Anticancer Drugs — MCQs
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Which of the following drugs is useful for the treatment of advanced prostate cancer?
What is true about Azathioprine?
Axicabtagene ciloleucel is indicated for which of the following conditions?
Venoocclusive disease of the liver is caused by which of the following agents?
Gemtuzumab acts against which antigen?
Alkalinization of urine is done during the administration of which of the following chemotherapeutic drugs?
Which of the following statements is true regarding methotrexate?
Ofatumumab is a monoclonal antibody against:
Pulmonary fibrosis is associated with the use of which of the following drugs?
A patient on treatment for leukemia develops chest pain, pulmonary infiltrates, and pleural effusion. What is the likely cause?
Anticancer Drugs Indian Medical PG Practice Questions and MCQs
Question 351: Which of the following drugs is useful for the treatment of advanced prostate cancer?
- A. Hydroxyurea (Correct Answer)
- B. Cisplatin
- C. Paclitaxel
- D. Carboplatin
Explanation: **Explanation:** **Correct Option: A. Hydroxyurea** Hydroxyurea is an antimetabolite that acts as a **Ribonucleotide Reductase inhibitor**, blocking the conversion of ribonucleotides to deoxyribonucleotides, thereby inhibiting DNA synthesis (S-phase specific). While hormonal therapies (like GnRH analogs and Anti-androgens) are the mainstays for advanced prostate cancer, Hydroxyurea is historically and clinically recognized as an alternative palliative treatment for **metastatic, hormone-refractory prostate cancer**. It helps in reducing tumor burden and managing symptoms when first-line therapies fail. **Incorrect Options:** * **B & D. Cisplatin and Carboplatin:** These are platinum compounds that cause DNA cross-linking. While they are "workhorse" drugs for many solid tumors (lung, ovary, bladder, and testicular cancers), they are not standard first-line or typical choices for prostate cancer, which is more responsive to hormonal manipulation and taxanes. * **C. Paclitaxel:** This is a taxane that stabilizes microtubules. While its cousin, **Docetaxel**, is the gold standard chemotherapy for metastatic castration-resistant prostate cancer (mCRPC), Paclitaxel itself is not the preferred agent for this specific malignancy. **High-Yield Clinical Pearls for NEET-PG:** * **Mechanism of Hydroxyurea:** Inhibits Ribonucleotide Reductase. * **Other uses of Hydroxyurea:** Myeloproliferative disorders (CML, Polycythemia Vera) and **Sickle Cell Anemia** (it increases HbF levels, preventing sickling). * **Side Effect:** Significant myelosuppression (dose-limiting) and cutaneous ulcers. * **Prostate Cancer Tip:** If the question asks for the "Drug of Choice" for metastatic prostate cancer, look for **GnRH agonists (Leuprolide)** or **Docetaxel**. Hydroxyurea is used in refractory cases.
Question 352: What is true about Azathioprine?
- A. It has more antitumor effect than immunosuppressant effect
- B. It is not a prodrug
- C. It selectively affects the differentiation of T cells (Correct Answer)
- D. It is a pyrimidine antimetabolite
Explanation: **Explanation:** **Azathioprine** is a potent immunosuppressant drug widely used in organ transplantation and autoimmune disorders [2]. **Why Option C is Correct:** Azathioprine is a purine analog that interferes with nucleic acid synthesis [1]. Its primary mechanism involves the inhibition of **de novo purine synthesis**, which is critical for rapidly dividing cells [1]. Lymphocytes (T cells and B cells) lack a robust "salvage pathway" and are uniquely dependent on de novo synthesis. Consequently, Azathioprine **selectively affects the proliferation and differentiation of T cells** more than other cell types, leading to suppressed cell-mediated immunity. **Analysis of Incorrect Options:** * **Option A:** Azathioprine has **more immunosuppressant effect** than antitumor effect [2]. While it is derived from 6-Mercaptopurine (6-MP), its clinical utility is almost exclusively as an immunosuppressant rather than a chemotherapy agent [1]. * **Option B:** It **is a prodrug**. After administration, it is non-enzymatically converted into **6-Mercaptopurine (6-MP)**, which is then further metabolized into active thio-guanine nucleotides [1]. * **Option C:** It is a **purine antimetabolite** (not pyrimidine) [1]. It acts as an analog of adenine and guanine [1]. **High-Yield Clinical Pearls for NEET-PG:** 1. **Drug Interaction:** Azathioprine/6-MP is metabolized by **Xanthine Oxidase**. If co-administered with **Allopurinol** (a xanthine oxidase inhibitor), the levels of Azathioprine rise significantly, leading to life-threatening bone marrow toxicity. The dose must be reduced by 75%. 2. **Pharmacogenomics:** Patients with a genetic deficiency of the enzyme **TPMT (Thiopurine Methyltransferase)** are at high risk for severe myelosuppression when taking Azathioprine. 3. **Clinical Use:** It is the drug of choice for maintaining remission in Crohn’s disease and is used in steroid-sparing regimens for Rheumatoid Arthritis and SLE [2].
