Anticancer Drugs — MCQs

Anticancer Drugs Indian Medical PG Practice Questions and MCQs

Question 371: Which of the following agents is known to cause epilation?

A. 5-Flurouracil
B. Cisplatin
C. Adriamycin (Correct Answer)
D. Methotrexate

Explanation: **Explanation:** **Adriamycin (Doxorubicin)**, an anthracycline antibiotic, is notorious for causing significant **alopecia (epilation)**. The underlying mechanism involves the drug’s interference with rapidly dividing cells. Hair follicles have a high mitotic index; Adriamycin inhibits Topoisomerase II and generates free radicals, leading to DNA damage in the hair bulb. This results in an "anagen effluvium," where hair loss is often complete and occurs within 1–3 weeks of treatment. **Analysis of Incorrect Options:** * **5-Fluorouracil (5-FU):** While it can cause thinning of hair, its hallmark toxicity is **Hand-Foot Syndrome** (palmar-plantar erythrodysesthesia) and GI mucosal ulceration. * **Cisplatin:** This platinum compound is primarily known for its dose-limiting **nephrotoxicity** and severe **emetogenicity**. It causes minimal hair loss compared to anthracyclines. * **Methotrexate:** An antimetabolite that primarily causes **myelosuppression** and **mucositis**. While it can cause some hair thinning, it rarely leads to the total epilation characteristic of Adriamycin. **High-Yield Clinical Pearls for NEET-PG:** 1. **Anthracycline Toxicity:** Apart from epilation, the most specific side effect is **Cardiotoxicity** (dilated cardiomyopathy). This is mediated by iron-dependent superoxide free radicals. 2. **Dexrazoxane:** An iron chelator used to prevent Adriamycin-induced cardiotoxicity. 3. **Radiation Recall:** Adriamycin can cause inflammatory skin reactions in previously irradiated areas. 4. **Red Urine:** Patients should be counseled that Adriamycin can cause harmless red discoloration of urine (not hematuria).

Question 372: What is the mechanism of action of 5-fluorouracil?

A. Antimetabolite (Correct Answer)
B. Direct DNA chelating agent
C. Anti-mitotic
D. Topoisomerase inhibitor

Explanation: **Explanation:** **5-Fluorouracil (5-FU)** is a pyrimidine analogue and is classified as an **Antimetabolite**. Its primary mechanism involves the inhibition of **thymidylate synthase**, the enzyme responsible for converting deoxyuridine monophosphate (dUMP) to deoxythymidine monophosphate (dTMP). By creating a "thymineless death" for the cell, it disrupts DNA synthesis during the **S-phase** of the cell cycle. **Why the other options are incorrect:** * **Direct DNA chelating agents:** These are typically platinum compounds (e.g., Cisplatin) or certain antibiotics (e.g., Bleomycin) that bind directly to DNA to cause cross-linking or strand breaks. * **Anti-mitotic:** These drugs (e.g., Vinca alkaloids like Vincristine or Taxanes like Paclitaxel) interfere with microtubule formation or disassembly, acting specifically on the **M-phase**. * **Topoisomerase inhibitors:** These agents (e.g., Etoposide, Irinotecan) inhibit enzymes that manage DNA supercoiling during replication and transcription. **Clinical Pearls for NEET-PG:** * **Synergy:** 5-FU is often administered with **Leucovorin (Folinic acid)**. Unlike its role in Methotrexate toxicity, Leucovorin *potentiates* 5-FU by stabilizing the binding of 5-FU to thymidylate synthase. * **Metabolism:** It is metabolized by the enzyme **Dihydropyrimidine dehydrogenase (DPD)**. Patients with DPD deficiency are at high risk of severe 5-FU toxicity. * **Side Effects:** A classic high-yield side effect is **Hand-Foot Syndrome** (palmar-plantar erythrodysesthesia). * **Topical Use:** Used for actinic keratosis and superficial basal cell carcinoma.

Question 373: Which of the following chemotherapeutic drugs has selective action on hypoxic tumor cells?

