Anticancer Drugs Practice Questions

Q: Trastuzumab is directed against which of the following targets?

Human epidermal growth factor receptor 2. **Explanation:** **Trastuzumab** is a recombinant humanized monoclonal antibody specifically designed to target the **Human Epidermal Growth Factor Receptor 2 (HER2/neu)**, a proto-oncogene. In about 20–30% of breast cancer cases, HER2 is overexpressed, leading to uncontrolled cell proliferation. Trastuzumab binds to the extracellular domain of this receptor, inhibiting downstream signaling pathways (like MAPK and PI3K/Akt) and inducing antibody-dependent cellular cytotoxicity (ADCC). **Analysis of Options:** * **Option A (Correct):** Trastuzumab targets **HER2**. It is the first-line treatment for HER2-positive breast cancer and is also used in HER2-positive metastatic gastric adenocarcinoma. * **Option B (Incorrect):** **Bevacizumab** is the monoclonal antibody directed against Vascular Endothelial Growth Factor A (VEGF-A), used to inhibit angiogenesis. * **Option C (Incorrect):** Platelet-derived growth factor (PDGF) receptors are typically targeted by small molecule tyrosine kinase inhibitors like **Imatinib** or **Dasatinib**, rather than Trastuzumab. * **Option D (Incorrect):** FGF-23 is involved in phosphate metabolism. **Burosumab** is the monoclonal antibody that targets FGF-23, used in X-linked hypophosphatemia. **High-Yield Clinical Pearls for NEET-PG:** 1. **Cardiotoxicity:** The most significant side effect of Trastuzumab is **cardiac dysfunction** (decreased LVEF/heart failure). Unlike anthracyclines, this toxicity is usually **reversible** and not dose-dependent. 2. **Drug-Drug Interaction:** Never co-administer Trastuzumab with **Doxorubicin** due to a synergistic increase in the risk of heart failure. 3. **Resistance:** If resistance to Trastuzumab develops, **Lapatinib** (a dual EGFR/HER2 tyrosine kinase inhibitor) or **Ado-trastuzumab emtansine** (an antibody-drug conjugate) can be used.

Q: Ipilimumab is a:

CTLA4 inhibitor. **Ipilimumab** is a recombinant human monoclonal antibody that acts as an **immune checkpoint inhibitor**. Its primary mechanism involves binding to and blocking **CTLA-4** (Cytotoxic T-Lymphocyte Antigen 4), a molecule expressed on the surface of T-cells. Normally, CTLA-4 acts as an "off switch" to prevent overactivation of the immune system. By inhibiting this checkpoint, Ipilimumab allows T-cells to remain active and mount an effective immune response against tumor cells. It is primarily used in the treatment of advanced (metastatic) melanoma [1].**Analysis of Incorrect Options:** * **Option A (Anti-CD30):** This describes **Brentuximab vedotin**, which is used in Hodgkin lymphoma and Anaplastic large cell lymphoma [1]. * **Option B (PD-L1 inhibitor):** Drugs in this class include **Atezolizumab, Durvalumab, and Avelumab**. (Note: Nivolumab and Pembrolizumab are PD-1 inhibitors, not PD-L1). * **Option D (PTPN22 inhibitor):** PTPN22 is a gene associated with autoimmune diseases (like Rheumatoid Arthritis); there are currently no standard anticancer monoclonal antibodies targeting this in clinical practice.**High-Yield Clinical Pearls for NEET-PG:**1. **Mechanism:** Ipilimumab works at the **priming phase** (lymph node level), whereas PD-1 inhibitors work at the **effector phase** (tumor microenvironment).2. **Adverse Effects:** Checkpoint inhibitors cause **immune-related Adverse Events (irAEs)**, such as colitis, dermatitis, and hypophysitis (pituitary inflammation), and anti-CTLA-4 antibodies can be associated with autoimmune toxicity [1].3. **FDA Approval:** It was the first checkpoint inhibitor to show a survival benefit in metastatic melanoma.

Q: Methotrexate is used for the management of all of the following conditions except?

