Anticancer Drugs — MCQs

Anticancer Drugs Indian Medical PG Practice Questions and MCQs

Question 321: Cardiomyopathy is a side effect caused by which of the following drugs?

A. Adriamycin (Correct Answer)
B. Emetine
C. Paclitaxel
D. Vincristine

Explanation: **Explanation:** **Adriamycin (Doxorubicin)** is the correct answer. It belongs to the Anthracycline class of antibiotics. The hallmark toxicity of anthracyclines is **cardiotoxicity**, which manifests in two forms: 1. **Acute:** Transient ECG changes (arrhythmias). 2. **Chronic:** Dose-dependent, irreversible **Dilated Cardiomyopathy** leading to Congestive Heart Failure (CHF). * **Mechanism:** The cardiotoxicity is mediated by the generation of **iron-dependent free radicals** (superoxide anions) that cause lipid peroxidation of the myocardial cell membrane. The heart is particularly vulnerable because it has low levels of the protective enzyme **catalase**. **Analysis of Incorrect Options:** * **B. Emetine:** While historically known to cause ECG changes and precordial pain, it is an amoebicide, not a standard anticancer drug, and is rarely used today due to its toxicity profile. * **C. Paclitaxel:** The primary dose-limiting toxicity is **peripheral neuropathy** and bone marrow suppression. While it can cause transient bradycardia, it does not typically cause cardiomyopathy. * **D. Vincristine:** This Vinca alkaloid is classic for causing **peripheral neuropathy** (paresthesia, loss of deep tendon reflexes) and autonomic dysfunction (constipation/paralytic ileus). It is notably **bone marrow sparing**. **High-Yield Clinical Pearls for NEET-PG:** * **Dexrazoxane:** An iron chelator used to prevent/reduce Adriamycin-induced cardiotoxicity. * **Lifetime Dose Limit:** To minimize cardiomyopathy risk, the cumulative dose of Doxorubicin should be kept below **450–550 mg/m²**. * **Monitoring:** Periodic **ECHO/MUGA scans** are mandatory to monitor the Left Ventricular Ejection Fraction (LVEF).

Question 322: Which of the following are alkylating agents?

A. Vincristine
B. Actinomycin-D
C. Chlorambucil
D. Cyclophosphamide (Correct Answer)

Explanation: **Explanation:** Alkylating agents are a class of cell cycle-nonspecific antineoplastic drugs that act by forming covalent bonds with DNA, specifically at the **N7 position of guanine**. This results in DNA cross-linking, strand breakage, and inhibition of DNA replication, ultimately leading to cell death (apoptosis). **Why Cyclophosphamide is correct:** **Cyclophosphamide** is a nitrogen mustard and a classic example of an alkylating agent. It is a prodrug activated in the liver by cytochrome P450 enzymes into its active forms, phosphoramide mustard and acrolein. It is widely used in treating lymphomas, leukemias, and solid tumors. **Analysis of Incorrect Options:** * **A. Vincristine:** This is a **Vinca alkaloid** (Antimitotic). It works by binding to tubulin and inhibiting microtubule polymerization, causing cell cycle arrest in the M-phase. * **B. Actinomycin-D (Dactinomycin):** This is an **Antitumor Antibiotic**. It acts by intercalating between DNA base pairs and inhibiting RNA synthesis by blocking RNA polymerase. * **C. Chlorambucil:** While Chlorambucil **is** also an alkylating agent (nitrogen mustard), in the context of single-choice NEET-PG questions, Cyclophosphamide is often the "most representative" or intended answer if only one can be selected. *Note: If this were a multiple-response question, both C and D would be correct.* **High-Yield Clinical Pearls for NEET-PG:** * **Acrolein Toxicity:** The metabolite acrolein causes **Hemorrhagic Cystitis**. This is prevented by aggressive hydration and the administration of **MESNA** (a sulfhydryl compound that neutralizes acrolein). * **Other Alkylating Agents:** Busulfan (causes pulmonary fibrosis), Nitrosoureas (Carmustine/Lomustine - cross the BBB), and Dacarbazine. * **Resistance:** Often occurs due to increased production of glutathione or enhanced DNA repair mechanisms (e.g., MGMT enzyme).