A. Mitomycin C (Correct Answer)
B. Cisplatin
C. Doxorubicin
D. 5-Fluorouracil

Explanation: **Explanation:** **Mitomycin C** is the correct answer because it acts as a **bioreductive alkylating agent**. It is a prodrug that requires enzymatic activation (reduction) to form a highly reactive DNA-crosslinking species. This activation process is significantly more efficient in **hypoxic environments** (low oxygen levels) compared to well-oxygenated tissues. Since the core of solid tumors is often poorly vascularized and hypoxic, Mitomycin C exhibits selective toxicity toward these cells, making it a unique tool in treating solid tumors like those of the stomach, pancreas, and bladder. **Analysis of Incorrect Options:** * **B. Cisplatin:** A platinum compound that causes DNA cross-linking. Its efficacy is actually **reduced** in hypoxic conditions because hypoxia can lead to decreased drug uptake and slower cell cycling. * **C. Doxorubicin:** An anthracycline that inhibits Topoisomerase II and generates free radicals. Its free-radical-mediated damage requires **oxygen**, making it less effective in hypoxic tumor zones. * **D. 5-Fluorouracil (5-FU):** An antimetabolite (pyrimidine analog) that inhibits thymidylate synthase. It is most effective against rapidly dividing cells in the S-phase and does not have a selective mechanism for hypoxia. **High-Yield Clinical Pearls for NEET-PG:** * **Dose-Limiting Toxicity:** Mitomycin C causes delayed and prolonged **bone marrow suppression** (thrombocytopenia and leukopenia). * **Specific Side Effect:** It is associated with **Hemolytic Uremic Syndrome (HUS)** and pulmonary fibrosis. * **Clinical Use:** Often used intravesically for superficial bladder cancer to prevent recurrence. * **Concept:** Tumors with high hypoxic fractions are generally resistant to radiotherapy; Mitomycin C is often used as a "hypoxic cell sensitizer" to bridge this gap.

Question 374: Bevacizumab is:

A. Monoclonal antibody against VEGF (Correct Answer)
B. Anti-IL-2 monoclonal antibody
C. Monoclonal antibody against FGFR
D. Monoclonal antibody against EGFR

Explanation: **Explanation:** **Bevacizumab** is a recombinant humanized monoclonal antibody that acts as a potent **angiogenesis inhibitor**. It works by specifically binding to and neutralizing **Vascular Endothelial Growth Factor (VEGF-A)**. By preventing VEGF from binding to its receptors (VEGFR-1 and VEGFR-2) on the surface of endothelial cells, it inhibits the formation of new blood vessels (neovascularization), thereby "starving" the tumor of oxygen and nutrients required for growth and metastasis. **Analysis of Incorrect Options:** * **Option B (Anti-IL-2):** Drugs like **Daclizumab** and **Basiliximab** are monoclonal antibodies against the IL-2 receptor (CD25), primarily used as immunosuppressants in renal transplants. * **Option C (Anti-FGFR):** While Fibroblast Growth Factor Receptor (FGFR) inhibitors exist (e.g., **Erdafitinib**), they are typically small molecule tyrosine kinase inhibitors rather than widely used monoclonal antibodies in standard NEET-PG curricula. * **Option D (Anti-EGFR):** Monoclonal antibodies against the Epidermal Growth Factor Receptor (EGFR) include **Cetuximab** and **Panitumumab**, commonly used in colorectal and head/neck cancers. **High-Yield Clinical Pearls for NEET-PG:** 1. **Clinical Uses:** Bevacizumab is used in metastatic colorectal cancer, non-small cell lung cancer (NSCLC), glioblastoma, and renal cell carcinoma. 2. **Ocular Use:** It is frequently used **off-label** (intravitreal injection) for **Wet Age-Related Macular Degeneration (ARMD)** and diabetic retinopathy to reduce macular edema. 3. **Key Side Effects:** The most characteristic adverse effects include **hypertension**, impaired wound healing, arterial thrombosis, and **proteinuria**. 4. **Suffix Tip:** Monoclonal antibodies ending in **"-umab"** are human, while **"-ximab"** are chimeric.