Sickle cell anemia. **Explanation:** **1. Why Sickle Cell Anemia is the Correct Answer:** Methotrexate (MTX) is a folate antagonist that inhibits the enzyme **dihydrofolate reductase (DHFR)**, leading to a decrease in DNA synthesis and cell proliferation [1]. It has no role in the management of Sickle Cell Anemia. The drug of choice for reducing the frequency of painful crises in Sickle Cell Anemia is **Hydroxyurea** [3], which acts by increasing the levels of Fetal Hemoglobin (HbF) [3]. **2. Analysis of Incorrect Options:** * **Rheumatoid Arthritis (RA):** MTX is the **"Anchor Drug"** and the first-line Disease-Modifying Anti-Rheumatic Drug (DMARD) for RA [2]. It acts by increasing adenosine levels, which exerts a potent anti-inflammatory effect. * **Psoriasis:** MTX is highly effective for severe, recalcitrant psoriasis and psoriatic arthritis due to its ability to inhibit the rapid proliferation of epidermal keratinocytes [2]. * **Organ Transplantation:** In low doses, MTX acts as an immunosuppressant used to prevent Graft-versus-Host Disease (GVHD) and organ rejection by inhibiting T-cell activation and proliferation [2]. **3. High-Yield Clinical Pearls for NEET-PG:** * **Mechanism:** Competitive inhibition of DHFR; cell cycle-specific for the **S-phase** [1]. * **Toxicity:** Bone marrow suppression (most common), hepatotoxicity (cirrhosis), and pulmonary fibrosis [4]. * **Rescue Therapy:** **Leucovorin (Folinic acid)** is used to "rescue" normal cells from MTX toxicity by bypassing the inhibited DHFR enzyme [1], [4]. * **Contraindication:** It is highly **teratogenic** (causes neural tube defects and fetal death) [4]. * **Other Uses:** Choriocarcinoma (Drug of choice), Ectopic pregnancy, and Osteosarcoma.

Q: Which chemotherapeutic agent is most commonly administered by continuous infusion?

Cytarabine (Ara-C). **Explanation:** **Why Cytarabine (Ara-C) is the Correct Answer:** Cytarabine is a **cell-cycle specific (S-phase)** antimetabolite. Its mechanism involves inhibition of DNA polymerase. The primary reason for continuous infusion is its **extremely short half-life** (approximately 10–20 minutes) due to rapid deamination by the enzyme cytidine deaminase in the blood and liver. To maintain therapeutic plasma concentrations and ensure that leukemic cells entering the S-phase at different times are exposed to the drug, it is traditionally administered via continuous intravenous infusion (e.g., in the "7+3" regimen for AML). **Analysis of Incorrect Options:** * **5-Fluorouracil (5-FU):** While 5-FU is frequently given as a continuous infusion in colorectal cancer to improve the safety profile and efficacy, it is also commonly given as a bolus. In the context of standard pharmacological teaching for competitive exams, Cytarabine’s pharmacokinetics make it the classic prototype for continuous infusion. * **Cisplatin:** This is a cell-cycle non-specific alkylating-like agent. It is typically administered as a short-term infusion with aggressive pre- and post-hydration to prevent nephrotoxicity, rather than a continuous maintenance infusion. * **Etoposide:** An inhibitor of Topoisomerase II, usually administered as an intermittent intravenous infusion over 30–60 minutes to avoid hypotension. **NEET-PG High-Yield Pearls:** * **Drug of Choice:** Cytarabine is the backbone of Induction therapy for **Acute Myeloid Leukemia (AML)**. * **Specific Toxicity:** High-dose Cytarabine (HiDAC) is associated with **Cerebellar toxicity** (ataxia, nystagmus) and conjunctivitis (prophylactic steroid drops are used). * **Mechanism:** It is a pyrimidine analog (specifically a Cytidine analog).

Q: Paclitaxel acts on which phase of the cell cycle?

M. **Explanation:** **Mechanism of Action (Why M phase is correct):** Paclitaxel belongs to the **Taxane** class of anticancer drugs. Its primary mechanism is the **stabilization of microtubules** [2]. Unlike Vinca alkaloids (which prevent microtubule assembly), Paclitaxel binds to the $\beta$-tubulin subunit and promotes the assembly of microtubules while inhibiting their disassembly (depolymerization) [2]. This results in the formation of non-functional, stable microtubule bundles, leading to "mitotic freeze." Consequently, the cell cannot form a functional mitotic spindle, arresting the cell cycle specifically in the **M (Mitosis) phase** [3, 5]. **Analysis of Incorrect Options:** * **G1 Phase:** Drugs like Corticosteroids or L-asparaginase typically act here. Paclitaxel requires the presence of mitotic spindles, which are absent in G1. * **S Phase:** This is the site of action for Antimetabolites (e.g., Methotrexate, 5-FU) and DNA polymerase inhibitors (e.g., Cytarabine), which interfere with DNA synthesis [3]. * **G2 Phase:** Drugs like Bleomycin and Etoposide primarily exert their effects in the late S or G2 phase [3]. **NEET-PG Clinical Pearls:** * **Source:** Paclitaxel is derived from the bark of the Pacific Yew tree (*Taxus brevifolia*) [2]. * **Adverse Effects:** The dose-limiting toxicity is **Bone Marrow Suppression** (Neutropenia). It is also notorious for causing **peripheral neuropathy** [1] and **hypersensitivity reactions** (often due to the Cremophor EL vehicle; premedication with dexamethasone and antihistamines is required) [1]. * **Albumin-bound Paclitaxel (Abraxane):** A newer formulation that reduces hypersensitivity risks [1]. * **Mnemonic:** **T**axanes **T**erminate (stabilize) the **T**ubules.

