Anticancer Drugs Practice Questions

Q: Venoocclusive disease of the liver is caused by which of the following agents?

Both Cyclophosphamide and Melphalan. **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.

Q: Which of the following statements is true regarding methotrexate?

Causes thrombocytopenia.. 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.

Q: Alkalinization of urine is done during the administration of which of the following chemotherapeutic drugs?

Methotrexate. **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.

Q: Ofatumumab is a monoclonal antibody against:

CD20. **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**.

Q: A patient on treatment for leukemia develops chest pain, pulmonary infiltrates, and pleural effusion. What is the likely cause?

Tretinoin. ### **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.

Q: Thalidomide was reintroduced for certain indications like multiple myeloma after being withdrawn due to side effects. Which of the following is NOT a side effect of thalidomide?

Diarrhea. **Explanation:** Thalidomide is an immunomodulatory drug (IMiD) used primarily in the treatment of Multiple Myeloma and Erythema Nodosum Leprosum (ENL). **Why Diarrhea is the correct answer:** Thalidomide is characteristically associated with **constipation**, not diarrhea. It has significant neurotoxic and sedative properties that slow down gastrointestinal motility. In contrast, its newer analogue, Lenalidomide, is more frequently associated with diarrhea. **Analysis of incorrect options:** * **Hypothyroidism:** Thalidomide can cause primary hypothyroidism. Patients on long-term therapy require regular monitoring of Thyroid Stimulating Hormone (TSH) levels. * **Teratogenicity:** This is the most infamous side effect of thalidomide. If taken during the first trimester of pregnancy, it causes **Phocomelia** (seal-like limbs) due to its anti-angiogenic properties. This led to its withdrawal in the 1960s (the "Thalidomide Tragedy"). * **Deep Vein Thrombosis (DVT):** Thalidomide significantly increases the risk of venous thromboembolism, especially when used in combination with high-dose dexamethasone or chemotherapy in myeloma patients. Prophylactic anticoagulation is often required. **High-Yield Clinical Pearls for NEET-PG:** 1. **Mechanism of Action:** It binds to a protein called **Cereblon**, part of the E3 ubiquitin ligase complex, leading to the degradation of transcription factors (IKZF1/3). 2. **Peripheral Neuropathy:** A common dose-limiting toxicity; it is usually a symmetrical, painful sensory neuropathy. 3. **STEPS Program:** Due to its teratogenic potential, it is distributed under a restricted program (System for Thalidomide Education and Prescribing Safety). 4. **Drug of Choice:** Thalidomide is the drug of choice for Type 2 Lepra Reaction (ENL).

Q: Which chemotherapeutic drug inhibits the polymerization of microtubules but is not associated with causing bone marrow suppression?

Vincristine. **Explanation:** The correct answer is **Vincristine**. This question tests the ability to differentiate between drugs within the same class based on their side-effect profiles, a common high-yield theme in NEET-PG. **1. Why Vincristine is correct:** Vincristine belongs to the **Vinca Alkaloids** class. Its mechanism of action involves binding to tubulin dimers, which **inhibits the polymerization** of microtubules, leading to mitotic arrest in the M-phase. A unique clinical feature of Vincristine is that it is **bone marrow sparing** (minimal myelosuppression). However, its dose-limiting toxicity is **peripheral neuropathy** (paresthesia, loss of reflexes, and foot drop). **2. Why the other options are incorrect:** * **Vinblastine:** Although it is also a Vinca alkaloid with the same mechanism (inhibiting polymerization), it is notorious for causing significant bone marrow suppression. (Mnemonic: **B**lastine **B**lasts the **B**one marrow). * **Cisplatin:** This is a platinum compound that acts by cross-linking DNA. It is highly emetogenic and nephrotoxic but does not act on microtubules. * **5-Fluorouracil:** This is an antimetabolite (pyrimidine analog) that inhibits thymidylate synthase. It causes significant myelosuppression and GI toxicity. **3. NEET-PG High-Yield Pearls:** * **Microtubule Inhibitors:** Remember that **Vinca alkaloids** (Vincristine, Vinblastine) inhibit *polymerization*, whereas **Taxanes** (Paclitaxel, Docetaxel) inhibit *depolymerization* (they "freeze" the spindle). * **Vincristine Side Effects:** Apart from neuropathy, it can cause **SIADH** and paralytic ileus. * **Fatal Administration:** Vincristine is **fatal if given intrathecally**; it must only be administered intravenously. * **Marrow Sparing Drugs:** Other notable marrow-sparing anticancer drugs include **Bleomycin** (pulmonary fibrosis) and **L-Asparaginase** (pancreatitis).

Q: Sipuleucel-T is a vaccine indicated for which condition?

Prostate carcinoma. **Explanation:** **Sipuleucel-T** is a revolutionary immunotherapy, specifically an **autologous cellular immunotherapy**, used in the management of advanced prostate cancer. **Why Prostate Carcinoma is Correct:** Sipuleucel-T is the first "cancer vaccine" approved by the FDA for the treatment of **asymptomatic or minimally symptomatic metastatic castrate-resistant prostate cancer (mCRPC)**. The process involves collecting a patient's own peripheral blood mononuclear cells (including antigen-presenting cells) via leukapheresis. These cells are activated ex-vivo with a recombinant fusion protein (PA2024) consisting of **Prostatic Acid Phosphatase (PAP)** linked to Granulocyte-Macrophage Colony-Stimulating Factor (GM-CSF). When re-infused, these "primed" cells stimulate a T-cell immune response against prostate cancer cells expressing PAP. **Why Other Options are Incorrect:** * **Renal Cell Carcinoma (RCC):** While RCC is highly immunogenic, standard immunotherapies involve Tyrosine Kinase Inhibitors (TKIs) or Checkpoint Inhibitors (Nivolumab/Pembrolizumab), not Sipuleucel-T. * **Testicular Tumor:** These are primarily treated with surgery (Radical Orchidectomy) and platinum-based chemotherapy (BEP regimen). * **Bladder Carcinoma:** Intravesical BCG is the standard immunotherapy for non-muscle invasive bladder cancer; Sipuleucel-T has no role here. **High-Yield Clinical Pearls for NEET-PG:** * **Indication:** Metastatic Castrate-Resistant Prostate Cancer (mCRPC) that is asymptomatic/minimally symptomatic. * **Target Antigen:** Prostatic Acid Phosphatase (PAP). * **Mechanism:** Active cellular immunotherapy (not a preventive vaccine). * **Survival:** It has been shown to improve overall survival (OS) but does not typically result in a decrease in PSA levels or tumor shrinkage on imaging.