Question 353: Axicabtagene ciloleucel is indicated for which of the following conditions?
- A. Relapsed myeloma
- B. T cell lymphoma
- C. Diffuse large B cell lymphoma (Correct Answer)
- D. Small cell lung cancer
Explanation: **Explanation:** **Axicabtagene ciloleucel (Yescarta)** is a pioneering **Chimeric Antigen Receptor (CAR) T-cell therapy**. It involves genetically engineering a patient’s own T-cells to express a receptor that targets the **CD19 antigen**, which is characteristically found on the surface of B-cells. 1. **Why Option C is Correct:** Axicabtagene ciloleucel is FDA-approved for the treatment of adult patients with **relapsed or refractory large B-cell lymphoma**, including **Diffuse Large B-Cell Lymphoma (DLBCL)**, primary mediastinal B-cell lymphoma, and high-grade B-cell lymphoma after two or more lines of systemic therapy. By targeting CD19, the engineered T-cells directly identify and eliminate the malignant B-cells. 2. **Why Other Options are Incorrect:** * **Relapsed Myeloma:** While CAR-T therapies exist for Multiple Myeloma (e.g., **Idecabtagene vicleucel**), they typically target **BCMA** (B-cell maturation antigen), not CD19. * **T-cell Lymphoma:** Axicabtagene targets CD19, which is a B-cell marker. It is ineffective against T-cell malignancies. * **Small Cell Lung Cancer:** This is a solid tumor of epithelial origin; CAR-T therapies are currently primarily utilized for hematological malignancies. **High-Yield Clinical Pearls for NEET-PG:** * **Mechanism:** Adoptive immunotherapy (CD19-directed CAR-T). * **Major Side Effects:** * **Cytokine Release Syndrome (CRS):** Managed with **Tocilizumab** (IL-6 inhibitor). * **ICANS:** Immune Effector Cell-Associated Neurotoxicity Syndrome. * **Other CAR-T drugs:** **Tisagenlecleucel** (indicated for DLBCL and B-cell ALL).
Question 354: Venoocclusive disease of the liver is caused by which of the following agents?
- A. Cyclophosphamide
- B. Melphalan
- C. Both Cyclophosphamide and Melphalan (Correct Answer)
- D. None of the above
Explanation: **Explanation:** **Sinusoidal Obstruction Syndrome (SOS)**, formerly known as **Veno-occlusive Disease (VOD)** of the liver, is a clinical syndrome characterized by hepatomegaly, jaundice, and fluid retention. It occurs due to toxic injury to the sinusoidal endothelial cells, leading to the occlusion of terminal hepatic venules. **Why the correct answer is C:** Both **Cyclophosphamide** and **Melphalan** are potent alkylating agents commonly used in high-dose conditioning regimens prior to Hematopoietic Stem Cell Transplantation (HSCT). * **Cyclophosphamide:** Its metabolite, acrolein, is primarily associated with hemorrhagic cystitis, but the drug is also a well-documented cause of hepatic VOD, especially when used in combination with total body irradiation. * **Melphalan:** High-dose melphalan is a standard treatment for Multiple Myeloma and is a recognized independent risk factor for the development of VOD. Since both drugs are implicated in the pathogenesis of this condition, Option C is the most accurate choice. **Analysis of incorrect options:** * **Option A & B:** While both are correct individually, they are incomplete. In the context of NEET-PG, when two drugs in the options are known to cause a specific side effect, the "Both" or "All of the above" option is the preferred answer. **High-Yield Clinical Pearls for NEET-PG:** 1. **Antidote for VOD:** **Defibrotide** is the drug of choice for treating severe hepatic veno-occlusive disease. 2. **Busulfan:** This is another high-yield alkylating agent frequently associated with VOD (often more so than cyclophosphamide). 3. **Acrolein Toxicity:** Remember that while acrolein causes VOD in the liver, it causes **hemorrhagic cystitis** in the bladder (prevented by **MESNA**). 4. **Other drugs causing VOD:** Azathioprine and 6-Thioguanine.
