * **D. Chronic Lymphocytic Leukemia (CLL):** CLL management typically involves BTK inhibitors (Ibrutinib), BCL-2 inhibitors (Venetoclax), or anti-CD20 monoclonal antibodies (Rituximab). **High-Yield Clinical Pearls for NEET-PG:** * **Mechanism:** Multi-kinase inhibitor (FLT3, KIT, PKC, and VEGFR). * **Other Indications:** Apart from AML, Midostaurin is also FDA-approved for **Advanced Systemic Mastocytosis** (targeting the KIT mutation). * **Side Effects:** Most common include nausea, vomiting, febrile neutropenia, and potential QTc prolongation. * **FLT3 Inhibitors:** Other drugs in this class include **Gilteritinib** (selective for FLT3) and **Sorafenib**.

Q: Which of the following drug classes is known to cause sterility?

Alkylating agents. **Explanation:** **Alkylating agents** (e.g., Cyclophosphamide, Busulfan, Procarbazine) are the most common class of antineoplastics associated with **gonadal toxicity and permanent sterility**. These drugs are cell-cycle non-specific and work by forming covalent bonds with DNA, leading to cross-linking and strand breaks. Because they target rapidly dividing cells, they significantly damage the germinal epithelium of the testes (causing oligospermia/azoospermia) and the ovarian follicles (leading to premature ovarian failure). The risk is dose-dependent and higher in post-pubertal patients. **Analysis of Incorrect Options:** * **Vinca Alkaloids (e.g., Vincristine):** These are M-phase specific drugs that inhibit microtubule polymerization. Their primary dose-limiting toxicity is **neurotoxicity** (peripheral neuropathy) rather than permanent sterility. * **Antimetabolites (e.g., Methotrexate, 5-FU):** These S-phase specific drugs interfere with DNA synthesis. While they can cause transient infertility during treatment, they are rarely associated with permanent gonadal failure compared to alkylating agents. * **Actinomycin D:** An antitumor antibiotic that intercalates into DNA. Its major toxicities include bone marrow suppression and GI upset, but it is not a classic cause of permanent sterility. **NEET-PG High-Yield Pearls:** * **Busulfan:** Specifically known for causing "Busulfan Lung" (pulmonary fibrosis) and severe marrow suppression before bone marrow transplant. * **Cyclophosphamide:** Associated with **Hemorrhagic Cystitis** (prevented by **MESNA** and hydration). * **Procarbazine:** Has high leukemogenic potential and can cause a **Disulfiram-like reaction** with alcohol. * **Ovarian protection:** GnRH agonists are sometimes used during chemotherapy to "quiet" the ovaries and reduce the risk of premature menopause.

Q: Which of the following drugs is NOT commonly used in the treatment of Non-Hodgkin lymphoma?

Cisplatin. **Explanation:** The standard first-line treatment for most types of Non-Hodgkin Lymphoma (NHL), particularly Diffuse Large B-Cell Lymphoma (DLBCL), is the **CHOP** or **R-CHOP** regimen. **Why Cisplatin is the Correct Answer:** While **Cisplatin** is a potent platinum-based alkylating agent, it is **not** part of the standard primary induction therapy for NHL. It is typically reserved for **salvage therapy** (e.g., DHAP or ESHAP regimens) in patients with relapsed or refractory disease. In contrast, the drugs listed in options A, B, and C are the core components of the standard frontline CHOP regimen. **Analysis of Incorrect Options:** * **Cyclophosphamide (C):** An alkylating agent (nitrogen mustard) that forms DNA cross-links. It is the "C" in CHOP. * **Doxorubicin (H):** An anthracycline antibiotic (Hydroxydaunorubicin) that inhibits Topoisomerase II and generates free radicals. It is the "H" in CHOP. * **Vincristine (O):** A vinca alkaloid that inhibits microtubule polymerization (Oncovin). It is the "O" in CHOP. * *(Note: The "P" in CHOP stands for Prednisolone).* **High-Yield Clinical Pearls for NEET-PG:** * **R-CHOP:** The addition of **Rituximab** (anti-CD20 monoclonal antibody) has significantly improved survival in CD20+ B-cell lymphomas. * **Dose-Limiting Toxicities:** * **Cyclophosphamide:** Hemorrhagic cystitis (prevented by **MESNA**). * **Doxorubicin:** Cardiotoxicity (dilated cardiomyopathy). * **Vincristine:** Peripheral neuropathy (areflexia/paresthesia) and paralytic ileus. * **Cisplatin:** Nephrotoxicity and Ototoxicity. * **Burkitt Lymphoma:** Often requires more intensive regimens like Hyper-CVAD rather than standard CHOP.

Q: Which drug arrests mitosis in metaphase?