Q: Which of the following causes minimum bone marrow suppression?

Bleomycin. **Explanation:** The correct answer is **Bleomycin**. Most conventional cytotoxic anticancer drugs are "myelosuppressive," meaning they target rapidly dividing cells in the bone marrow, leading to leukopenia, anemia, and thrombocytopenia. However, certain drugs are known for their **"bone marrow sparing"** properties. **1. Why Bleomycin is correct:** Bleomycin is a glycopeptide antibiotic that works by inducing free radical formation, causing single and double-strand DNA breaks. Its dose-limiting toxicity is **pulmonary fibrosis**, not myelosuppression. This is because the enzyme that inactivates the drug (bleomycin hydrolase) is present in high concentrations in the bone marrow but is deficient in the lungs and skin. **2. Why the other options are incorrect:** * **5-Fluorouracil (5-FU):** An antimetabolite (pyrimidine analog) that inhibits thymidylate synthase. It causes significant myelosuppression (nadir at 9–14 days) and GI toxicity. * **Cytarabine (Ara-C):** A potent S-phase specific antimetabolite. It is notorious for causing severe, prolonged bone marrow suppression, which is actually the therapeutic goal when treating acute myeloid leukemia (AML). * **Topotecan:** A Topoisomerase I inhibitor. Its primary dose-limiting toxicity is neutropenia (up to 80% of patients). **High-Yield Clinical Pearls for NEET-PG:** * **Mnemonic for Bone Marrow Sparing Drugs:** "**B**etter **V**ictory **L**ess **C**omplications" → **B**leomycin, **V**incristine, **L**-asparaginase, **C**isplatin (Cisplatin is relatively less myelosuppressive compared to Carboplatin). * **Specific Toxicities to Remember:** * Bleomycin: Pulmonary fibrosis & Skin hyperpigmentation. * Vincristine: Peripheral neuropathy (Microtubule inhibitor). * L-asparaginase: Pancreatitis & Clotting factor deficiency. * Cyclophosphamide: Hemorrhagic cystitis (prevented by **MESNA**).

Question 1

Venoocclusive disease of the liver is caused by which of the following agents?

Accepted Answer

Both Cyclophosphamide and Melphalan

Answer

Cyclophosphamide

Answer

Melphalan

Answer

None of the above

Question 2

A 25-year-old female presents with palpable lumps in the axilla and supra-clavicular region. Following clinical examination and diagnostic procedures including X-ray, USG-guided biopsy, and HPE, a diagnosis was established. Flow cytometry revealed CD15 and CD30 positivity. The patient was initiated on chemotherapy and subsequently developed skin lesions. Which of the following chemotherapeutic agents is most likely responsible for these skin manifestations?

Accepted Answer

Bleomycin

Answer

Daunorubicin

Answer

Capecitabine

Answer

Cyclophosphamide

Question 3

Which of the following statements is true regarding methotrexate?

Accepted Answer

Causes thrombocytopenia.

Answer

Oral bioavailability is 30-40%.

Answer

Does not interfere with the action of IL-1.

Answer

Not useful in Crohn's disease.

Question 4

Alkalinization of urine is done during the administration of which of the following chemotherapeutic drugs?

Accepted Answer

Methotrexate

Answer

Ara-C

Answer

Cisplatin

Answer

Ifosfamide

Question 5

Ofatumumab is a monoclonal antibody against:

Accepted Answer

CD20

Answer

CD19

Answer

CD79a

Answer

CD25

Question 6

A patient on treatment for leukemia develops chest pain, pulmonary infiltrates, and pleural effusion. What is the likely cause?

Accepted Answer

Tretinoin

Answer

Daunorubicin

Answer

Hydroxyurea

Answer

Cytarabine

Question 7

Thalidomide was reintroduced for certain indications like multiple myeloma after being withdrawn due to side effects. Which of the following is NOT a side effect of thalidomide?

Accepted Answer

Diarrhea

Answer

Hypothyroidism

Answer

Teratogenicity

Answer

Deep Vein Thrombosis

Question 8

Which chemotherapeutic drug inhibits the polymerization of microtubules but is not associated with causing bone marrow suppression?

Accepted Answer

Vincristine

Answer

Cisplatin

Answer

Vinblastine

Answer

5-Fluorouracil

Question 9

Sipuleucel-T is a vaccine indicated for which condition?

Accepted Answer

Prostate carcinoma

Answer

Renal cell carcinoma

Answer

Testicular tumor

Answer

Bladder carcinoma

Question 10

Which of the following causes minimum bone marrow suppression?

Accepted Answer

Bleomycin

Answer

5-Fluorouracil

Answer

Cytarabine

Answer

Topotecan

Anticancer Drugs — MCQs

Anticancer Drugs — MCQs

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