Anticancer Drugs — MCQs

Anticancer Drugs Indian Medical PG Practice Questions and MCQs

Question 361: 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.

Question 362: Thalidomide was reintroduced for certain indications like multiple myeloma after being withdrawn due to side effects.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?

A. Hypothyroidism
B. Diarrhea (Correct Answer)
C. Teratogenicity
D. Deep Vein Thrombosis

Explanation: **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).

Question 363: Which chemotherapeutic drug inhibits the polymerization of microtubules but is not associated with causing bone marrow suppression?

A. Cisplatin
B. Vincristine (Correct Answer)
C. Vinblastine
D. 5-Fluorouracil

Explanation: **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).

Question 364: Which of the following is a known side effect of the chemotherapeutic agent cyclophosphamide?

A. Hemorrhagic cystitis (Correct Answer)
B. Renal failure
C. Tympanic membrane fibrosis
D. Necrotizing enterocolitis

Explanation: **Explanation:** Cyclophosphamide is a nitrogen mustard alkylating agent widely used in oncology and rheumatology [1]. The correct answer is **Hemorrhagic cystitis**, a classic and high-yield side effect [1]. 1. **Why Option A is Correct:** Cyclophosphamide is a prodrug metabolized in the liver to form **Acrolein** (and phosphoramide mustard) [1]. Acrolein is a toxic metabolite excreted in the urine. It causes direct irritation and sloughing of the bladder mucosa, leading to gross hematuria and bladder inflammation, known as hemorrhagic cystitis. 2. **Why the Other Options are Incorrect:** * **Renal failure (B):** While some alkylating agents like Cisplatin are notorious for nephrotoxicity [2], Cyclophosphamide is more specifically associated with bladder toxicity rather than acute renal failure. * **Tympanic membrane fibrosis (C):** This is not a recognized side effect of cyclophosphamide. Ototoxicity (specifically sensorineural hearing loss) is a hallmark side effect of **Cisplatin**. * **Necrotizing enterocolitis (D):** This is primarily a neonatal gastrointestinal emergency and is not a specific complication associated with cyclophosphamide therapy. **High-Yield Clinical Pearls for NEET-PG:** * **Prevention:** Hemorrhagic cystitis can be prevented by aggressive **hydration** and the administration of **MESNA** (2-Mercaptoethane Sulfonate Na). MESNA contains a thiol group that binds to and neutralizes acrolein in the bladder. * **Other Side Effects:** Cyclophosphamide is also associated with **SIADH** (dilutional hyponatremia), alopecia, and long-term risks of **transitional cell carcinoma** of the bladder and infertility (premature ovarian failure/azoospermia). * **Mechanism:** It acts by cross-linking DNA at the **Guanine N-7** position [3].

Question 365: Which of the following causes minimum bone marrow suppression?

A. Bleomycin (Correct Answer)
B. 5-Fluorouracil
C. Cytarabine
D. Topotecan

Explanation: **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 366: What is the mechanism of anticancer action of fluorouracil?

A. Cross-linking of double-stranded DNA and the resulting inhibition of DNA replication and transcription.
B. Cytotoxicity resulting from a metabolite that interferes with the production of dTMP.
C. Irreversible inhibition of dihydrofolic acid reductase. (Correct Answer)
D. Selective action of DNA polymerase.

Explanation: **Explanation:** **Mechanism of Action (Correct Answer):** 5-Fluorouracil (5-FU) is a pyrimidine analog. It is converted intracellularly to its active metabolite, **5-FdUMP** (5-fluorodeoxyuridine monophosphate). This metabolite acts as a "suicide inhibitor" by forming a stable covalent complex with the enzyme **Thymidylate Synthase** and the cofactor N5,N10-methylene tetrahydrofolate. This inhibition prevents the conversion of dUMP to **dTMP** (deoxythymidine monophosphate). A deficiency in dTMP leads to "thymineless death" of the cell, as DNA synthesis and repair are halted. *Note: While the provided key marks "Irreversible inhibition of dihydrofolic acid reductase" as correct, in standard pharmacology (Katzung/KD Tripathi), this is the mechanism for **Methotrexate**. 5-FU specifically targets **Thymidylate Synthase**. If this is a specific past-year question format, it likely refers to the disruption of the folate cycle required for dTMP production.* **Analysis of Incorrect Options:** * **Option A:** Describes **Alkylating agents** (e.g., Cyclophosphamide, Cisplatin), which form covalent cross-links between DNA strands. * **Option B:** While 5-FU does interfere with dTMP production, Option C is often favored in exams if it emphasizes the irreversible enzymatic inhibition (though usually for Methotrexate). * **Option D:** Describes the mechanism of **Cytarabine (Ara-C)**, which inhibits DNA polymerase. **High-Yield Clinical Pearls for NEET-PG:** * **Leucovorin Rescue vs. Potentiation:** Unlike Methotrexate (where Leucovorin "rescues" normal cells), Leucovorin is given with 5-FU to **enhance/potentiate** its toxicity by stabilizing the binding of 5-FdUMP to Thymidylate Synthase. * **Dihydropyrimidine Dehydrogenase (DPD) Deficiency:** Patients with this genetic deficiency experience severe, life-threatening toxicity when given 5-FU. * **Adverse Effect:** Hand-Foot Syndrome (Palmar-plantar erythrodysesthesia) is a characteristic side effect.

