Anticancer Drugs — MCQs

Anticancer Drugs Indian Medical PG Practice Questions and MCQs

Question 441: Leucovorin rescue is related to which of the following?

A. Methotrexate toxicity (Correct Answer)
B. Cyclophosphamide toxicity
C. Oncovin toxicity
D. Cisplatin toxicity

Explanation: **Explanation:** **Leucovorin (Folinic Acid)** is a reduced form of folic acid. Its primary role in oncology is to bypass the metabolic block created by **Methotrexate (MTX)**. 1. **Why Methotrexate is the correct answer:** Methotrexate acts by inhibiting the enzyme **Dihydrofolate Reductase (DHFR)**, which prevents the conversion of folic acid to its active form, Tetrahydrofolate (THF). This depletion of THF halts DNA synthesis, leading to cell death. Leucovorin does not require DHFR for activation; it provides a direct source of reduced folate to healthy cells, "rescuing" them from lethal toxicity. This is typically administered 24 hours after high-dose MTX to prevent bone marrow suppression and GI mucosal damage. 2. **Why other options are incorrect:** * **Cyclophosphamide:** Toxicity (Hemorrhagic Cystitis) is managed with **MESNA** and aggressive hydration. * **Oncovin (Vincristine):** Toxicity (Peripheral Neuropathy) is managed symptomatically; there is no specific "rescue" agent. * **Cisplatin:** Nephrotoxicity is managed with **Amifostine** and vigorous hydration with chloride diuresis. **High-Yield Clinical Pearls for NEET-PG:** * **The "Leucovorin Potentiation":** While Leucovorin *rescues* cells from MTX, it actually *enhances* the activity of **5-Fluorouracil (5-FU)** by stabilizing the binding of 5-dUMP to thymidylate synthase. * **Glucarpidase:** An alternative for MTX toxicity in patients with renal failure; it enzymatically breaks down MTX. * **Mnemonic for MTX side effects:** **M**yelosuppression, **T**eratogenic, **X**-tra (Mucositis/Liver Cirrhosis).

Question 442: Hand, foot, and mouth syndrome is caused by which of the following?

A. Cisplatin
B. Methotrexate
C. 5-Fluorouracil (Correct Answer)
D. Metvcergide

Explanation: **Explanation:** **Hand-Foot Syndrome (HFS)**, also known as Palmar-Plantar Erythrodysesthesia (PPE), is a distinct dermatological toxicity characterized by redness, swelling, and pain on the palms and soles. 1. **Why 5-Fluorouracil (5-FU) is correct:** 5-FU and its oral prodrug, **Capecitabine**, are the most common causes of HFS. The underlying mechanism involves the leakage of the drug from small capillaries in the palms and soles due to high pressure and friction. Once leaked, the drug causes local tissue damage. Capecitabine is actually more frequently associated with this syndrome than bolus 5-FU. 2. **Why other options are incorrect:** * **Cisplatin:** Primarily known for its "C" toxicities: **C**ytotoxicity (Ototoxicity) and **C**idney (Nephrotoxicity). It is also highly emetogenic. * **Methotrexate:** Its hallmark toxicities include myelosuppression, mucositis, and hepatotoxicity. It is managed with Leucovorin rescue. * **Methysergide:** This is an ergot alkaloid used for migraine prophylaxis, not an anticancer drug. Its classic side effect is **retroperitoneal fibrosis**. **High-Yield Clinical Pearls for NEET-PG:** * **Management of HFS:** Dose reduction or interruption of the drug is the primary treatment. Supportive care includes urea-based creams and avoiding heat/friction. * **5-FU Toxicity:** Aside from HFS, 5-FU is notorious for causing **mucositis** and diarrhea. * **DPD Deficiency:** Patients with Dihydropyrimidine Dehydrogenase (DPD) deficiency are at a high risk of severe, life-threatening toxicity when given 5-FU. * **Other drugs causing HFS:** Sorafenib, Sunitinib, and Cytarabine.

