Anticancer Drugs Practice Questions

Q: Alemtuzumab is an antibody against which target molecule?

CD-52. **Explanation:** **Alemtuzumab** is a recombinant DNA-derived humanized monoclonal antibody (IgG1 kappa) directed against the **CD52** antigen. CD52 is a glycoprotein expressed at high levels on the surface of nearly all B and T lymphocytes, natural killer (NK) cells, monocytes, and macrophages. When Alemtuzumab binds to CD52, it triggers antibody-dependent cellular cytotoxicity (ADCC) and complement-mediated lysis, leading to profound and long-lasting lymphopenia. **Analysis of Incorrect Options:** * **A. CD-20:** This is the target for **Rituximab**, Ofatumumab, and Obinutuzumab. These are primarily used in B-cell non-Hodgkin lymphomas and Chronic Lymphocytic Leukemia (CLL). * **B. VEGF:** Vascular Endothelial Growth Factor is targeted by **Bevacizumab**. It acts as an angiogenesis inhibitor used in colorectal, lung, and renal cancers. * **C. EGFR:** Epidermal Growth Factor Receptor is targeted by **Cetuximab** and Panitumumab (monoclonal antibodies) or Erlotinib and Gefitinib (tyrosine kinase inhibitors). **Clinical Pearls for NEET-PG:** * **Indications:** Alemtuzumab is used in the treatment of **B-cell Chronic Lymphocytic Leukemia (B-CLL)** and relapsing-remitting **Multiple Sclerosis (MS)**. * **Adverse Effects:** Due to severe lymphopenia, patients are at high risk for **opportunistic infections** (e.g., CMV reactivation, PCP pneumonia). Prophylaxis is often required. * **Mnemonic:** "Alemtu-**52**-mab" (Rhyme "two" with "52") helps remember the CD marker. * **Other CD targets to remember:** CD3 (Muromonab), CD25 (Daclizumab/Basiliximab), CD33 (Gemtuzumab).

Q: Which of the following drugs binds to tubulin and arrests the metaphase of the cell cycle?

Vincristine. **Explanation:** **Vincristine (Option A)** is the correct answer. It belongs to the **Vinca Alkaloids** class of antineoplastic agents. These drugs act as "spindle poisons" by binding specifically to **tubulin dimers**, preventing their polymerization into microtubules. This disruption prevents the formation of the mitotic spindle, leading to **cell cycle arrest in the Metaphase (M-phase)**. **Analysis of Incorrect Options:** * **Carmustine (Option B):** A Nitrosourea (Alkylating agent) that works by cross-linking DNA strands. It is cell-cycle non-specific and is notable for its high lipid solubility, allowing it to cross the blood-brain barrier (used in brain tumors). * **Infliximab (Option C):** A monoclonal antibody against **TNF-alpha**. It is used in the treatment of autoimmune conditions like Crohn’s disease and Rheumatoid Arthritis, not as a cytotoxic microtubule inhibitor. * **Methotrexate (Option D):** An Antimetabolite that inhibits **Dihydrofolate Reductase (DHFR)**. It interferes with DNA synthesis (S-phase) by depleting tetrahydrofolate levels. **High-Yield Clinical Pearls for NEET-PG:** * **Vinca Alkaloids (Vincristine, Vinblastine):** Prevent **assembly** (polymerization) of microtubules. * **Taxanes (Paclitaxel, Docetaxel):** Prevent **disassembly** (depolymerization) of microtubules; they "freeze" the spindle. * **Dose-Limiting Toxicity:** Vincristine is notorious for **Peripheral Neuropathy** (paresthesia, foot drop) but is relatively bone marrow-sparing. In contrast, Vinblastine is known for significant **Bone Marrow Suppression** ("Blast" = Bone marrow). * **Contraindication:** Vincristine must **never** be given intrathecally, as it is fatal (causes ascending myeloencephalopathy).