Question 323: Which of the following antineoplastic drugs is known to cause pulmonary toxicity?

A. Bleomycin (Correct Answer)
B. 5-fluorouracil
C. Cisplatin
D. Vincristine

Explanation: **Explanation:** **Bleomycin (Option A)** is the correct answer. It is a cytotoxic antibiotic that acts by generating free radicals, which cause oxidative damage and double-stranded breaks in DNA. The primary dose-limiting toxicity of Bleomycin is **pulmonary fibrosis**. This occurs because the lungs lack the enzyme **bleomycin hydrolase**, which normally inactivates the drug. Without this enzyme, the drug accumulates in lung tissue, leading to inflammation and eventual fibrosis. **Why other options are incorrect:** * **5-Fluorouracil (Option B):** An antimetabolite primarily known for causing gastrointestinal toxicity (mucositis, diarrhea) and **Hand-Foot Syndrome** (palmar-plantar erythrodysesthesia). * **Cisplatin (Option C):** A platinum compound notorious for **nephrotoxicity** and **ototoxicity**. It is also highly emetogenic. * **Vincristine (Option D):** A vinca alkaloid that inhibits microtubule assembly. Its hallmark toxicity is **peripheral neuropathy** (paresthesia, loss of reflexes) and autonomic dysfunction (constipation). Notably, it is "bone marrow sparing." **High-Yield Clinical Pearls for NEET-PG:** 1. **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. 2. **Oxygen Warning:** Patients with a history of Bleomycin use are at high risk of severe lung injury if exposed to high concentrations of inspired oxygen (e.g., during surgery). 3. **Busulfan:** Another high-yield drug associated with "Busulfan Lung" (interstitial fibrosis). 4. **Skin Toxicity:** Bleomycin can also cause **flagellate hyperpigmentation** of the skin.

Question 324: Neutropenia develops in a patient undergoing cancer chemotherapy. Administration of which one of the following agents would accelerate recovery of neutrophil counts?

A. Leucovorin
B. Filgrastim (Correct Answer)
C. Prednisone
D. Vitamin B12

Explanation: ### Explanation **Correct Option: B. Filgrastim** Filgrastim is a recombinant human **Granulocyte Colony-Stimulating Factor (G-CSF)**. It acts on the bone marrow to stimulate the proliferation and differentiation of progenitor cells into mature neutrophils. In patients undergoing chemotherapy, it is specifically used to reduce the duration and severity of **neutropenia**, thereby decreasing the risk of life-threatening infections (febrile neutropenia). **Why the other options are incorrect:** * **A. Leucovorin (Folinic Acid):** This is a reduced form of folic acid used as a "rescue" therapy following high-dose **Methotrexate** to protect healthy cells from toxicity. It does not directly stimulate neutrophil production. * **C. Prednisone:** While glucocorticoids can cause "pseudoneutrophilia" (by decreasing the margination of neutrophils from blood vessel walls into tissues), they are not used to treat chemotherapy-induced bone marrow suppression. In fact, long-term use can increase infection risk. * **D. Vitamin B12:** This is used to treat megaloblastic anemia caused by B12 deficiency. It has no role in recovering neutrophil counts depleted by cytotoxic chemotherapy. **High-Yield Clinical Pearls for NEET-PG:** * **Sargramostim:** A recombinant **GM-CSF** (Granulocyte-Macrophage CSF) that stimulates both neutrophils and macrophages. * **Oprelvekin (IL-11):** Used to treat chemotherapy-induced **thrombocytopenia** (stimulates platelet production). * **Epoetin Alfa:** A recombinant Erythropoietin used to treat chemotherapy-induced **anemia**. * **Timing:** G-CSF is typically administered 24–72 hours after the completion of chemotherapy; it should not be given simultaneously with cytotoxic drugs as it may worsen myelosuppression. * **Common Side Effect:** The most frequent side effect of Filgrastim is **medullary bone pain**.

Question 325: Which of the following is not an antimetabolite?