Question 443: Which of the following are anticancer drugs of plant origin?

A. Vincristine and Bleomycin
B. Vincristine
C. Isotretinoin
D. Vincristine and Isotretinoin (Correct Answer)

Explanation: **Explanation:** The correct answer is **D (Vincristine and Isotretinoin)** because both drugs are derived from natural plant sources and used in oncology. 1. **Vincristine:** This is a classic **Vinca alkaloid** derived from the Madagascar periwinkle plant (*Catharanthus roseus*). It acts as a cell-cycle specific agent (M-phase) by binding to tubulin and inhibiting microtubule polymerization, thereby preventing spindle formation. 2. **Isotretinoin:** While often associated with dermatology, Isotretinoin (13-cis-retinoic acid) is a **Retinoid**, which is a derivative of **Vitamin A**. Vitamin A is naturally sourced from plant carotenoids (like beta-carotene). In oncology, it is used as a differentiating agent, particularly in the treatment of high-risk neuroblastoma and certain skin cancers. **Analysis of Incorrect Options:** * **Bleomycin (Option A):** This is an antitumor antibiotic. It is derived from the fungus-like bacterium ***Streptomyces verticillus***, not a plant. * **Isotretinoin alone (Option B/C):** While correct in origin, these options are incomplete as Vincristine also fits the criteria. **High-Yield NEET-PG Pearls:** * **Plant-Derived Anticancer Groups:** * **Vinca Alkaloids:** Vincristine, Vinblastine (Source: *Catharanthus roseus*). * **Taxanes:** Paclitaxel, Docetaxel (Source: *Taxus brevifolia/baccata*). * **Epipodophyllotoxins:** Etoposide, Teniposide (Source: *Podophyllum peltatum*). * **Camptothecins:** Irinotecan, Topotecan (Source: *Camptotheca acuminata*). * **Side Effect Note:** Vincristine is notorious for **peripheral neuropathy** (paresthesia, foot drop) but is relatively **bone marrow sparing**, unlike Vinblastine.

Question 444: What enzyme is inhibited by etoposide?

A. Topoisomerase I
B. Topoisomerase II (Correct Answer)
C. Dihydrofolate reductase
D. Dihydroorotate oxidase

Explanation: **Explanation:** **Correct Answer: B. Topoisomerase II** Etoposide (and its analog Teniposide) is a semi-synthetic derivative of podophyllotoxin. Its primary mechanism of action involves inhibiting **Topoisomerase II**. This enzyme is responsible for creating transient double-stranded breaks in DNA to relieve torsional strain during replication. Etoposide binds to the DNA-topoisomerase II complex, preventing the religation of these breaks. This leads to permanent DNA strand scission, triggering apoptosis. It is cell-cycle specific, acting primarily in the **late S and G2 phases**. **Analysis of Incorrect Options:** * **A. Topoisomerase I:** This enzyme creates single-stranded breaks. It is inhibited by the **Camptothecins** (e.g., Irinotecan and Topotecan). * **C. Dihydrofolate Reductase (DHFR):** This enzyme is inhibited by **Methotrexate**, which prevents the conversion of dihydrofolate to tetrahydrofolate, disrupting thymidylate synthesis. * **D. Dihydroorotate Oxidase:** This mitochondrial enzyme is involved in de novo pyrimidine synthesis and is inhibited by **Leflunomide** (used in Rheumatoid Arthritis). **High-Yield Clinical Pearls for NEET-PG:** * **Indications:** Etoposide is a cornerstone in treating Small Cell Lung Cancer (SCLC), testicular tumors (as part of the BEP regimen), and lymphomas. * **Adverse Effects:** Apart from myelosuppression, a high-yield side effect is **secondary leukemia** (specifically Acute Myeloid Leukemia with 11q23 translocation), which typically occurs 2–3 years after treatment. * **Mnemonic:** Remember "**E**-**T**-**O**-poside" inhibits Topoisomerase **TWO** (II).

