Anticancer Drugs Practice Questions

Q: Which of the following monoclonal antibodies is used for the treatment of colorectal carcinoma?

Cetuximab. **Explanation:** **Correct Answer: B. Cetuximab** Cetuximab is a recombinant human/mouse chimeric monoclonal antibody that targets the **Epidermal Growth Factor Receptor (EGFR)**. In colorectal carcinoma, EGFR is often overexpressed, leading to uncontrolled cell proliferation. By binding to the extracellular domain of EGFR, Cetuximab inhibits downstream signaling pathways (like KRAS/MAPK). * **High-Yield Note:** It is only effective in patients with **wild-type KRAS** genes. If a patient has a KRAS mutation, the pathway remains "on" regardless of EGFR inhibition, making the drug ineffective. **Incorrect Options:** * **A. Pembrolizumab:** This is a **PD-1 inhibitor** (checkpoint inhibitor). While used for various solid tumors, its specific indication in colorectal cancer is limited to cases with **Microsatellite Instability-High (MSI-H)** or mismatch repair deficiency (dMMR), rather than being the primary targeted therapy for general colorectal carcinoma. * **C. Rituximab:** This is a chimeric monoclonal antibody against **CD20**, primarily found on B-cells. It is used in the treatment of Non-Hodgkin Lymphoma (NHL), Chronic Lymphocytic Leukemia (CLL), and autoimmune conditions like Rheumatoid Arthritis. * **D. Natalizumab:** This antibody targets **α4-integrin**. It is used in the management of **Multiple Sclerosis** and Crohn’s disease by preventing leukocyte migration into inflamed tissues. **Clinical Pearls for NEET-PG:** 1. **Panitumumab** is another EGFR inhibitor used in colorectal cancer (fully humanized). 2. **Bevacizumab** (anti-VEGF) is also used in colorectal cancer to inhibit angiogenesis. 3. **Side Effect:** EGFR inhibitors like Cetuximab characteristically cause an **acneiform skin rash**; the presence of the rash often correlates with a positive therapeutic response.

Q: Irreversible ototoxicity is caused by which of the following drugs?

Cisplatin. **Explanation:** **Cisplatin** is a potent platinum-based alkylating agent used for various solid tumors. Its most characteristic dose-limiting toxicities are **nephrotoxicity** and **ototoxicity**. The ototoxicity is typically **bilateral, progressive, and irreversible**. It occurs because cisplatin induces the formation of reactive oxygen species (ROS) in the stria vascularis and hair cells of the cochlea, leading to permanent cell death. It initially affects high-frequency hearing (tinnitus is an early sign) before progressing to lower frequencies. **Analysis of Incorrect Options:** * **Cyclophosphamide:** Known primarily for **hemorrhagic cystitis** (due to the metabolite acrolein) and bone marrow suppression. It does not cause significant ototoxicity. * **Bleomycin:** Its most notorious side effect is **pulmonary fibrosis** and skin hyperpigmentation. It is "myelosuppressive-sparing" and does not affect hearing. * **Chlorambucil:** An alkylating agent used mainly in Chronic Lymphocytic Leukemia (CLL). Its primary toxicity is myelosuppression and potential secondary malignancies; it is not associated with ototoxicity. **Clinical Pearls for NEET-PG:** * **Amifostine:** A cytoprotective agent (free radical scavenger) that can be used to reduce cisplatin-induced nephrotoxicity. * **Vigorous Hydration:** The primary preventive measure for cisplatin-induced renal damage. * **Emetogenic Potential:** Cisplatin is the most highly emetogenic chemotherapy drug (requires NK1 receptor antagonists like Aprepitant). * **Other Ototoxic Drugs:** Remember the mnemonic "SALTA" (Salicylates, Aminoglycosides, Loop diuretics, Thalidomide, Antimalarials/Anticancer like Cisplatin).

Q: Which of the following drugs has the least bone marrow suppression?