Vinca Alkaloids. **Explanation:** The correct answer is **Vinca Alkaloids (Option C)**. **Mechanism of Action:** Vinca alkaloids (e.g., Vincristine, Vinblastine) are **cell cycle-specific** agents that act during the **M-phase (Mitosis)**. They bind to tubulin and inhibit its polymerization into microtubules. This prevents the formation of the mitotic spindle, which is essential for chromosome separation. Consequently, the cell cannot progress beyond metaphase, leading to **mitotic arrest** and subsequent apoptosis. **Analysis of Incorrect Options:** * **A. Busulfan:** An **Alkylating agent** that works by cross-linking DNA strands. It is cell cycle-nonspecific and is notably used in chronic myeloid leukemia (CML) and bone marrow ablation. * **B. 5-Fluorouracil (5-FU):** An **Antimetabolite (Pyrimidine analog)** that inhibits thymidylate synthase. It acts specifically during the **S-phase** (DNA synthesis) of the cell cycle. * **C. Methotrexate:** A **Folate antagonist** that inhibits dihydrofolate reductase (DHFR). Like 5-FU, it is **S-phase specific**, preventing the synthesis of DNA, RNA, and proteins. **High-Yield Clinical Pearls for NEET-PG:** * **Vincristine vs. Vinblastine Toxicity:** Remember the mnemonic: **"Vincristine blasts the Nerves"** (Peripheral neuropathy is the dose-limiting toxicity) and **"Vinblastine blasts the Bone marrow"** (Bone marrow suppression is the dose-limiting toxicity). * **Taxanes (e.g., Paclitaxel):** These also act on the M-phase but have the *opposite* mechanism—they **stabilize** microtubules (preventing depolymerization), "freezing" the cell in mitosis. * **Vinca Alkaloids** are fatal if administered intrathecally; they must only be given intravenously.

Q: What is the drug of choice for Choriocarcinoma?

Methotrexate. **Explanation:** **Methotrexate (MTX)** is the drug of choice for **Choriocarcinoma** (a highly malignant trophoblastic tumor). The underlying medical concept is that choriocarcinoma cells are exquisitely sensitive to folate antagonists. Methotrexate works by inhibiting the enzyme **Dihydrofolate Reductase (DHFR)**, preventing the conversion of dihydrofolate to tetrahydrofolate. This halts DNA synthesis and cell proliferation. In low-risk gestational trophoblastic neoplasia (GTN), MTX is used as monotherapy (often with Leucovorin rescue), achieving nearly 100% cure rates. **Analysis of Incorrect Options:** * **B. Actinomycin-D (Dactinomycin):** While highly effective and used as a second-line agent or in combination (EMA-CO regimen) for high-risk cases, it is generally considered the alternative to Methotrexate, not the primary drug of choice for initial single-agent therapy. * **C. Vincristine:** This is a vinca alkaloid that inhibits microtubule assembly. It is part of the EMA-CO regimen for high-risk choriocarcinoma but is never used as a first-line monotherapy. * **D. 6-Thioguanine:** This is a purine analog primarily used in the treatment of Acute Myeloid Leukemia (AML). It has no significant role in the management of choriocarcinoma. **High-Yield Clinical Pearls for NEET-PG:** * **Leucovorin (Folinic Acid) Rescue:** Used to minimize MTX toxicity by providing a source of reduced folate that bypasses DHFR. * **Monitoring:** Therapeutic success in choriocarcinoma is uniquely monitored using **serum β-hCG levels**. * **Other uses of MTX:** Ectopic pregnancy (medical management), Rheumatoid Arthritis (Disease-modifying antirheumatic drug - DMARD), and Psoriasis. * **Side Effects:** Hepatotoxicity, pulmonary fibrosis, and mucositis.

Q: Which of the following is an indication for the use of folinic acid?

Counteracting toxicity of high-dose methotrexate therapy. ### Explanation **Correct Option: B. Counteracting toxicity of high-dose methotrexate therapy** **Mechanism of Action:** Methotrexate (MTX) is a folate antagonist that inhibits the enzyme **dihydrofolate reductase (DHFR)**. This inhibition prevents the conversion of dihydrofolate to tetrahydrofolate (THF), the active form of folic acid required for DNA synthesis. **Folinic acid (Leucovorin)** is a reduced form of folate (5-formyl-THF) that does not require DHFR for its activity. When administered after high-dose MTX, it "bypasses" the metabolic block, providing a source of active folate to healthy cells. This process is known as **"Leucovorin Rescue,"** and it prevents lethal bone marrow and gastrointestinal toxicity. **Analysis of Incorrect Options:** * **Option A:** Prophylaxis of neural tube defects requires **Folic acid**, not folinic acid. Folic acid is sufficient for supplementation in pregnancy as DHFR activity is normal. * **Option C:** Pernicious anemia is caused by **Vitamin B12 deficiency**. While folate can temporarily improve the hematological profile, it fails to treat the underlying neurological damage and is therefore contraindicated as monotherapy. * **Option D:** Anemia of renal failure is primarily due to a deficiency of **Erythropoietin**, which is the standard treatment. **High-Yield NEET-PG Pearls:** * **Leucovorin/Folinic Acid** is also used to **potentiate** the action of **5-Fluorouracil (5-FU)** in colorectal cancer by stabilizing the binding of 5-dUMP to thymidylate synthase. * **Glucarpidase** is an alternative used for MTX toxicity in patients with renal failure (it enzymatically degrades MTX). * **Methotrexate Toxicity:** Common side effects include myelosuppression, mucositis, and nephrotoxicity (due to crystalluria). Always ensure adequate hydration and urinary alkalinization.