Question 375: All of the following drugs are components of the MOPP cancer chemotherapy regimen EXCEPT:

A. Procarbazine
B. Vincristine
C. Mechlorethamine
D. Methotrexate (Correct Answer)

Explanation: **Explanation:** The **MOPP regimen** was the first highly effective combination chemotherapy used for the treatment of **Hodgkin Lymphoma**. The acronym stands for: * **M: Mechlorethamine** (Nitrogen mustard; an alkylating agent) * **O: Oncovin** (Brand name for **Vincristine**; a microtubule inhibitor) * **P: Procarbazine** (A methylhydrazine derivative/alkylating agent) [1] * **P: Prednisolone** (A glucocorticoid) **Why Methotrexate is the correct answer:** Methotrexate is a folate antagonist (antimetabolite) [2] used in various regimens like CMF (Breast cancer) or for maintenance in ALL, but it is **not** a component of the MOPP regimen. **Analysis of Incorrect Options:** * **Mechlorethamine:** It is the "M" in MOPP. It is a bifunctional alkylating agent that causes DNA cross-linking. * **Vincristine (Oncovin):** It is the "O" in MOPP. It acts by binding to tubulin and inhibiting microtubule assembly, leading to M-phase arrest. * **Procarbazine:** It is the first "P" in MOPP [1]. It is unique because it also acts as a weak MAO inhibitor. **High-Yield Clinical Pearls for NEET-PG:** 1. **ABVD Regimen:** Due to the high risk of secondary malignancies (like AML) and infertility associated with MOPP, it has largely been replaced by the **ABVD regimen** (Adriamycin, Bleomycin, Vinblastine, Dacarbazine) as the gold standard for Hodgkin Lymphoma. 2. **Procarbazine Side Effect:** It can cause a **Disulfiram-like reaction** with alcohol and hypertensive crises with tyramine-rich foods (due to MAO inhibition). 3. **Vincristine Side Effect:** The dose-limiting toxicity is **peripheral neuropathy** (areflexia, foot drop), unlike Vinblastine, which is more bone marrow suppressive ("Blastine blasts the marrow").

Question 376: Which of the following agents is recommended as the first-line drug for the treatment of gastrointestinal stromal tumors (GIST)?

A. Sorafenib
B. Gefitinib
C. Imatinib (Correct Answer)
D. Erlotinib

Explanation: ### Explanation **Correct Answer: C. Imatinib** **Mechanism and Rationale:** Gastrointestinal Stromal Tumors (GIST) are primarily driven by activating mutations in the **KIT (CD117)** proto-oncogene (a receptor tyrosine kinase) or, less commonly, the **PDGFRA** gene [3]. **Imatinib** is a 2-phenylaminopyrimidine derivative that acts as a selective tyrosine kinase inhibitor (TKI) [2]. It works by binding to the ATP-binding pocket of the KIT and PDGFRA receptors, effectively blocking downstream signaling pathways that lead to cell proliferation [3]. Due to its high efficacy and targeted nature, it is the established **first-line therapy** for both metastatic and unresectable GIST, as well as adjuvant therapy following surgical resection [1, 3]. **Analysis of Incorrect Options:** * **A. Sorafenib:** This is a multi-kinase inhibitor (targeting VEGF, BRAF, and Raf-1) primarily used as first-line therapy for **Hepatocellular Carcinoma (HCC)** and Advanced Renal Cell Carcinoma. * **B. Gefitinib:** This is a selective **EGFR** (Epidermal Growth Factor Receptor) tyrosine kinase inhibitor. It is used as first-line therapy for Non-Small Cell Lung Cancer (NSCLC) with specific EGFR mutations. * **D. Erlotinib:** Similar to Gefitinib, it targets **EGFR** and is used in NSCLC and pancreatic cancer. It does not have significant activity against the KIT mutations found in GIST. **High-Yield Clinical Pearls for NEET-PG:** * **Imatinib Indications:** Also the first-line drug for **Chronic Myeloid Leukemia (CML)**, targeting the **BCR-ABL** (Philadelphia chromosome) fusion protein [3]. * **Resistance:** If a GIST patient develops resistance to Imatinib, the second-line agent of choice is **Sunitinib**, followed by Regorafenib. * **Side Effects:** A classic side effect of Imatinib is **periorbital edema** (fluid retention). * **Diagnostic Marker:** Over 95% of GISTs are positive for **CD117** on immunohistochemistry.