Vincristine. The correct answer is **Vincristine**. ### **Explanation** The primary dose-limiting toxicity of most cytotoxic chemotherapy agents is **myelosuppression** (bone marrow suppression). However, certain drugs are known for being "bone marrow sparing." **Vincristine**, a Vinca alkaloid that inhibits microtubule assembly (mitotic inhibitor), is unique because it causes **minimal to no bone marrow suppression**. Its dose-limiting toxicity is instead **peripheral neuropathy** (paresthesia, loss of deep tendon reflexes, and autonomic dysfunction like constipation). ### **Analysis of Incorrect Options** * **Cisplatin:** A platinum compound known for being highly emetogenic and nephrotoxic, but it also causes significant cumulative myelosuppression. * **Cyclophosphamide:** An alkylating agent that causes significant neutropenia. Its other classic side effect is hemorrhagic cystitis (prevented by Mesna). * **Methotrexate:** An antimetabolite (folate antagonist) that is highly myelosuppressive. This effect is managed using "Leucovorin rescue." ### **High-Yield Clinical Pearls for NEET-PG** * **Bone Marrow Sparing Agents:** Remember the mnemonic **"V-B-L-S"** for drugs with minimal myelosuppression: **V**incristine, **B**leomycin (Lung fibrosis), **L**-Asparaginase (Pancreatitis/Thrombosis), and **S**teroids. * **Vincristine vs. Vinblastine:** While they belong to the same class, **V**inblastine "**B**lasts" the bone marrow (highly myelosuppressive), whereas **V**incristine spares it. * **Vincristine Warning:** It is **fatal if given intrathecally**; it must only be administered intravenously.

Q: A patient undergoing chemotherapy for two weeks for a mediastinal tumor develops high-frequency hearing loss. What is the most probable cause of this condition?

Cisplatin. ### Explanation **Correct Option: A. Cisplatin** Cisplatin is a potent platinum-based alkylating agent used for various solid tumors (e.g., testicular, lung, and mediastinal tumors). Its most characteristic dose-limiting toxicities are **nephrotoxicity** and **ototoxicity**. * **Mechanism of Ototoxicity:** Cisplatin causes the generation of reactive oxygen species (ROS) in the **stria vascularis** and destroys the **outer hair cells** of the organ of Corti. * **Clinical Presentation:** It typically presents as bilateral, irreversible, **high-frequency hearing loss** (tinnitus is often the first sign). This aligns perfectly with the patient's symptoms. **Why Incorrect Options are Wrong:** * **B. Etoposide:** A topoisomerase II inhibitor primarily associated with **myelosuppression** and secondary leukemias. It does not cause hearing loss. * **C. Doxorubicin:** An anthracycline antibiotic famous for **cardiotoxicity** (dilated cardiomyopathy) due to free radical generation in the myocardium. * **D. Methotrexate:** An antimetabolite (folate antagonist) known for **mucositis**, bone marrow suppression, and hepatotoxicity. It is not ototoxic. **High-Yield Clinical Pearls for NEET-PG:** * **Amifostine:** A cytoprotective agent (free radical scavenger) used to reduce cisplatin-induced nephrotoxicity. * **Vigorous Hydration:** The primary strategy to prevent cisplatin-induced renal damage. * **Emetic Potential:** Cisplatin is the most highly emetogenic chemotherapy drug (requires NK1 receptor antagonists like Aprepitant). * **Other Ototoxic Drugs:** Loop diuretics (Furosemide), Aminoglycosides (Gentamicin), and Vancomycin. When combined with Cisplatin, the risk of permanent deafness increases significantly.

Q: Which of the following is an anti-CD20 monoclonal antibody?

Tositumomab. **Explanation:** **Tositumomab** is a murine IgG1 monoclonal antibody directed against the **CD20 antigen**, which is primarily expressed on the surface of normal and malignant B-lymphocytes. It is often used as a radiopharmaceutical (Iodine-131 tositumomab) for the treatment of relapsed or refractory follicular lymphoma. By binding to CD20, it induces cell death through antibody-dependent cell-mediated cytotoxicity (ADCC), complement-dependent cytotoxicity (CDC), and apoptosis. **Analysis of Incorrect Options:** * **Alemtuzumab (Option A):** This is a monoclonal antibody directed against **CD52**, found on B and T lymphocytes. It is used in Chronic Lymphocytic Leukemia (CLL) and Multiple Sclerosis. * **Bevacizumab (Option B):** This is an angiogenesis inhibitor that targets **VEGF (Vascular Endothelial Growth Factor)**, not a surface cluster of differentiation (CD) marker. It is used in colorectal, lung, and renal cancers. * **Gemtuzumab (Option C):** This is an antibody-drug conjugate directed against **CD33**, which is expressed on leukemic blasts in Acute Myeloid Leukemia (AML). **High-Yield Clinical Pearls for NEET-PG:** * **CD20 Inhibitors:** Other high-yield anti-CD20 antibodies include **Rituximab** (chimeric), **Ofatumumab** (human), and **Obinutuzumab**. * **Mnemonic for CD Markers:** * **C**-D**20** = **R**ituximab (**20** looks like **R** flipped). * **C**-D**33** = **G**emtuzumab (**3** looks like **G**). * **C**-D**52** = **A**lemtuzumab (**5-2** = 3; but remember it as the "A" drug). * **Trastuzumab** targets **HER2/neu** (ErbB2) and is a classic question for breast cancer management.