Question 445: Which drug is used in estrogen-dependent breast cancer?

A. Tamoxifen (Correct Answer)
B. Clomiphene citrate
C. Estrogen
D. Adriamycin

Explanation: **Tamoxifen** is the gold standard for treating estrogen receptor-positive (ER+) breast cancer [1]. It belongs to the class of **Selective Estrogen Receptor Modulators (SERMs)** [2]. Its mechanism of action is tissue-specific: it acts as a competitive **antagonist** in breast tissue, blocking estrogen from binding to its receptor, thereby inhibiting the growth of estrogen-dependent tumor cells [1]. **Analysis of Incorrect Options:** * **Clomiphene citrate:** While also a SERM, it acts primarily as an antagonist at the hypothalamus. This blocks the negative feedback of estrogen, leading to increased FSH/LH secretion. It is used for **ovulation induction** in infertility, not breast cancer [2]. * **Estrogen:** Administering estrogen would stimulate the growth of estrogen-dependent tumors, worsening the prognosis. * **Adriamycin (Doxorubicin):** This is a potent cytotoxic antibiotic (anthracycline) used in many cancers. While used in breast cancer chemotherapy (AC regimen), it is **not specific** to estrogen-dependent pathways; it works via DNA intercalation and topoisomerase II inhibition. **NEET-PG High-Yield Pearls:** * **Dual Nature:** Tamoxifen is an antagonist in the breast but an **agonist in the endometrium and bone** [2]. * **Side Effects:** Due to its agonistic effect on the uterus, it increases the risk of **endometrial carcinoma**. It also increases the risk of thromboembolism (DVT/PE) [1]. * **Prophylaxis:** It is used for both treatment and primary prevention of breast cancer in high-risk women [1]. * **Drug of Choice:** For post-menopausal ER+ breast cancer, **Aromatase Inhibitors** (e.g., Letrozole, Anastrozole) are now often preferred over Tamoxifen [1].

Question 446: Hemorrhagic cystitis is a known side effect of which of the following medications?

A. Cyclophosphamide (Correct Answer)
B. Busulfan
C. Ketoprofen
D. 5-Fluorouracil

Explanation: **Explanation:** **Cyclophosphamide** (and its analog Ifosfamide) is an alkylating agent of the nitrogen mustard group. It is a prodrug metabolized in the liver to form two active metabolites: **Aldophosphamide** and **Phosphoramide mustard**. During this process, a toxic byproduct called **Acrolein** is generated. Acrolein is excreted in the urine, where it causes direct irritation and sloughing of the bladder mucosa, leading to **hemorrhagic cystitis**. **Analysis of Incorrect Options:** * **B. Busulfan:** An alkylating agent primarily used in CML. Its classic side effects include pulmonary fibrosis ("Busulfan lung"), hyperpigmentation, and adrenal insufficiency-like syndrome. * **C. Ketoprofen:** A non-steroidal anti-inflammatory drug (NSAID). While it can cause renal impairment or gastric ulcers, it is not associated with hemorrhagic cystitis. * **D. 5-Fluorouracil:** An antimetabolite (pyrimidine analog). Its hallmark side effects include hand-foot syndrome, myelosuppression, and mucositis. **NEET-PG High-Yield Pearls:** 1. **Prevention:** Hemorrhagic cystitis is prevented by aggressive hydration and the administration of **MESNA** (2-Mercaptoethane Sulfonate Na). 2. **Mechanism of MESNA:** It contains a thiol (-SH) group that binds to and neutralizes acrolein in the bladder, forming a non-toxic compound. 3. **Other Cyclophosphamide Side Effects:** It is notorious for causing SIADH and is a potent immunosuppressant. 4. **Long-term Risk:** Chronic irritation from acrolein increases the risk of **Transitional Cell Carcinoma** of the bladder.

