Anticancer Drugs Practice Questions

Q: A patient receiving anti-cancer therapy developed neutropenia. Which of the following drugs can be used to prevent neutropenia in the next cycle of chemotherapy?

Filgrastim. **Explanation:** **1. Why Filgrastim is Correct:** Filgrastim is a recombinant **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 clinical oncology, it is the standard of care for the primary and secondary prophylaxis of **Chemotherapy-Induced Neutropenia (CIN)**. By accelerating neutrophil recovery, it reduces the risk of febrile neutropenia and prevents delays in subsequent chemotherapy cycles. **2. Why the Other Options are Incorrect:** * **Prednisolone:** While corticosteroids are used in cancer (e.g., for lympholysis in leukemias or as anti-emetics), they do not treat neutropenia. In fact, they can cause "pseudoleukocytosis" by demarginating neutrophils, but they do not increase actual production and may mask signs of infection. * **Vitamin B12 & Folic Acid:** These are essential for DNA synthesis and are used to treat **megaloblastic anemia**. While their deficiency can cause pancytopenia, they have no role in reversing bone marrow suppression caused by cytotoxic drugs like alkylating agents or antimetabolites. **3. High-Yield Clinical Pearls for NEET-PG:** * **Sargramostim:** A recombinant **GM-CSF** (Granulocyte-Macrophage CSF) that stimulates both neutrophils and macrophages. * **Pegfilgrastim:** A pegylated (long-acting) form of Filgrastim, administered once per cycle. * **Common Side Effect:** The most frequent side effect of G-CSF therapy is **bone pain** (due to marrow expansion). * **Timing:** G-CSF should not be given within 24 hours of chemotherapy as it may worsen myelosuppression by stimulating rapidly dividing cells while the chemo is still active.

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

Adriamycin. **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).

Q: What is the mechanism of action of 5-fluorouracil?

Antimetabolite. **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.

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

Mitomycin C. **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.

Q: Bevacizumab is:

Monoclonal antibody against VEGF. **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.

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

Methotrexate. **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").

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

Imatinib. ### 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.

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

Folinic acid. **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.

Q: Bevacizumab is:

Anti VEGF antibody. **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 1

A patient receiving anti-cancer therapy developed neutropenia. Which of the following drugs can be used to prevent neutropenia in the next cycle of chemotherapy?

Accepted Answer

Filgrastim

Answer

Prednisolone

Answer

Vitamin B12

Answer

Folic Acid

Question 2

Which of the following agents is known to cause epilation?

Accepted Answer

Adriamycin

Answer

5-Flurouracil

Answer

Cisplatin

Answer

Methotrexate

Question 3

What is the mechanism of action of 5-fluorouracil?

Accepted Answer

Antimetabolite

Answer

Direct DNA chelating agent

Answer

Anti-mitotic

Answer

Topoisomerase inhibitor

Question 4

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

Accepted Answer

Mitomycin C

Answer

Cisplatin

Answer

Doxorubicin

Answer

5-Fluorouracil

Question 5

Bevacizumab is:

Accepted Answer

Monoclonal antibody against VEGF

Answer

Anti-IL-2 monoclonal antibody

Answer

Monoclonal antibody against FGFR

Answer

Monoclonal antibody against EGFR

Question 6

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

Accepted Answer

Methotrexate

Answer

Procarbazine

Answer

Vincristine

Answer

Mechlorethamine

Question 7

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

Accepted Answer

Imatinib

Answer

Sorafenib

Answer

Gefitinib

Answer

Erlotinib

Question 8

Amifostine is protective to all EXCEPT:

Accepted Answer

Salivary glands

Answer

Skin

Answer

CNS

Answer

GIT

Question 9

Methotrexate toxicity is prevented by giving which of the following?

Accepted Answer

Folinic acid

Answer

Folic acid

Answer

Citric acid

Answer

Glucaric acid

Question 10

Bevacizumab is:

Accepted Answer

Anti VEGF antibody

Answer

Histone deacetylase inhibitor

Answer

Proteasome inhibitor

Answer

Her2 neu inhibitor

Anticancer Drugs — MCQs

Anticancer Drugs — MCQs

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