Q: What is the mechanism of action of tacrolimus?

Calcineurin inhibitor. **Explanation:** **Mechanism of Action (Correct Answer: B)** Tacrolimus (FK506) is a potent immunosuppressant that belongs to the class of **Calcineurin Inhibitors**. It binds to an intracellular protein called **FK-binding protein (FKBP-12)**. This tacrolimus-FKBP complex then inhibits calcineurin, a phosphatase responsible for dephosphorylating the **Nuclear Factor of Activated T-cells (NFAT)**. Without dephosphorylation, NFAT cannot enter the nucleus to promote the transcription of **Interleukin-2 (IL-2)** and other cytokines, thereby preventing T-lymphocyte activation. **Analysis of Incorrect Options:** * **A. Folate antagonist:** This describes drugs like **Methotrexate**, which inhibit dihydrofolate reductase (DHFR) to interfere with DNA synthesis. * **C. Antimetabolite:** This refers to drugs like **5-Fluorouracil, Azathioprine, or Cytarabine** that mimic natural substrates to inhibit nucleic acid synthesis. * **D. CD 20 antibody:** This is the mechanism of **Rituximab**, a monoclonal antibody used in B-cell lymphomas and certain autoimmune conditions. **High-Yield Clinical Pearls for NEET-PG:** * **Clinical Use:** Primary drug for preventing organ rejection in liver, kidney, and heart transplants; also used topically for atopic dermatitis. * **Side Effects:** Nephrotoxicity (most common), neurotoxicity (tremors, seizures), and **post-transplant diabetes mellitus (PTDM)**. * **Comparison:** Unlike Cyclosporine (which binds to Cyclophilin), Tacrolimus is more potent and does **not** typically cause gingival hyperplasia or hirsutism. * **Metabolism:** It is metabolized by **CYP3A4**; therefore, grapefruit juice and macrolides can increase its toxicity.

Q: Red discoloration of urine is seen with which of the following medications?

Doxorubicin. **Explanation:** **Doxorubicin** (and its analog Daunorubicin) is an Anthracycline antibiotic used in cancer chemotherapy. The correct answer is Doxorubicin because it is a **naturally red-colored compound**. After administration, the drug and its metabolites are excreted via the kidneys, leading to a benign but striking **red discoloration of the urine** (chromaturia). Patients should be counseled about this side effect to prevent unnecessary alarm. **Analysis of Incorrect Options:** * **Methotrexate:** An antimetabolite (folate antagonist) primarily known for causing myelosuppression, mucositis, and hepatotoxicity. It does not typically change urine color. * **Cytarabine (Ara-C):** A pyrimidine antagonist used in leukemias. Its major dose-limiting toxicity is myelosuppression and cerebellar ataxia at high doses. * **Cisplatin:** A platinum compound known for its significant **nephrotoxicity** and ototoxicity. While it affects the kidneys, it does not cause red discoloration of urine. **High-Yield Clinical Pearls for NEET-PG:** * **Cardiotoxicity:** The most serious side effect of Doxorubicin is cumulative, dose-dependent cardiotoxicity (dilated cardiomyopathy). **Dexrazoxane** is the iron-chelating agent used to prevent this. * **Mechanism:** Anthracyclines work by inhibiting **Topoisomerase II**, intercalating DNA, and generating free radicals. * **Other "Red" Drugs:** Apart from Doxorubicin, **Rifampin** (antitubercular) and **Clofazimine** (antileprotic) are classic causes of red/orange discoloration of body fluids. * **Cyclophosphamide:** Contrast this with Doxorubicin; Cyclophosphamide causes **Hemorrhagic Cystitis** (bloody urine), which is prevented by **MESNA**.