Q: Sodium 2-mercaptoethanesulfonate is used as a protective agent in:

Cancer chemotherapy. **Explanation:** **Sodium 2-mercaptoethanesulfonate (MESNA)** is a sulfhydryl compound used specifically as a cytoprotective agent in cancer chemotherapy to prevent **hemorrhagic cystitis**. **Why it is the correct answer:** Chemotherapeutic agents like **Cyclophosphamide** and **Ifosfamide** (oxazaphosphorines) are metabolized into **acrolein**, a highly reactive and toxic metabolite. Acrolein accumulates in the urinary bladder, causing irritation and sloughing of the bladder mucosa, leading to gross hematuria (hemorrhagic cystitis). MESNA works by concentrating in the urine, where its free thiol (-SH) group binds to and neutralizes acrolein, forming a non-toxic stable thioether. **Why other options are incorrect:** * **Radiotherapy:** While radioprotectors like *Amifostine* (a free radical scavenger) are used to protect salivary glands and lungs, MESNA has no role in mitigating radiation damage. * **Lithotripsy:** This is a procedure to break kidney stones; it does not involve chemical toxicity requiring a thiol-based protector. * **Hepatic encephalopathy:** This condition is managed with Lactulose, Rifaximin, or Neomycin to reduce ammonia levels, not MESNA. **High-Yield Clinical Pearls for NEET-PG:** * **Mnemonic:** **M**ESNA **E**mpties **S**pecific **N**oxious **A**crolein. * **Hydration:** Vigorous intravenous hydration is always used alongside MESNA to further dilute acrolein. * **Ifosfamide vs. Cyclophosphamide:** MESNA is *mandatory* with Ifosfamide (due to higher acrolein production) but used with high-dose Cyclophosphamide. * **Other Protective Agents:** * **Dexrazoxane:** Prevents Doxorubicin-induced cardiotoxicity. * **Leucovorin (Folinic acid):** "Rescue" for Methotrexate toxicity. * **Amifostine:** Prevents Cisplatin-induced nephrotoxicity.

Q: Dose reduction should be done for which of the following anticancer drugs if Allopurinol is used?

6-Mercaptopurine. **Explanation:** The correct answer is **6-Mercaptopurine (6-MP)**. This is a classic drug-drug interaction frequently tested in NEET-PG. **1. Why 6-Mercaptopurine is correct:** 6-Mercaptopurine is a purine analog metabolized primarily by the enzyme **Xanthine Oxidase (XO)** into inactive metabolites (6-thiouric acid). **Allopurinol** is a potent inhibitor of Xanthine Oxidase. When administered together, Allopurinol prevents the degradation of 6-MP, leading to toxic plasma levels and severe bone marrow suppression. Therefore, if Allopurinol is used (often to prevent Tumor Lysis Syndrome), the dose of 6-MP must be reduced to **25-33% of the original dose**. **2. Why other options are incorrect:** * **Methotrexate:** It is a folate antagonist. Its metabolism is not dependent on Xanthine Oxidase; it is primarily excreted renally. * **Mitoxantrone:** An anthracenedione (topoisomerase II inhibitor) metabolized by the liver via oxidation and conjugation. * **Mitomycin-C:** An alkylating agent that requires enzymatic activation in tissues; it is not metabolized by Xanthine Oxidase. **3. Clinical Pearls for NEET-PG:** * **Azathioprine:** Since Azathioprine is a prodrug that is converted into 6-MP, it also requires a similar dose reduction when used with Allopurinol. * **Tumor Lysis Syndrome (TLS):** Allopurinol is used in TLS to prevent hyperuricemia. In patients with leukemia/lymphoma receiving 6-MP, this interaction is a major clinical concern. * **Alternative:** **Febuxostat** (another XO inhibitor) also interacts with 6-MP. If a patient must take full-dose 6-MP, **Rasburicase** (recombinant urate oxidase) is a safer alternative for managing uric acid as it does not inhibit XO.

Q: A 50-year-old lady with severe rheumatoid disease causing joint pains and functional limitation is treated with methotrexate, requiring folinic rescue therapy. What is the mechanism by which methotrexate acts?