A. Methotrexate
B. 5-Fluorouracil
C. Gemcitabine
D. Vincristine (Correct Answer)

Explanation: **Explanation:** The correct answer is **Vincristine** because it belongs to the class of **Vinca Alkaloids**, which are **Mitotic Inhibitors** (M-phase specific), not antimetabolites. **1. Why Vincristine is the correct answer:** Antimetabolites work by interfering with DNA and RNA synthesis, primarily during the **S-phase** of the cell cycle. Vincristine, however, acts by binding to **tubulin** and inhibiting its polymerization into microtubules. This prevents the formation of the mitotic spindle, leading to cell cycle arrest in the **M-phase**. **2. Why the other options are incorrect:** * **Methotrexate (Option A):** A classic **Folate Antagonist**. It inhibits the enzyme *Dihydrofolate Reductase (DHFR)*, preventing the synthesis of tetrahydrofolate required for purine and thymidylate production. * **5-Fluorouracil (Option B):** A **Pyrimidine Analog**. It is converted to 5-dFUMP, which inhibits *Thymidylate Synthase*, leading to "thymineless death" of the cell. * **Gemcitabine (Option C):** A **Pyrimidine (Cytidine) Analog**. It inhibits *Ribonucleotide Reductase* and competes with dCTP for incorporation into DNA, causing chain termination. **Clinical Pearls for NEET-PG:** * **Vincristine Side Effect:** Characterized by **Peripheral Neuropathy** (stocking-glove pattern) and paralytic ileus. Notably, it is **bone marrow sparing** (unlike Vinblastine). * **Methotrexate Toxicity:** Managed with **Leucovorin (Folinic acid) rescue**. * **5-FU Toxicity:** Can cause **Hand-Foot Syndrome** (Palmar-plantar erythrodysesthesia). * **Cell Cycle Specificity:** Remember that all antimetabolites are **S-phase specific**, while Vinca alkaloids and Taxanes are **M-phase specific**.

Question 326: Which of the following is an adenosine deaminase inhibitor?

A. Pentostatin (Correct Answer)
B. TxA2
C. Cladribine
D. All of the above

Explanation: **Explanation:** **1. Correct Answer: Pentostatin** Pentostatin (2'-deoxycoformycin) is a potent, irreversible inhibitor of the enzyme **Adenosine Deaminase (ADA)**. ADA is essential for the purine salvage pathway, converting adenosine to inosine and deoxyadenosine to deoxyinosine. Inhibition of ADA leads to the toxic accumulation of intracellular deoxyadenosine triphosphate (dATP). High levels of dATP inhibit ribonucleotide reductase, thereby stalling DNA synthesis and inducing apoptosis, particularly in lymphocytes. It is the drug of choice for **Hairy Cell Leukemia**. **2. Analysis of Incorrect Options:** * **TxA2 (Thromboxane A2):** This is a lipid signaling molecule (eicosanoid) produced by platelets. It promotes platelet aggregation and vasoconstriction. It is not an anticancer drug or an enzyme inhibitor in this context. * **Cladribine:** While also used for Hairy Cell Leukemia, Cladribine is a **purine nucleoside analog** (resistant to degradation by ADA). It mimics adenosine and incorporates into DNA, causing strand breaks. It does not inhibit the ADA enzyme itself. * **All of the above:** Incorrect, as only Pentostatin fits the specific mechanism of ADA inhibition. **3. High-Yield Clinical Pearls for NEET-PG:** * **Drug of Choice:** Both Pentostatin and Cladribine are highly effective for Hairy Cell Leukemia, but their mechanisms differ (Pentostatin = ADA inhibitor; Cladribine = Purine analog). * **ADA Deficiency:** Congenital deficiency of Adenosine Deaminase leads to **SCID (Severe Combined Immunodeficiency)** due to the accumulation of dATP, which is toxic to T and B cells. * **Other Purine Analogs:** Remember **Fludarabine** (used in CLL) and **6-Mercaptopurine** (inhibits PRPP amidotransferase).

Question 327: Denileukin diftitox is used in which of the following conditions?