Question 355: Gemtuzumab acts against which antigen?
- A. CD11a
- B. CD22
- C. CD33 (Correct Answer)
- D. CD45
Explanation: **Explanation:** **Gemtuzumab ozogamicin** is a humanized monoclonal antibody conjugated to a cytotoxic derivative of calicheamicin. 1. **Why CD33 is correct:** Gemtuzumab specifically targets the **CD33 antigen**, a transmembrane glycoprotein expressed on the surface of myeloid cells. It is found on the leukemic blasts of approximately 90% of patients with **Acute Myeloid Leukemia (AML)**. Once the drug binds to CD33, the complex is internalized, releasing calicheamicin, which causes double-stranded DNA breaks and subsequent cell death. 2. **Why other options are incorrect:** * **CD11a:** This is a subunit of LFA-1. The drug **Efalizumab** (previously used for psoriasis) targets CD11a. * **CD22:** This is expressed on B-cells. Drugs targeting CD22 include **Inotuzumab ozogamicin** (used in ALL) and **Moxetumonab pasudotox** (used in Hairy Cell Leukemia). * **CD45:** Known as Leukocyte Common Antigen (LCA), it is expressed on all hematopoietic cells. There are currently no standard monoclonal antibody therapies targeting CD45 in routine clinical use for AML. **High-Yield Clinical Pearls for NEET-PG:** * **Indication:** Gemtuzumab is primarily used for CD33-positive **Acute Myeloid Leukemia (AML)**. * **Black Box Warning:** It is associated with a high risk of **Hepatotoxicity**, specifically **Veno-Occlusive Disease (VOD)** or Sinusoidal Obstruction Syndrome. * **Suffix "ozogamicin":** Indicates the drug is an antibody-drug conjugate (ADC) linked to calicheamicin.
Question 356: Alkalinization of urine is done during the administration of which of the following chemotherapeutic drugs?
- A. Ara-C
- B. Methotrexate (Correct Answer)
- C. Cisplatin
- D. Ifosfamide
Explanation: **Explanation:** **Methotrexate (MTX)** is the correct answer because it is a weak acid that is primarily excreted by the kidneys. At high doses, MTX and its metabolite (7-OH-methotrexate) are poorly soluble in acidic urine, leading to the formation of crystals in the renal tubules (**crystalluria**). This can cause acute kidney injury (AKI) due to obstructive nephropathy. **Alkalinization of urine** (using Sodium Bicarbonate) increases the ionization of Methotrexate, significantly enhancing its solubility and renal clearance, thereby preventing nephrotoxicity. **Analysis of Incorrect Options:** * **Ara-C (Cytarabine):** Its dose-limiting toxicity is bone marrow suppression and cerebellar ataxia (at high doses). It does not require urinary alkalinization. * **Cisplatin:** It is highly nephrotoxic (causing ATN), but the prevention strategy involves **aggressive hydration** and the use of **Amifostine** (a cytoprotective agent) or osmotic diuresis (Mannitol), not alkalinization. * **Ifosfamide:** Along with Cyclophosphamide, it causes **hemorrhagic cystitis** due to the metabolite **Acrolein**. This is prevented by vigorous hydration and the administration of **MESNA**, which neutralizes acrolein in the bladder. **High-Yield Clinical Pearls for NEET-PG:** * **Leucovorin Rescue:** Folinic acid (Leucovorin) is used to "rescue" normal cells from MTX toxicity by bypassing the inhibited Dihydrofolate Reductase (DHFR) enzyme. * **Glucarpidase:** An enzyme used as an antidote for MTX toxicity in patients with renal failure. * **Drug Interactions:** NSAIDs, Penicillins, and Probenecid decrease MTX excretion by competing for organic anion transporters (OAT), increasing toxicity.