Question 377: Amifostine is protective to all EXCEPT:

A. Salivary glands (Correct Answer)
B. Skin
C. CNS
D. GIT

Explanation: Amifostine is a cytoprotective adjuvant (a prodrug) used to reduce the toxicities of chemotherapy (specifically Cisplatin) and radiotherapy. It is converted by alkaline phosphatase into an active thiol metabolite (WR-1065) that scavenges free radicals. The question asks what Amifostine is protective to EXCEPT. Amifostine is specifically FDA-approved and clinically indicated to protect the salivary glands (preventing xerostomia) during radiation for head and neck cancers. Therefore, it is protective to the salivary glands. *Note: In the context of this specific MCQ format, if "Salivary glands" is marked as the correct answer for an "EXCEPT" question, it implies a technical error in the question stem or a specific focus on its lack of protection for the CNS.* **Analysis of Options** * **CNS (Option C):** This is the actual physiological exception. Amifostine does not cross the blood-brain barrier (BBB). Therefore, it provides no protection to the Central Nervous System. * **Salivary Glands (Option A):** Highly protected. It reduces the incidence of moderate-to-severe xerostomia. * **Skin (Option B) & GIT (Option D):** These tissues have high alkaline phosphatase activity and a neutral pH, allowing Amifostine to accumulate and provide protection against radiation-induced dermatitis and mucositis. **High-Yield Clinical Pearls for NEET-PG** 1. **Mechanism:** It is a selective cytoprotectant because normal cells have higher alkaline phosphatase activity and better vascularity (higher pH) than tumor cells, allowing the drug to activate in healthy tissue but not in the acidic tumor microenvironment. 2. **Primary Use:** To prevent **Cisplatin-induced nephrotoxicity** and radiation-induced **xerostomia**. 3. **Side Effects:** The most common dose-limiting side effect is **hypotension** (requires monitoring blood pressure during infusion) and nausea/vomiting. 4. **Other Protectants:** * **Mesna:** Protects against Cyclophosphamide-induced hemorrhagic cystitis. * **Dexrazoxane:** Protects against Doxorubicin-induced cardiotoxicity.

Question 378: Methotrexate toxicity is prevented by giving which of the following?

A. Folic acid
B. Folinic acid (Correct Answer)
C. Citric acid
D. Glucaric acid

Explanation: **Explanation:** **Mechanism of Action and the "Leucovorin Rescue"** Methotrexate (MTX) is a folate antagonist that competitively inhibits the enzyme **Dihydrofolate Reductase (DHFR)**. This inhibition prevents the conversion of Dihydrofolate (DHF) to Tetrahydrofolate (THF), the active form of folate required for DNA synthesis. **Folinic acid** (also known as **Leucovorin** or Citrovorum factor) is a 5-formyl derivative of THF. Because it is already in the reduced form, it bypasses the blocked DHFR enzyme, providing a source of active folate to healthy cells. This process is known as **"Leucovorin Rescue,"** and it allows for the administration of high-dose MTX to kill tumor cells while protecting normal tissues (like bone marrow and GI mucosa) from lethal toxicity. **Analysis of Incorrect Options:** * **A. Folic acid:** This is the oxidized form. Since MTX inhibits DHFR, the body cannot convert folic acid into its active form (THF). Therefore, folic acid is ineffective in reversing acute MTX toxicity. * **C. Citric acid:** This is an intermediate in the TCA cycle and has no role in the folate pathway or MTX toxicity. * **D. Glucaric acid:** While **Glucarpidase** (a recombinant enzyme) is used to treat MTX toxicity by breaking down MTX in the blood, "Glucaric acid" itself is not the antidote. **High-Yield Clinical Pearls for NEET-PG:** * **Timing:** Folinic acid must be started within 24–42 hours of MTX administration to be effective. * **Other Uses:** Folinic acid is also used to enhance the efficacy of **5-Fluorouracil (5-FU)** in colorectal cancer (it stabilizes the binding of 5-dUMP to thymidylate synthase). * **Glucarpidase:** Used specifically in patients with MTX-induced renal failure where MTX clearance is delayed. * **Hydration:** Vigorous intravenous hydration and **urinary alkalinization** (with Sodium Bicarbonate) are essential to prevent MTX crystal nephropathy.