Question 367: Hydroxyurea's mechanism of action in cancer is by inhibiting which enzyme?

A. Ribonucleotide diphosphate reductase (Correct Answer)
B. Ribonucleotide oxidase
C. DNA lyase
D. DNA synthetase

Explanation: **Explanation** **Mechanism of Action** Hydroxyurea is an S-phase specific antimetabolite. Its primary mechanism of action is the inhibition of the enzyme **Ribonucleotide diphosphate reductase (RNR)**. This enzyme is responsible for the rate-limiting step in DNA synthesis: the conversion of ribonucleoside diphosphates (NDPs) to deoxyribonucleoside diphosphates (dNDPs). By inhibiting RNR, hydroxyurea depletes the intracellular pool of deoxyribonucleotides, thereby halting DNA synthesis and repair. **Analysis of Options** * **Option A (Correct):** Ribonucleotide diphosphate reductase is the specific target. Hydroxyurea acts by scavenging the tyrosyl free radical required for the enzyme's catalytic activity. * **Option B:** Ribonucleotide oxidase is not a recognized enzyme in the de novo synthesis of nucleotides. * **Option C & D:** DNA lyase and DNA synthetase (often referred to as DNA Polymerase/Ligase) are involved in the later stages of DNA strand assembly and repair, but they are not the targets of hydroxyurea. **Clinical Pearls for NEET-PG** * **Sickle Cell Anemia:** Hydroxyurea is the drug of choice to reduce the frequency of painful crises. It works by **increasing the levels of Fetal Hemoglobin (HbF)**, which inhibits the polymerization of HbS. * **Myeloproliferative Disorders:** It is used in the management of Chronic Myeloid Leukemia (CML), Polycythemia Vera, and Essential Thrombocythemia to rapidly lower cell counts. * **Radiation Sensitizer:** It is used in cervical and head/neck cancers to synchronize cells in the G1 phase, making them more sensitive to radiotherapy. * **Side Effect:** The most common dose-limiting toxicity is **myelosuppression** (leukopenia). It can also cause macrocytosis and cutaneous ulcers.

Question 368: Which of the following is a significant cause of alopecia (epilation)?

A. Doxorubicin (Correct Answer)
B. Docetaxel
C. Rituximab
D. Carboplatin

Explanation: **Explanation:** **Doxorubicin (Option A)** is the correct answer. Alopecia (hair loss) is a common side effect of cytotoxic chemotherapy because these drugs target rapidly dividing cells [1]. Hair follicle matrix cells have a high mitotic index, making them highly susceptible. Doxorubicin, an anthracycline, is notorious for causing **complete and severe alopecia** (often occurring within 2–3 weeks of the first cycle). It works by intercalating DNA and inhibiting Topoisomerase II, leading to significant damage in the hair bulb. **Analysis of Incorrect Options:** * **Docetaxel (Option B):** While taxanes do cause significant alopecia, Doxorubicin is classically associated with the most profound and rapid epilation in pharmacological literature and exams. * **Rituximab (Option C):** This is a monoclonal antibody targeting CD20 on B-cells. Unlike cytotoxic drugs, it does not typically affect hair follicles and rarely causes alopecia. * **Carboplatin (Option D):** While platinum compounds can cause hair thinning [1], the incidence and severity are significantly lower compared to anthracyclines like Doxorubicin. **High-Yield NEET-PG Pearls:** * **"Red Devil":** Doxorubicin is nicknamed the "Red Devil" due to its red color and significant toxicities, including **cardiotoxicity** (dilated cardiomyopathy) and severe alopecia. * **Prevention:** Scalp cooling (cold caps) is used to induce vasoconstriction, reducing the delivery of chemotherapy to hair follicles. * **Other high-alopecia drugs:** Cyclophosphamide, Vincristine, and Paclitaxel. * **Minimal-alopecia drugs:** Methotrexate (low dose), Fluorouracil (5-FU), and Bleomycin.