Question 357: Which of the following statements is true regarding methotrexate?
- A. Oral bioavailability is 30-40%.
- B. Does not interfere with the action of IL-1.
- C. Causes thrombocytopenia. (Correct Answer)
- D. Not useful in Crohn's disease.
Explanation: Methotrexate (MTX) is a folate antimetabolite that acts as a competitive inhibitor of the enzyme dihydrofolate reductase (DHFR) [1]. This inhibition prevents the conversion of dihydrofolate to tetrahydrofolate, halting DNA synthesis and cell proliferation [1]. 1. Why Option C is Correct: Methotrexate is a potent myelosuppressant. It inhibits the rapidly dividing cells of the bone marrow, leading to a decrease in all cell lines (pancytopenia) [2]. Thrombocytopenia (low platelet count) is a common and dose-limiting adverse effect of MTX therapy [3]. 2. Why Other Options are Incorrect: * Option A: At low doses (used in RA or psoriasis), MTX has high oral bioavailability (>70%). Bioavailability only decreases at higher doses due to saturation of intestinal transporters. * Option B: MTX has potent anti-inflammatory effects. It increases extracellular adenosine levels, which interferes with the action of IL-1 and other pro-inflammatory cytokines (TNF-α, IL-6). * Option D: MTX is an established second-line therapy for Crohn’s disease, particularly for maintaining remission in patients who are steroid-dependent or resistant to thiopurines. 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 [1]. * Antidote for Toxicity: Glucarpidase can be used to rapidly reduce toxic plasma concentrations of MTX. * Monitoring: Always monitor Liver Function Tests (LFTs) as MTX can cause hepatic fibrosis/cirrhosis with long-term use. * Contraindication: It is highly teratogenic (Category X) and must be avoided in pregnancy.
Question 358: Ofatumumab is a monoclonal antibody against:
- A. CD19
- B. CD79a
- C. CD20 (Correct Answer)
- D. CD25
Explanation: **Explanation:** **Ofatumumab** is a fully humanized monoclonal antibody that targets the **CD20** antigen. CD20 is a transmembrane protein expressed on the surface of B-lymphocytes, from the pre-B cell stage through mature B cells (but not on plasma cells). **Why Option C is Correct:** Ofatumumab binds to a unique epitope on the CD20 molecule (distinct from the binding site of Rituximab), encompassing both the small and large extracellular loops. This binding triggers B-cell lysis primarily through **Complement-Dependent Cytotoxicity (CDC)** and Antibody-Dependent Cellular Cytotoxicity (ADCC). It is clinically used in the treatment of Chronic Lymphocytic Leukemia (CLL) and Relapsing Multiple Sclerosis (RMS). **Why Other Options are Incorrect:** * **CD19 (Option A):** Targeted by drugs like **Blinatumomab** (a BiTE) and CAR-T cell therapies (e.g., Tisagenlecleucel). CD19 is a biomarker for B-cell lineage but is not the target for Ofatumumab. * **CD79a (Option B):** Part of the B-cell receptor complex. While used in immunohistochemistry to identify B-cell neoplasms, it is not a common target for current monoclonal antibody therapy in this context. * **CD25 (Option C):** This is the alpha chain of the IL-2 receptor. It is targeted by **Basiliximab** and **Daclizumab**, primarily used to prevent transplant rejection. **High-Yield Clinical Pearls for NEET-PG:** * **Anti-CD20 Trio:** Remember **Rituximab** (chimeric), **Ofatumumab** (fully human), and **Obinutuzumab** (type II, glycoengineered). * **Ofatumumab Advantage:** Being a fully human antibody, it has a lower risk of infusion-related reactions compared to the chimeric Rituximab. * **Key Indication:** It is a first-line subcutaneous B-cell depleting therapy for **Multiple Sclerosis**.