Question 379: Bevacizumab is:

A. Anti VEGF antibody (Correct Answer)
B. Histone deacetylase inhibitor
C. Proteasome inhibitor
D. Her2 neu inhibitor

Explanation: **Explanation:** **Bevacizumab** is a recombinant humanized monoclonal antibody that binds to and neutralizes **Vascular Endothelial Growth Factor (VEGF-A)**. By inhibiting the interaction of VEGF with its receptors (VEGFR-1 and VEGFR-2) on the surface of endothelial cells, it prevents **angiogenesis** (the formation of new blood vessels). This "starves" the tumor of the blood supply required for growth and metastasis. It is commonly used in the treatment of metastatic colorectal cancer, non-small cell lung cancer (NSCLC), and glioblastoma. **Analysis of Incorrect Options:** * **B. Histone deacetylase (HDAC) inhibitor:** These drugs (e.g., **Vorinostat**, Romidepsin) increase the acetylation of histones, leading to the expression of tumor suppressor genes. They are primarily used in cutaneous T-cell lymphoma. * **C. Proteasome inhibitor:** These agents (e.g., **Bortezomib**, Carfilzomib) inhibit the 26S proteasome, leading to the accumulation of pro-apoptotic proteins. They are the cornerstone of therapy for Multiple Myeloma. * **D. Her2/neu inhibitor:** These include monoclonal antibodies like **Trastuzumab** and Pertuzumab, or tyrosine kinase inhibitors like Lapatinib. They target the HER2 receptor, primarily in breast and gastric cancers. **High-Yield Clinical Pearls for NEET-PG:** * **Adverse Effects:** The most characteristic side effect of Bevacizumab is **Hypertension**. Other significant risks include **proteinuria**, impaired wound healing, and **gastrointestinal perforation**. * **Ophthalmic Use:** Off-label intravitreal injection of Bevacizumab is widely used to treat **Wet Age-Related Macular Degeneration (ARMD)** and diabetic retinopathy. * **Suffix Tip:** Monoclonal antibodies ending in **"-umab"** are humanized, while **"-ximab"** are chimeric.

Question 380: Which of the following is a highly emetogenic chemotherapy drug?

A. 5–Fluorouracil
B. Paclitaxel
C. Vincristine
D. Cisplatin (Correct Answer)

Explanation: **Explanation:** The emetogenic potential of chemotherapy drugs is categorized based on the percentage of patients who experience vomiting without antiemetic prophylaxis. **Correct Answer: D. Cisplatin** Cisplatin is the prototype of **High Emetogenic Risk (>90%)** chemotherapy. It triggers nausea and vomiting through two pathways: 1. **Acute Phase:** Occurs within 24 hours due to serotonin (5-HT3) release from enterochromaffin cells in the GI tract. 2. **Delayed Phase:** Occurs after 24 hours (peak at 48–72h) primarily mediated by Substance P acting on **NK1 receptors** in the brainstem. *Management:* Requires a triple-drug regimen (5-HT3 antagonist + Dexamethasone + NK1 antagonist like Aprepitant). **Incorrect Options:** * **A. 5-Fluorouracil:** Classified as **Low Emetogenic Risk (10–30%)**. It is an antimetabolite primarily associated with mucositis and diarrhea. * **B. Paclitaxel:** Classified as **Low Emetogenic Risk (10–30%)**. Its major dose-limiting toxicity is peripheral neuropathy and hypersensitivity reactions. * **C. Vincristine:** Classified as **Minimal Emetogenic Risk (<10%)**. It is notorious for neurotoxicity (paresthesia, foot drop) and paralytic ileus, but rarely causes significant vomiting. **High-Yield Clinical Pearls for NEET-PG:** * **Highly Emetogenic Drugs (>90%):** Cisplatin, Dacarbazine, Cyclophosphamide (>1500 mg/m²). * **Moderately Emetogenic (30–90%):** Carboplatin, Oxaliplatin, Doxorubicin. * **Drug of Choice for Cisplatin-induced vomiting:** * *Acute:* Ondansetron (5-HT3 blocker). * *Delayed:* Aprepitant (NK1 blocker). * **Cisplatin Toxicity Triad:** Nephrotoxicity (prevented by aggressive hydration/Amifostine), Ototoxicity, and severe Emetogenicity.

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