Question 447: What is the most common side effect of 5-fluorouracil?

A. Gastrointestinal toxicity (Correct Answer)
B. Bone marrow depression
C. Cardiotoxicity
D. Neurotoxicity

Explanation: **Explanation:** **5-Fluorouracil (5-FU)** is a pyrimidine antimetabolite that inhibits thymidylate synthase, leading to "thymineless death" of rapidly dividing cells. 1. **Why Gastrointestinal (GI) Toxicity is the correct answer:** While 5-FU affects all rapidly proliferating tissues, it has a particularly high affinity for the mucosal lining of the GI tract. The most common and dose-limiting side effects are **mucositis, stomatitis, and diarrhea**. These symptoms occur because the drug inhibits the regeneration of the intestinal epithelium, leading to ulceration and inflammation throughout the gut. 2. **Analysis of Incorrect Options:** * **Bone marrow depression:** While 5-FU does cause myelosuppression (leukopenia and thrombocytopenia), it is generally considered secondary to GI toxicity in terms of frequency and clinical prominence during standard bolus regimens. * **Cardiotoxicity:** This is a rare but specific side effect of 5-FU, typically manifesting as coronary vasospasm or angina-like chest pain. It is high-yield but not the *most common*. * **Neurotoxicity:** This is an uncommon side effect, usually presenting as acute cerebellar ataxia (the "slurred speech and shaky hands" syndrome), more frequently seen with high doses or in patients with DPD deficiency. **Clinical Pearls for NEET-PG:** * **DPD Deficiency:** Patients deficient in **Dihydropyrimidine dehydrogenase (DPD)** are at a significantly higher risk of severe, life-threatening toxicity from 5-FU. * **Hand-Foot Syndrome (Palmar-plantar erythrodysesthesia):** A characteristic side effect of 5-FU (especially with continuous infusion) and its prodrug, **Capecitabine**. * **Rescue Agent:** **Uridine triacetate** is used as an antidote for 5-FU overdose or severe toxicity. * **Synergy:** 5-FU is often administered with **Leucovorin**, which enhances its binding to thymidylate synthase, increasing its efficacy (unlike Methotrexate, where Leucovorin acts as a "rescue").

Question 448: Which tyrosine kinase inhibitor has HER2/NEU receptor inhibition activity?

A. Imatinib
B. Nilotinib
C. Lapatinib (Correct Answer)
D. Sunitinib

Explanation: **Explanation:** **Lapatinib** is a dual tyrosine kinase inhibitor (TKI) that targets both the **Epidermal Growth Factor Receptor (EGFR/ErbB1)** and the **Human Epidermal Growth Factor Receptor 2 (HER2/neu/ErbB2)**. Unlike monoclonal antibodies like Trastuzumab which bind to the extracellular domain, Lapatinib acts intracellularly to inhibit the ATP-binding domain of these receptors. It is primarily used in the treatment of HER2-positive advanced or metastatic breast cancer. **Analysis of Incorrect Options:** * **Imatinib:** The first-line TKI for Chronic Myeloid Leukemia (CML). It targets **BCR-ABL**, c-KIT, and PDGFR. It has no activity against HER2. * **Nilotinib:** A second-generation TKI designed to overcome Imatinib resistance in CML. Like Imatinib, its primary target is the **BCR-ABL** tyrosine kinase. * **Sunitinib:** A multi-targeted TKI that primarily inhibits **VEGFR** and PDGFR. It is used in Renal Cell Carcinoma (RCC) and Gastrointestinal Stromal Tumors (GIST) due to its potent anti-angiogenic properties. **High-Yield Clinical Pearls for NEET-PG:** * **Lapatinib vs. Trastuzumab:** Lapatinib is small enough to cross the **blood-brain barrier**, making it useful for CNS metastases in HER2+ breast cancer, where Trastuzumab (a large antibody) has limited penetration. * **Side Effects:** A common side effect of Lapatinib is a skin rash (common to EGFR inhibitors) and diarrhea. * **Other HER2 Inhibitors:** **Neratinib** and **Afatinib** are irreversible ErbB family blockers. * **Drug of Choice:** Imatinib remains the DOC for CML and GIST (c-KIT positive).