Question 359: Pulmonary fibrosis is associated with the use of which of the following drugs?
- A. Bleomycin (Correct Answer)
- B. Cisplatin
- C. Methotrexate
- D. Actinomycin D
Explanation: **Explanation:** **Bleomycin** is a glycopeptide antibiotic used in cancer chemotherapy (e.g., Hodgkin lymphoma, testicular cancer) that acts by inducing DNA strand breaks through free radical generation. The most characteristic and dose-limiting toxicity of Bleomycin is **pulmonary fibrosis**. This occurs because the lungs lack the enzyme **bleomycin hydrolase**, which normally inactivates the drug. Consequently, the drug accumulates in lung tissue, leading to oxidative stress, cytokine release, and subsequent fibroblast proliferation. **Analysis of Incorrect Options:** * **Cisplatin:** Primarily known for its **nephrotoxicity** (prevented by aggressive hydration and amifostine) and severe **ototoxicity**. It is not typically associated with pulmonary fibrosis. * **Methotrexate:** An antimetabolite (DHFR inhibitor) whose chief toxicities include **myelosuppression**, mucositis, and hepatotoxicity. While it can cause acute pneumonitis, chronic fibrosis is classic for Bleomycin. * **Actinomycin D (Dactinomycin):** An antitumor antibiotic used mainly in pediatric tumors (Wilms tumor). Its major side effects are **bone marrow suppression** and alopecia. **High-Yield Clinical Pearls for NEET-PG:** * **Monitoring:** Patients on Bleomycin should undergo regular **Pulmonary Function Tests (PFTs)**; a decrease in DLCO (Diffusing capacity of the lungs for carbon monoxide) is an early sign of toxicity. * **Risk Factor:** High concentrations of inspired oxygen (FiO2) during surgery can exacerbate Bleomycin-induced lung injury. * **Other drugs causing Pulmonary Fibrosis:** Remember the mnemonic **"BAM"** — **B**leomycin, **A**miodarone, **M**ethysergide, and **B**usulfan.
Question 360: A patient on treatment for leukemia develops chest pain, pulmonary infiltrates, and pleural effusion. What is the likely cause?
- A. Daunorubicin
- B. Hydroxyurea
- C. Cytarabine
- D. Tretinoin (Correct Answer)
Explanation: ### **Explanation** The clinical presentation of chest pain, pulmonary infiltrates, and pleural effusion in a patient being treated for leukemia (specifically Acute Promyelocytic Leukemia - APL) describes **Differentiation Syndrome** (formerly known as Retinoic Acid Syndrome). **1. Why Tretinoin is Correct:** Tretinoin (All-Trans Retinoic Acid or ATRA) induces the maturation of malignant promyelocytes. During this process, these cells release inflammatory cytokines and express adhesion molecules, leading to massive pulmonary infiltration and capillary leak. This manifests clinically as fever, dyspnea, weight gain, pleural/pericardial effusions, and pulmonary infiltrates. * **Management:** High-dose intravenous **Dexamethasone** is the treatment of choice. **2. Why Other Options are Incorrect:** * **Daunorubicin:** An anthracycline primarily associated with **cardiotoxicity** (dilated cardiomyopathy and congestive heart failure) rather than acute pulmonary infiltrates. * **Hydroxyurea:** Primarily causes myelosuppression and cutaneous side effects (hyperpigmentation, leg ulcers). While it can cause rare interstitial pneumonitis, it is not the classic cause of this acute triad in leukemia treatment. * **Cytarabine:** Known for causing **"Ara-C Syndrome"** (fever, rash, conjunctivitis) and cerebellar toxicity at high doses. While it can cause non-cardiogenic pulmonary edema, the context of APL treatment strongly points toward Tretinoin. **3. High-Yield Clinical Pearls for NEET-PG:** * **APL Marker:** Associated with **t(15;17)** translocation, involving the PML-RARα gene. * **Differentiation Syndrome:** Can also be caused by **Arsenic Trioxide**, another first-line agent for APL. * **Emergency Management:** Do not wait for radiological confirmation; if Differentiation Syndrome is suspected, start steroids immediately to prevent mortality.
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
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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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