Q: All of the following are true about rituximab except?

Dose-independent pharmacokinetics. **Explanation:** Rituximab is a landmark therapeutic agent in oncology and rheumatology. The correct answer is **D** because Rituximab exhibits **dose-dependent (non-linear) pharmacokinetics**, not dose-independent. Its clearance is influenced by the "tumor burden"; as CD-20 receptors are saturated and B-cells are depleted, the clearance rate decreases and the half-life increases. **Analysis of Options:** * **Option A (True):** Rituximab is a **chimeric** (mouse/human) monoclonal antibody. It specifically targets the **CD-20 antigen** found on the surface of normal and malignant B-lymphocytes. * **Option B (True):** The **most common side effect** is an **infusion-related reaction** (fever, chills, rigors), typically occurring during the first infusion due to cytokine release. Pre-medication with acetaminophen and antihistamines is standard practice. * **Option C (True):** Rituximab holds the historical distinction of being the **first monoclonal antibody approved by the FDA (1997)** for the treatment of cancer, specifically for relapsed or refractory low-grade B-cell non-Hodgkin's lymphoma. **High-Yield Clinical Pearls for NEET-PG:** 1. **Mechanism of Action:** Causes B-cell lysis via Antibody-Dependent Cellular Cytotoxicity (ADCC), Complement-Dependent Cytotoxicity (CDC), and apoptosis. 2. **Major Risk:** It can cause **Reactivation of Hepatitis B**. Screening for HBsAg and anti-HBc is mandatory before starting therapy. 3. **Rare but Fatal Side Effect:** Progressive Multifocal Leukoencephalopathy (PML) due to JC virus reactivation. 4. **Clinical Uses:** NHL, CLL, Rheumatoid Arthritis (refractory to TNF inhibitors), Wegener’s Granulomatosis, and Pemphigus Vulgaris.

Q: Which of the following anticancer drugs has a high emetogenic potential?

Cisplatin. **Explanation:** **Cisplatin** is the correct answer because it is classified as a **highly emetogenic** chemotherapy agent (Level 5, >90% frequency of emesis without prophylaxis). The underlying mechanism involves the release of serotonin (5-HT) from enterochromaffin cells in the GI tract and the stimulation of the Chemoreceptor Trigger Zone (CTZ) in the area postrema. Due to its high emetic potential, patients receiving Cisplatin require aggressive prophylactic antiemetic therapy, typically a "triple regimen" consisting of a 5-HT3 antagonist (e.g., Ondansetron), a NK1 receptor antagonist (e.g., Aprepitant), and Dexamethasone. **Analysis of Incorrect Options:** * **Chlorambucil (A):** An alkylating agent used primarily in CLL. It is administered orally and has **low emetogenic potential**. * **Vincristine (B):** A vinca alkaloid that inhibits microtubule assembly. It is notorious for peripheral neuropathy but has **minimal emetogenic potential**. * **6-Mercaptopurine (C):** A purine antimetabolite used in ALL maintenance therapy. It is associated with bone marrow suppression and hepatotoxicity but has **low emetogenic potential**. **High-Yield Clinical Pearls for NEET-PG:** * **Cisplatin Toxicity Profile:** Remember the "3 Ns"—**N**ephrotoxicity (prevented by aggressive hydration/Amifostine), **N**eurotoxicity (peripheral neuropathy), and **N**ausea/Vomiting (highly emetogenic). It also causes **Ototoxicity** (high-frequency hearing loss). * **Highly Emetogenic Drugs:** Apart from Cisplatin, other high-risk drugs include Cyclophosphamide (>1500 mg/m²), Dacarbazine, and Anthracycline/Cyclophosphamide combinations (AC regimen). * **Drug of Choice for Cisplatin-induced vomiting:** 5-HT3 antagonists (Ondansetron) are the mainstay for acute emesis, while Aprepitant is preferred for delayed emesis.