A. Breast carcinoma
B. AML
C. Cutaneous T cell lymphoma (Correct Answer)
D. Burkitt's lymphoma

Explanation: Denileukin diftitox is a unique antineoplastic agent classified as a fusion toxin. It is engineered by combining the cytotoxic fragments of the Diphtheria toxin with the receptor-binding domain of Interleukin-2 (IL-2).1. **Why Cutaneous T-cell Lymphoma (CTCL) is correct:** The mechanism of action relies on the expression of **CD25**, which is the alpha subunit of the IL-2 receptor. This receptor is highly expressed on the malignant T-cells of patients with CTCL (Mycosis Fungoides/Sézary Syndrome). The drug binds to the IL-2 receptor, is internalized via endocytosis, and releases the diphtheria toxin fragment into the cytosol. This inhibits protein synthesis by inactivating **Elongation Factor-2 (EF-2)**, leading to cell death.2. **Why other options are incorrect:** * **Breast Carcinoma:** Typically treated with hormonal therapy (Tamoxifen), HER2 inhibitors (Trastuzumab), or taxanes; these cells do not characteristically express the IL-2 receptor. * **AML:** Treatment involves cytarabine and anthracyclines; CD25 is not a primary target in standard AML protocols. * **Burkitt’s Lymphoma:** A B-cell malignancy associated with c-myc translocation; it is treated with aggressive regimens like R-CODOX-M/IVAC, targeting B-cell markers (CD20) rather than IL-2 receptors.**High-Yield Clinical Pearls for NEET-PG:** * **Mechanism:** Inhibition of EF-2 (similar to *Pseudomonas* exotoxin and *Corynebacterium diphtheriae* toxin). * **Target:** CD25 (IL-2 receptor). * **Key Side Effect:** **Vascular Leak Syndrome** (hypotension, edema, and hypoalbuminemia) is a classic board-relevant adverse effect. * **Indication:** Specifically FDA-approved for persistent or recurrent CTCL.

Question 328: Imatinib is used in the treatment of which condition?

A. Chronic Myeloid Leukemia (CML) (Correct Answer)
B. Myelodysplastic Syndromes (MDS)
C. Acute Lymphoblastic Leukemia (ALL)
D. All of the above

Explanation: ### Explanation **1. Why Option A is Correct:** Imatinib is the prototype of a class of drugs known as **Tyrosine Kinase Inhibitors (TKIs)** [2]. It is the first-line treatment for **Chronic Myeloid Leukemia (CML)** [2], [3]. The underlying pathophysiology of CML involves the **Philadelphia chromosome (t[9;22])**, which creates the **BCR-ABL fusion gene** [4]. This gene produces a constitutively active tyrosine kinase protein that drives uncontrolled white blood cell proliferation [4]. Imatinib works by binding to the ATP-binding site of the BCR-ABL enzyme, effectively "turning off" the signal for cell division [1], [3]. **2. Why Other Options are Incorrect:** * **Myelodysplastic Syndromes (MDS):** These are a group of bone marrow failure disorders. While some specific subtypes (like those with 5q deletion) respond to Lenalidomide, Imatinib is not a standard treatment for MDS. * **Acute Lymphoblastic Leukemia (ALL):** While Imatinib is used in a specific subset of ALL (Philadelphia chromosome-positive or Ph+ ALL), it is not the primary treatment for ALL in general, which usually requires intensive multi-agent chemotherapy [1]. * **All of the above:** Since Imatinib is specifically targeted toward the BCR-ABL mutation, its primary and most definitive indication remains CML. **3. High-Yield Clinical Pearls for NEET-PG:** * **Mechanism:** Competitive inhibition of the ATP-binding site of BCR-ABL tyrosine kinase [3]. * **Other Indications:** Imatinib is also highly effective in **Gastrointestinal Stromal Tumors (GIST)** because it inhibits the **c-KIT** tyrosine kinase. * **Side Effects:** The most characteristic side effect is **periorbital edema** (fluid retention). Others include muscle cramps and GI upset. * **Resistance:** Resistance to Imatinib often occurs due to point mutations in the BCR-ABL kinase domain (e.g., the **T315I mutation**), which necessitates the use of second-generation TKIs like **Dasatinib** or **Nilotinib**, or the third-generation **Ponatinib** [1].