Binding to dihydrofolate reductase. **Explanation:** **Mechanism of Action (Correct Answer: C):** Methotrexate (MTX) is a folate antimetabolite. It acts by **competitively inhibiting the enzyme Dihydrofolate Reductase (DHFR)**. Under normal conditions, DHFR reduces dihydrofolate into tetrahydrofolate (THF), which is a crucial co-factor for the synthesis of thymidylate and purine nucleotides. By binding to DHFR with an affinity 1,000 times greater than the natural substrate, MTX depletes the cellular pool of THF, leading to a "thymineless death" of rapidly dividing cells. **Analysis of Incorrect Options:** * **Option A:** MTX does not increase folic acid excretion; it interferes with its intracellular metabolism. * **Option B:** DNA binding is the mechanism of Alkylating agents (e.g., Cyclophosphamide) or Antitumor antibiotics (e.g., Doxorubicin), not antimetabolites. * **Option D:** MTX **decreases** nucleotide synthesis by inhibiting the formation of precursors required for DNA and RNA production. **High-Yield Clinical Pearls for NEET-PG:** * **Folinic Acid (Leucovorin) Rescue:** As mentioned in the stem, Leucovorin is a reduced form of folate that bypasses the DHFR block. It is used to "rescue" normal cells from MTX toxicity (e.g., bone marrow suppression, mucositis). * **Resistance:** The most common mechanism of resistance to MTX is the production of **altered DHFR** with reduced affinity for the drug or decreased polyglutamation. * **Toxicity:** Watch for **Hepatotoxicity** (cirrhosis with long-term use in RA) and **Pulmonary fibrosis**. * **Drug Interaction:** NSAIDs and Penicillins decrease the renal excretion of MTX, increasing its toxicity.

Q: Leucovorin rescue is indicated in which of the following toxicities?

Methotrexate toxicity. Methotrexate 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 [1]. **Leucovorin (Folinic Acid)** is a reduced form of folate that does not require DHFR for activation. By providing a source of active folate, Leucovorin bypasses the metabolic block, "rescuing" normal cells (especially bone marrow and GI mucosa) from lethal MTX toxicity [1, 2]. This is typically administered 24 hours after high-dose MTX [3].

Q: Which of the following anti-cancer drugs does not possess anti-inflammatory or immunosuppressive properties?

L-Asparaginase. **Explanation:** The correct answer is **L-Asparaginase**. **1. Why L-Asparaginase is correct:** L-Asparaginase is a unique enzyme used primarily in **Acute Lymphoblastic Leukemia (ALL)**. Its mechanism involves degrading circulating **L-asparagine** into aspartic acid and ammonia. Since leukemic cells lack the enzyme *asparagine synthetase*, they cannot synthesize asparagine endogenously and die due to protein synthesis inhibition. Unlike most cytotoxic drugs, L-Asparaginase is **not a general bone marrow suppressant** and does not interfere with the proliferation of normal T or B lymphocytes in a way that provides anti-inflammatory or immunosuppressive benefits. Its side effect profile is distinct, focusing on hypersensitivity, pancreatitis, and clotting factor deficiencies. **2. Why the other options are incorrect:** * **Methotrexate (MTX):** A folate antagonist that inhibits dihydrofolate reductase. It is a potent immunosuppressant and is the "gold standard" Disease-Modifying Antirheumatic Drug (DMARD) for **Rheumatoid Arthritis**. * **Azathioprine:** A purine antimetabolite (prodrug of 6-Mercaptopurine) that inhibits lymphocyte proliferation. It is widely used for **organ transplant rejection** and autoimmune conditions like SLE. * **Cyclophosphamide:** An alkylating agent that suppresses both B-cell and T-cell functions. It is used in severe autoimmune diseases like **Wegener’s Granulomatosis** and Lupus Nephritis. **3. NEET-PG High-Yield Pearls:** * **L-Asparaginase Toxicity:** Look for "Acute Pancreatitis" or "Thrombosis/Bleeding" (due to decreased synthesis of clotting factors and Antithrombin III) in clinical vignettes. * **Unique Property:** It is one of the few anticancer drugs that is **bone marrow sparing**. * **Resistance:** Occurs due to increased expression of asparagine synthetase by tumor cells.

Q: Ifosfamide is classified as which of the following types of agents?