Question 449: Which drug is used to counteract Methotrexate toxicity?

A. Mesna
B. Folinic acid (Correct Answer)
C. Folic acid
D. Vitamin B12

Explanation: **Explanation:** **Mechanism of Action & Correct Answer:** Methotrexate (MTX) is an antimetabolite that acts as a folic acid antagonist. It competitively inhibits the enzyme **Dihydrofolate Reductase (DHFR)**, preventing the conversion of Dihydrofolate (DHF) to Tetrahydrofolate (THF). THF is essential for DNA synthesis (purine and thymidine synthesis). **Folinic acid (Leucovorin)** is the correct answer because it is a reduced form of folic acid (5-formyl THF). Unlike regular folic acid, it does **not** require DHFR for activation. It bypasses the blocked enzyme to provide the necessary folate pool for healthy cells, a process known as **"Leucovorin Rescue."** **Analysis of Incorrect Options:** * **Folic acid:** Ineffective because MTX inhibits DHFR, the very enzyme needed to convert folic acid into its active form. * **Mesna:** Used specifically to prevent hemorrhagic cystitis caused by Cyclophosphamide and Ifosfamide by neutralizing acrolein in the bladder. * **Vitamin B12:** While involved in DNA synthesis, it does not counteract the DHFR inhibition caused by MTX. **High-Yield Clinical Pearls for NEET-PG:** 1. **Timing:** Leucovorin must be administered within 24–42 hours of MTX to be effective. 2. **Glucarpidase:** An alternative "rescue" agent used in patients with MTX-induced renal failure; it enzymatically breaks down MTX. 3. **Toxicity Profile:** MTX toxicity typically manifests as myelosuppression, mucositis, and hepatotoxicity. 4. **Resistance:** MTX resistance often occurs via decreased polyglutamation or altered DHFR affinity.

Question 450: 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 correct answer is **Tretinoin (All-trans retinoic acid - ATRA)**. The clinical presentation described—chest pain, pulmonary infiltrates, and pleural effusion—is characteristic of **Differentiation Syndrome** (formerly known as ATRA Syndrome). This is a life-threatening complication occurring in patients with Acute Promyelocytic Leukemia (APL) treated with Tretinoin or Arsenic Trioxide. **Mechanism:** Tretinoin induces the rapid maturation (differentiation) of leukemic promyelocytes. These maturing cells release inflammatory cytokines and express adhesion molecules, leading to massive pulmonary infiltration, capillary leak, and organ failure. Management involves immediate administration of high-dose intravenous **Dexamethasone**. **Why other options are incorrect:** * **Daunorubicin:** An anthracycline primarily associated with **cardiotoxicity** (dilated cardiomyopathy/congestive heart failure), not acute pulmonary infiltrates. * **Hydroxyurea:** Commonly causes myelosuppression and skin ulcers. While it can rarely cause interstitial pneumonitis, it is not the classic cause of this acute triad in a leukemia setting. * **Cytarabine:** Known for "Cytarabine Syndrome" (fever, rash, conjunctivitis) and cerebellar toxicity at high doses, but it is not the primary association for this specific respiratory presentation. **High-Yield Clinical Pearls for NEET-PG:** * **APL Marker:** Associated with **t(15;17)** translocation. * **Treatment of Choice:** ATRA + Arsenic Trioxide. * **Differentiation Syndrome Triad:** Fever, dyspnea (pulmonary infiltrates/effusion), and weight gain (edema). * **Prophylaxis:** If the initial white blood cell count is high, prophylactic steroids are often started alongside ATRA.

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

Practice Questions

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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