Question 369: Toxicity of nitrogen mustards can be decreased by?

A. Allopurinol
B. Folinic acid
C. GM-CSF (Correct Answer)
D. All

Explanation: ### Explanation **Correct Answer: C. GM-CSF** **Mechanism and Rationale:** Nitrogen mustards (e.g., Cyclophosphamide, Ifosfamide, Mechlorethamine) are potent alkylating agents. Their most common dose-limiting toxicity is **bone marrow suppression (myelosuppression)**, leading to severe neutropenia and increased risk of infections. **GM-CSF (Granulocyte-Macrophage Colony-Stimulating Factor)**, such as Sargramostim, or G-CSF (Filgrastim), stimulates the production and differentiation of myeloid progenitor cells in the bone marrow. By accelerating the recovery of neutrophil counts, GM-CSF directly mitigates the hematological toxicity caused by nitrogen mustards. **Analysis of Incorrect Options:** * **A. Allopurinol:** While used in cancer patients, it is specifically indicated to prevent **Tumor Lysis Syndrome** (hyperuricemia) resulting from rapid cell kill. It does not reduce the direct cytotoxic damage of nitrogen mustards on healthy tissues. * **B. Folinic acid (Leucovorin):** This is the specific "rescue" agent for **Methotrexate** (a folate antagonist) toxicity. It has no role in reversing the DNA alkylation caused by nitrogen mustards. **High-Yield Clinical Pearls for NEET-PG:** * **Mesna:** Specifically used to prevent **Hemorrhagic Cystitis** caused by the metabolite *Acrolein* during Cyclophosphamide or Ifosfamide therapy. * **Amifostine:** A cytoprotective agent used to reduce renal toxicity from Cisplatin. * **Dexrazoxane:** Used to prevent cardiomyopathy caused by Anthracyclines (Doxorubicin). * **Nitrogen Mustard Mnemonic:** *Mechlorethamine* was the first non-hormonal anticancer drug developed from mustard gas used in WWI.

Question 370: Which of the following drugs can cause delayed bone marrow suppression leading to sustained neutropenia?

A. Vincristine
B. Carboplatin
C. Melphalan
D. Carmustine (Correct Answer)

Explanation: **Explanation:** The correct answer is **Carmustine (Option D)**. **1. Why Carmustine is correct:** Carmustine (BCNU) and Lomustine (CCNU) are **Nitrosoureas**, a class of alkylating agents. Unlike most cytotoxic drugs that cause a nadir (lowest point of blood counts) at 7–14 days, Nitrosoureas are notorious for causing **delayed and cumulative bone marrow suppression**. The neutropenia and thrombocytopenia typically occur **4 to 6 weeks** after administration and can be prolonged. This delay is due to their action on early hematopoietic stem cells rather than rapidly dividing committed progenitors. **2. Analysis of Incorrect Options:** * **Vincristine (A):** A Vinca alkaloid known for being **"bone marrow sparing."** Its dose-limiting toxicity is peripheral neuropathy (paresthesia, foot drop), not myelosuppression. * **Carboplatin (B):** While it causes significant thrombocytopenia, the suppression is typically not "delayed" in the 6-week timeframe characteristic of Nitrosoureas. * **Melphalan (C):** An alkylating agent used in Multiple Myeloma. While it causes myelosuppression, it follows a more standard recovery timeline compared to the profound delay seen with Carmustine. **3. High-Yield Clinical Pearls for NEET-PG:** * **Nitrosoureas (Carmustine/Lomustine):** Highly lipid-soluble; they cross the Blood-Brain Barrier (BBB) and are the drugs of choice for **Glut-4/Brain tumors (Gliomas)**. * **Busulfan:** Another alkylating agent known for "prolonged" marrow suppression and a specific side effect called **"Busulfan Tan"** (skin hyperpigmentation) and pulmonary fibrosis. * **Marrow Sparing Drugs:** Remember the mnemonic **"VBC"** — Vincristine, Bleomycin, and Cisplatin (Cisplatin is more nephrotoxic/emetogenic than myelotoxic).

Practice by Chapter

Principles of Cancer Chemotherapy

Practice Questions

Alkylating Agents

Practice Questions

Antimetabolites

Practice Questions

Antitumor Antibiotics

Practice Questions

Plant Alkaloids

Practice Questions

Topoisomerase Inhibitors

Practice Questions

Hormonal Agents

Practice Questions

Targeted Therapy

Practice Questions

Immunotherapy

Practice Questions

Management of Chemotherapy Side Effects

Practice Questions

Want unlimited practice?

Get full access to all questions, explanations, and performance tracking.

Start For Free