Alkylating agent. **Explanation:** **Ifosfamide** is a nitrogen mustard and a structural isomer of cyclophosphamide. It belongs to the **Alkylating Agents** class of chemotherapy. 1. **Why the correct answer is right:** Alkylating agents work by attaching an alkyl group to DNA, typically at the **N7 position of guanine**. This leads to DNA cross-linking (inter-strand and intra-strand), which inhibits DNA replication and transcription, ultimately triggering apoptosis. Like cyclophosphamide, ifosfamide is a **prodrug** that requires activation by hepatic cytochrome P450 enzymes (specifically CYP3A4 and CYP2B6) to form its active metabolite, ifosfamide mustard. 2. **Why the incorrect options are wrong:** * **Antimetabolites (e.g., 5-Fluorouracil, Methotrexate):** These drugs interfere with normal metabolic processes, usually by mimicking nucleotides to inhibit DNA synthesis during the S-phase. * **Folate Antagonists (e.g., Methotrexate):** A sub-class of antimetabolites that specifically inhibit the enzyme dihydrofolate reductase (DHFR). * **Plant Alkaloids (e.g., Vincristine, Paclitaxel):** These agents act on microtubules (mitotic inhibitors) rather than directly alkylating DNA. 3. **NEET-PG High-Yield Clinical Pearls:** * **Acrolein Toxicity:** Metabolism of ifosfamide releases acrolein, which causes **Hemorrhagic Cystitis**. * **Prevention:** Always co-administer with **MESNA** (2-Mercaptoethane sulfonate Na) and aggressive hydration to neutralize acrolein in the bladder. * **Neurotoxicity:** Ifosfamide is more neurotoxic than cyclophosphamide due to the production of chloroacetaldehyde; this can present as encephalopathy. * **Spectrum:** It is widely used in the treatment of testicular cancer, sarcomas, and lymphomas.

Q: Which of the following antiumor agents works by impairing de novo purine synthesis?

Methotrexate (antifolate). ### Explanation **Correct Option: C. Methotrexate (antifolate)** Methotrexate is a folate antagonist that competitively inhibits the enzyme **Dihydrofolate Reductase (DHFR)**. This inhibition prevents the conversion of dihydrofolate (DHF) to tetrahydrofolate (THF). THF is a crucial one-carbon carrier required for the **de novo synthesis of purines** (adenine and guanine) and the conversion of dUMP to dTMP (pyrimidine synthesis) [2], [4]. By depleting the pool of THF, methotrexate effectively halts DNA synthesis and cell replication [2]. **Analysis of Incorrect Options:** * **A. Acycloguanosine (Acyclovir):** This is an antiviral agent, not primarily an antitumor drug. It acts as a guanosine analog that inhibits viral DNA polymerase, specifically in Herpes Simplex and Varicella-Zoster viruses. * **B. 5-Fluorouracil (5-FU):** While 5-FU is an antimetabolite, it primarily inhibits **Thymidylate Synthase** [1], [5]. This impairs **pyrimidine synthesis** (specifically dTMP) rather than de novo purine synthesis [5]. * **D. Allopurinol:** This is a xanthine oxidase inhibitor used to treat gout and prevent tumor lysis syndrome [3]. It inhibits the **catabolism** of purines (preventing uric acid formation) rather than their de novo synthesis [3]. **High-Yield Clinical Pearls for NEET-PG:** * **Rescue Therapy:** High-dose Methotrexate toxicity is managed with **Leucovorin (Folinic acid)**, which bypasses the inhibited DHFR enzyme to provide a source of reduced folate [1], [2]. * **Specific Toxicity:** Methotrexate can cause myelosuppression, mucositis, and nephrotoxicity (due to crystalluria) [1]. * **Other Purine Synthesis Inhibitors:** Apart from Methotrexate, drugs like **6-Mercaptopurine (6-MP)** and **6-Thioguanine** also inhibit de novo purine synthesis by acting as pseudo-feedback inhibitors of glutamine-PRPP amidotransferase [3].

Q: Crizotinib is used in the treatment of which of the following conditions?