Q: Which type of alkylating antineoplastic drug is Lomustine?

Nitrosoureas. **Explanation:** Alkylating agents are a class of antineoplastic drugs that act by attaching alkyl groups to DNA, leading to cross-linking and strand breaks. **Lomustine (CCNU)** belongs to the **Nitrosourea** sub-class. **Why Nitrosoureas is correct:** Nitrosoureas, including **Lomustine, Carmustine (BCNU), and Semustine**, are highly lipid-soluble, non-ionized compounds. This characteristic allows them to readily cross the **blood-brain barrier (BBB)**. Consequently, they are the drugs of choice for treating primary brain tumors (e.g., glioblastoma multiforme) and meningeal leukemia. **Analysis of Incorrect Options:** * **Nitrogen mustards:** This group includes drugs like Cyclophosphamide, Ifosfamide, and Mechlorethamine. While they are alkylating agents, their chemical structure and clinical applications differ from nitrosoureas. * **Alkyl sulfonate:** The classic example is **Busulfan**, primarily used in Chronic Myeloid Leukemia (CML) and known for causing pulmonary fibrosis. * **Triazine:** This group includes **Dacarbazine and Temozolomide**. While Temozolomide also crosses the BBB, Lomustine is chemically classified specifically as a nitrosourea. **High-Yield Clinical Pearls for NEET-PG:** * **Mechanism:** Nitrosoureas require non-enzymatic activation to form carbonium ions that alkylate DNA. * **Toxicity:** A unique feature of nitrosoureas is **delayed myelosuppression** (occurring 4–6 weeks after administration). * **Mnemonic:** Remember the "mustines" (**Car**mustine, **Lo**mustine, **Se**mustine) are **Nitrosoureas** that go to the **CNS**.

Q: Methotrexate is often used as a chemotherapeutic agent to treat patients with leukemia. This drug is effective because it inhibits cells in which phase of the cell cycle?

S phase. **Explanation:** **Mechanism of Action (Why S phase is correct):** Methotrexate (MTX) is a folate antagonist and a classic example of a **Cell Cycle Specific (CCS)** drug. It works by competitively inhibiting the enzyme **Dihydrofolate Reductase (DHFR)**. This inhibition prevents the conversion of dihydrofolate to tetrahydrofolate (the active form). Tetrahydrofolate is a crucial cofactor required for the synthesis of thymidylate and purine nucleotides. Since DNA synthesis and replication occur exclusively during the **S phase (Synthesis phase)** of the cell cycle, MTX exerts its cytotoxic effect by halting DNA production during this specific window. **Analysis of Incorrect Options:** * **G1 phase (Gap 1):** This is the pre-synthetic phase where organelles and proteins are produced. While some drugs like L-asparaginase act here, MTX does not target the metabolic processes specific to G1. * **G2 phase (Gap 2):** This phase involves the synthesis of RNA and proteins required for spindle formation. Drugs like **Bleomycin** and **Etoposide** primarily act in the G2 phase. * **M phase (Mitosis):** This involves physical cell division. Drugs that target microtubules, such as **Vinca alkaloids** (Vincristine, Vinblastine) and **Taxanes** (Paclitaxel), are specific to the M phase. **High-Yield Clinical Pearls for NEET-PG:** * **Rescue Therapy:** High-dose MTX toxicity is managed with **Leucovorin (Folinic acid)**, which bypasses the blocked DHFR enzyme to provide a source of reduced folate to healthy cells. * **Resistance:** Most common mechanism of resistance is a change in the affinity of DHFR or decreased uptake by the folate carrier. * **Adverse Effects:** Nephrotoxicity (due to crystalluria), Hepatotoxicity (cirrhosis with long-term use), and Pulmonary fibrosis. * **Other Uses:** Apart from leukemia, it is a first-line Disease-Modifying Antirheumatic Drug (DMARD) for Rheumatoid Arthritis and is used for Ectopic Pregnancy and Psoriasis.

Q: Which enzyme deficiency leads to serious side effects with 5-Fluorouracil?