Q: Fluorouracil undergoes in vivo chemical changes resulting in a covalent complex bound to both thymidylate synthase and methylene-tetrahydrofolate. What type of inhibition is responsible for the subsequent blockage of deoxythymidilate formation and cell division?

Irreversible inhibition. **Explanation:** **Mechanism of Action (Why C is correct):** 5-Fluorouracil (5-FU) is a pyrimidine analog that acts as a "suicide inhibitor." Once inside the cell, it is converted to **5-FdUMP** (5-fluorodeoxyuridine monophosphate). This metabolite acts as a false substrate and forms a stable, **covalent ternary complex** with the enzyme **Thymidylate Synthase (TS)** and the cofactor **5,10-methylene tetrahydrofolate**. Because the bond is covalent and the enzyme is permanently inactivated, this is classified as **Irreversible Inhibition**. This prevents the conversion of dUMP to dTMP, leading to a "thymineless death" of the cell. **Analysis of Incorrect Options:** * **A. Allosteric inhibition:** This involves binding to a site other than the active site to induce a conformational change. 5-FU binds directly to the active site. * **B. Competitive inhibition:** While 5-FdUMP competes for the active site initially, the formation of a permanent covalent bond makes the inhibition irreversible (non-competitive in kinetics over time), as it cannot be reversed by increasing substrate concentration. * **D. Noncovalent inhibition:** The hallmark of 5-FU’s action is the formation of a **covalent** bond; noncovalent interactions are reversible and weaker. **NEET-PG High-Yield Pearls:** * **Rescue Agent:** Leucovorin (folinic acid) is administered with 5-FU not to reduce toxicity, but to **potentiate** its efficacy by stabilizing the ternary complex. * **Rate-limiting Enzyme:** Dihydropyrimidine dehydrogenase (DPD) degrades 5-FU. Patients with **DPD deficiency** are at high risk of severe 5-FU toxicity (pancytopenia, mucosal ulceration). * **Specific Toxicity:** Hand-foot syndrome (palmar-plantar erythrodysesthesia) is a characteristic side effect.

Question 1

Midostaurin is a new drug used for the treatment of which of the following conditions?

Accepted Answer

Acute Myeloid Leukemia (AML)

Answer

Chronic Myeloid Leukemia (CML)

Answer

Acute Lymphoblastic Leukemia (ALL)

Answer

Chronic Lymphocytic Leukemia (CLL)

Question 2

Which of the following drug classes is known to cause sterility?

Accepted Answer

Alkylating agents

Answer

Vinca alkaloids

Answer

Antimetabolites

Answer

Actinomycin D

Question 3

Which of the following drugs is NOT commonly used in the treatment of Non-Hodgkin lymphoma?

Accepted Answer

Cisplatin

Answer

Doxorubicin

Answer

Cyclophosphamide

Answer

Vincristine

Question 4

Which drug arrests mitosis in metaphase?

Accepted Answer

Vinca Alkaloids

Answer

Busulfan

Answer

5-fluorouracil

Answer

Methotrexate

Question 5

What is the drug of choice for Choriocarcinoma?

Accepted Answer

Methotrexate

Answer

Actinomycin-D

Answer

Vincristine

Answer

6-thioguanine

Question 6

Which of the following medications are essential for ameliorating the toxicity of pemetrexed?

Accepted Answer

Folinic acid and vitamin B12

Answer

Folic acid and vitamin B12

Answer

Vitamin B6 and Vitamin B1

Answer

Folic acid and dexamethasone

Question 7

Which of the following is an indication for the use of folinic acid?

Accepted Answer

Counteracting toxicity of high-dose methotrexate therapy

Answer

Prophylaxis of neural tube defects in the offspring of women receiving anticonvulsant medications

Answer

Pernicious anemia

Answer

Anemia associated with renal failure

Question 8

All of the following are true about rituximab except?

Accepted Answer

Dose-independent pharmacokinetics

Answer

Chimeric monoclonal antibody against CD-20 B cell antigen

Answer

Most common side effect is infusion reaction

Answer

First FDA drug approved for resistant lymphomas

Question 9

Which of the following anticancer drugs has a high emetogenic potential?

Accepted Answer

Cisplatin

Answer

Chlorambucil

Answer

Vincristine

Answer

6-Mercaptopurine

Question 10

Fluorouracil undergoes in vivo chemical changes resulting in a covalent complex bound to both thymidylate synthase and methylene-tetrahydrofolate. What type of inhibition is responsible for the subsequent blockage of deoxythymidilate formation and cell division?

Accepted Answer

Irreversible inhibition

Answer

Allosteric inhibition

Answer

Competitive inhibition

Answer

Noncovalent inhibition

Anticancer Drugs — MCQs

Anticancer Drugs — MCQs

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