ALK positive Non-small cell carcinoma of lung. **Explanation:** **Crizotinib** is a first-generation tyrosine kinase inhibitor (TKI) that primarily targets the **ALK (Anaplastic Lymphoma Kinase)** protein. In approximately 3–5% of Non-Small Cell Lung Cancer (NSCLC) cases, a chromosomal rearrangement occurs (typically the EML4-ALK fusion gene), leading to constitutive activation of ALK signaling, which drives tumor growth. Crizotinib effectively inhibits this signaling pathway, making it the standard initial therapy for **ALK-positive NSCLC**. **Analysis of Incorrect Options:** * **Option A & C (FLT-3 positive):** FLT-3 mutations are hallmark drivers in **Acute Myeloid Leukemia (AML)**. The drugs used for FLT-3 positive AML include **Midostaurin** and **Gilteritinib**, not Crizotinib. * **Option D (BRCA-2 positive):** BRCA mutations involve DNA repair pathways. The treatment of choice for BRCA-positive metastatic breast or ovarian carcinoma involves **PARP inhibitors** such as **Olaparib** or **Niraparib**. **Clinical Pearls for NEET-PG:** * **Mechanism:** Crizotinib inhibits ALK, **ROS1**, and **c-MET** tyrosine kinases. * **Resistance:** Most patients eventually develop resistance to Crizotinib (often via the L1196M "gatekeeper" mutation). Second-generation ALK inhibitors like **Ceritinib**, **Alectinib**, and **Brigatinib** are used to overcome this. * **Side Effects:** Notable side effects include **visual disturbances** (flashes of light), hepatotoxicity, and QT interval prolongation. * **High-Yield Association:** Always associate **ALK rearrangement** with **younger age** and **non-smokers** in the context of lung adenocarcinoma.

Question 1

Alemtuzumab is an antibody against which target molecule?

Accepted Answer

CD-52

Answer

CD-20

Answer

VEGF

Answer

EGFR

Question 2

Which of the following drugs binds to tubulin and arrests the metaphase of the cell cycle?

Accepted Answer

Vincristine

Answer

Carmustine

Answer

Infliximab

Answer

Methotrexate

Question 3

Sodium 2-mercaptoethanesulfonate is used as a protective agent in:

Accepted Answer

Cancer chemotherapy

Answer

Radiotherapy

Answer

Lithotripsy

Answer

Hepatic encephalopathy

Question 4

Dose reduction should be done for which of the following anticancer drugs if Allopurinol is used?

Accepted Answer

6-Mercaptopurine

Answer

Methotrexate

Answer

Mitoxantrone

Answer

Mitomycin-C

Question 5

A 50-year-old lady with severe rheumatoid disease causing joint pains and functional limitation is treated with methotrexate, requiring folinic rescue therapy. What is the mechanism by which methotrexate acts?

Accepted Answer

Binding to dihydrofolate reductase

Answer

Increasing folic acid excretion

Answer

DNA binding

Answer

Increasing nucleotide synthesis

Question 6

Leucovorin rescue is indicated in which of the following toxicities?

Accepted Answer

Methotrexate toxicity

Answer

Cyclophosphamide toxicity

Answer

Vincristine toxicity

Answer

Cisplatin toxicity

Question 7

Which of the following anti-cancer drugs does not possess anti-inflammatory or immunosuppressive properties?

Accepted Answer

L-Asparaginase

Answer

Methotrexate

Answer

Azathioprine

Answer

Cyclophosphamide

Question 8

Ifosfamide is classified as which of the following types of agents?

Accepted Answer

Alkylating agent

Answer

Antimetabolite

Answer

Folate antagonist

Answer

Plant alkaloid

Question 9

Which of the following antiumor agents works by impairing de novo purine synthesis?

Accepted Answer

Methotrexate (antifolate)

Answer

Acyloguanosine

Answer

5-Fluorouracil

Answer

Allopurinol

Question 10

Crizotinib is used in the treatment of which of the following conditions?

Accepted Answer

ALK positive Non-small cell carcinoma of lung

Answer

FLT-3 positive Non-small cell carcinoma of lung

Answer

FLT-3 positive Acute myeloid leukemia

Answer

BRCA-2 positive metastatic breast carcinoma

Anticancer Drugs — MCQs

Anticancer Drugs — MCQs

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