Dihydropyrimidine dehydrogenase. **Explanation:** **1. Why Dihydropyrimidine dehydrogenase (DPD) is correct:** 5-Fluorouracil (5-FU) is a pyrimidine antimetabolite used in treating solid tumors (e.g., colorectal and breast cancer). **DPD is the rate-limiting enzyme responsible for the catabolism (breakdown) of over 80% of administered 5-FU** into inactive metabolites. If a patient has a genetic deficiency of DPD, 5-FU is not cleared efficiently, leading to toxic accumulation. This results in severe, potentially life-threatening side effects, including profound myelosuppression, severe mucositis, and neurotoxicity. **2. Why the other options are incorrect:** * **CYP2D6:** This is a Cytochrome P450 enzyme involved in the metabolism of drugs like Tamoxifen, codeine, and beta-blockers. It does not play a role in 5-FU metabolism. * **Uridine diphosphate (UDP):** While 5-FU is converted into active metabolites like F-dUMP and FUTP (which involve uridine pathways), the *deficiency* of UDP itself is not the clinical marker for 5-FU toxicity. (Note: Uridine triacetate is actually used as an antidote for 5-FU overdose). * **Purine:** 5-FU is a **pyrimidine** analogue, not a purine. Enzymes related to purine metabolism (like TPMT) are relevant for drugs like 6-Mercaptopurine, not 5-FU. **3. High-Yield Clinical Pearls for NEET-PG:** * **Mechanism of Action:** 5-FU inhibits **Thymidylate Synthase**, leading to "thymineless death" of cells. * **Antidote:** **Uridine triacetate** is the specific FDA-approved antidote for 5-FU or Capecitabine overdose/toxicity. * **Hand-Foot Syndrome:** A common dermatological side effect associated with 5-FU and its prodrug, Capecitabine. * **Comparison:** While **DPD** deficiency affects 5-FU, **TPMT** (Thiopurine Methyltransferase) deficiency leads to toxicity with **6-Mercaptopurine** and **Azathioprine**.

Question 1

Which of the following monoclonal antibodies is used for the treatment of colorectal carcinoma?

Accepted Answer

Cetuximab

Answer

Pembrolizumab

Answer

Rituximab

Answer

Natalizumab

Question 2

Irreversible ototoxicity is caused by which of the following drugs?

Accepted Answer

Cisplatin

Answer

Cyclophosphamide

Answer

Bleomycin

Answer

Chlorambucil

Question 3

Which of the following drugs has the least bone marrow suppression?

Accepted Answer

Vincristine

Answer

Cisplatin

Answer

Cyclophosphamide

Answer

Methotrexate

Question 4

A patient undergoing chemotherapy for two weeks for a mediastinal tumor develops high-frequency hearing loss. What is the most probable cause of this condition?

Accepted Answer

Cisplatin

Answer

Etoposide

Answer

Doxorubicin

Answer

Methotrexate

Question 5

Which of the following is an anti-CD20 monoclonal antibody?

Accepted Answer

Tositumomab

Answer

Alemtuzumab

Answer

Bevacizumab

Answer

Gemtuzumab

Question 6

What is the mechanism of action of tacrolimus?

Accepted Answer

Calcineurin inhibitor

Answer

Folate antagonist

Answer

Antimetabolite

Answer

CD 20 antibody

Question 7

Red discoloration of urine is seen with which of the following medications?

Accepted Answer

Doxorubicin

Answer

Methotrexate

Answer

Cytarabine

Answer

Cisplatin

Question 8

Which type of alkylating antineoplastic drug is Lomustine?

Accepted Answer

Nitrosoureas

Answer

Nitrogen mustards

Answer

Alkyl sulfonate

Answer

Triazine

Question 9

Methotrexate is often used as a chemotherapeutic agent to treat patients with leukemia. This drug is effective because it inhibits cells in which phase of the cell cycle?

Accepted Answer

S phase

Answer

G1 phase

Answer

G2 phase

Answer

M phase

Question 10

Which enzyme deficiency leads to serious side effects with 5-Fluorouracil?

Accepted Answer

Dihydropyrimidine dehydrogenase

Answer

CYP2D6

Answer

Uridine diphosphate

Answer

Purine

Anticancer Drugs — MCQs

Anticancer Drugs — MCQs

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