Question 329: What is the main side effect of Imatinib mesylate?

A. Leg ulcers
B. Fluid retention (Correct Answer)
C. Flagellate hyperpigmentation
D. Irreversible myelosuppression

Explanation: Imatinib mesylate is a selective Tyrosine Kinase Inhibitor (TKI) that targets the BCR-ABL protein (Philadelphia chromosome), as well as c-KIT and PDGFR [1]. It is the first-line treatment for Chronic Myeloid Leukemia (CML) [1] and Gastrointestinal Stromal Tumors (GIST) [2]. 1. Why Fluid Retention is Correct: The most characteristic and common side effect of Imatinib is fluid retention, which typically manifests as periorbital edema (puffiness around the eyes) and peripheral edema. In severe cases, it can lead to pleural effusion or ascites. This occurs due to the inhibition of the Platelet-Derived Growth Factor Receptor (PDGFR) [1], which regulates interstitial fluid pressure. 2. Analysis of Incorrect Options: * A. Leg ulcers: These are classically associated with Hydroxyurea, often used in myeloproliferative disorders. * C. Flagellate hyperpigmentation: This is a pathognomonic side effect of Bleomycin [3]. It presents as linear, whip-like streaks on the trunk. * D. Irreversible myelosuppression: While Imatinib can cause myelosuppression (neutropenia/thrombocytopenia), it is usually reversible upon dose adjustment. Irreversible bone marrow suppression is more characteristic of Busulfan or high-dose radiation. High-Yield Clinical Pearls for NEET-PG: * Mechanism: Inhibits the ATP-binding site of the BCR-ABL tyrosine kinase [1]. * Drug of Choice (DOC): Chronic Myeloid Leukemia (CML) [1]. * Other Side Effects: Muscle cramps, GI upset, and skin rashes. * Metabolism: Metabolized by CYP3A4; therefore, grapefruit juice should be avoided as it increases drug toxicity [2].

Question 330: What is the most common side effect of cisplatin in a patient being treated for esophageal carcinoma?

A. Acute tubular necrosis (Correct Answer)
B. Thrombocytopenia
C. Hepatic failure
D. Cardiomyopathy

Explanation: **Explanation:** **Cisplatin** is a potent platinum-based alkylating agent used extensively in solid tumors like esophageal, lung, and germ cell carcinomas. **1. Why Acute Tubular Necrosis (ATN) is correct:** The dose-limiting toxicity of Cisplatin is **nephrotoxicity**. Cisplatin accumulates in the proximal convoluted tubule (PCT) and the S3 segment of the straight tubule, leading to oxidative stress and apoptosis of tubular cells. This manifests clinically as **Acute Tubular Necrosis**, characterized by a decrease in GFR and an increase in serum creatinine. To mitigate this, patients are typically managed with aggressive **pre-treatment hydration** (saline diuresis) and the administration of **Amifostine** (a cytoprotective free-radical scavenger). **2. Why the other options are incorrect:** * **Thrombocytopenia:** While Cisplatin causes mild bone marrow suppression, it is notably **less myelosuppressive** than most other anticancer drugs (like Carboplatin). * **Hepatic failure:** Cisplatin is not typically associated with significant hepatotoxicity; its primary elimination is renal. * **Cardiomyopathy:** This is a classic side effect of **Anthracyclines** (e.g., Doxorubicin), not Cisplatin. **High-Yield Clinical Pearls for NEET-PG:** * **Mnemonic for Cisplatin Toxicity:** "3 N's" — **N**ephrotoxicity (ATN), **N**eurotoxicity (Peripheral neuropathy), and **N**eusea/Vomiting (it is highly emetogenic). * **Ototoxicity:** Cisplatin causes high-frequency hearing loss (tinnitus/deafness) which is often irreversible. * **Electrolyte Imbalance:** It frequently causes **hypomagnesemia** due to renal wasting. * **Amifostine:** Specifically used to reduce Cisplatin-induced nephrotoxicity.

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

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Immunotherapy

Practice Questions

Management of Chemotherapy Side Effects

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