Q: Methotrexate blocks the synthesis of thymidine monophosphate by inhibiting the activity of which enzyme?

Dihydrofolate reductase. ### **Explanation** **Correct Option: A. Dihydrofolate Reductase (DHFR)** Methotrexate (MTX) is a folate antimetabolite. It acts as a structural analog of folic acid and binds to the active site of **Dihydrofolate Reductase (DHFR)** with an affinity 1,000 times greater than the natural substrate. * **Mechanism:** By inhibiting DHFR, MTX prevents the conversion of dihydrofolate (DHF) to tetrahydrofolate (THF). * **Result:** THF is a crucial co-factor for the enzyme **Thymidylate Synthase**, which converts dUMP to dTMP (Thymidine monophosphate). Depletion of THF leads to a "thymineless death" of the cell, halting DNA synthesis and repair. **Analysis of Incorrect Options:** * **B. Orotate phosphoribosyl transferase:** This enzyme is involved in the **de novo synthesis of pyrimidines** (converting orotic acid to OMP). It is inhibited by 5-Fluorouracil (5-FU) metabolites, not Methotrexate. * **C. Ribonucleotide reductase:** This enzyme converts ribonucleotides to deoxyribonucleotides. It is the primary target of **Hydroxyurea**. * **D. Dihydroorotase:** This is an early-stage enzyme in pyrimidine biosynthesis. It is not a major target for common clinical antineoplastic agents. --- ### **High-Yield Clinical Pearls for NEET-PG** * **Leucovorin Rescue:** Folinic acid (Leucovorin) is given to "bypass" the blocked DHFR enzyme in normal cells during high-dose MTX therapy, preventing lethal hematological toxicity. * **Resistance Mechanism:** The most common cause of MTX resistance is the **amplification of the DHFR gene** or mutations in the DHFR enzyme. * **Polyglutamation:** Inside the cell, MTX undergoes polyglutamation, which traps the drug inside the cell and increases its inhibitory potency. * **Toxicity:** Watch for **Mucositis** (earliest sign), Nephrotoxicity (due to crystalluria), and Hepatotoxicity (cirrhosis with long-term use in Psoriasis/RA).

Q: Which of the following drugs is not categorized under anti-VEGF agents?

5-Fluorouracil. ### Explanation **Correct Answer: B. 5-Fluorouracil** **Why 5-Fluorouracil is the correct answer:** 5-Fluorouracil (5-FU) is an **Antimetabolite** (specifically a pyrimidine analog). Its primary mechanism of action is the inhibition of **thymidylate synthase**, which prevents the conversion of dUMP to dTMP. This leads to "thymineless death" of the cell by disrupting DNA synthesis. It does not directly target Vascular Endothelial Growth Factor (VEGF) or its receptors. **Analysis of Incorrect Options:** * **Bevacizumab:** A recombinant humanized **monoclonal antibody** that binds directly to circulating **VEGF-A** ligands, preventing them from binding to their receptors. It is widely used in colorectal and lung cancers. * **Ranibizumab:** A monoclonal antibody fragment (Fab) derived from bevacizumab. It is specifically designed for intravitreal injection to treat **neovascular (wet) Age-related Macular Degeneration (AMD)** by inhibiting VEGF. * **Sunitinib:** An oral **multi-targeted tyrosine kinase inhibitor (TKI)**. It inhibits the intracellular domain of **VEGFR-1, 2, and 3**, as well as PDGFR. It is a first-line agent for Renal Cell Carcinoma (RCC). **NEET-PG High-Yield Pearls:** 1. **VEGF Inhibitor Classification:** * **Antibodies (Ligand binders):** Bevacizumab, Ranibizumab, Aflibercept (VEGF Trap). * **Tyrosine Kinase Inhibitors (Receptor blockers):** Sunitinib, Sorafenib, Pazopanib. 2. **Side Effects of Anti-VEGFs:** Hypertension (most common), proteinuria, impaired wound healing, and arterial thrombosis. 3. **5-FU Toxicity:** Hand-foot syndrome (palmar-plantar erythrodysesthesia) and myelosuppression. Its action is enhanced by **Leucovorin** (folinic acid), which stabilizes the binding of 5-FU to thymidylate synthase.

Q: "Radiation recall syndrome" is seen with all of the following except?

Bleomycin. **Explanation:** **Radiation Recall Syndrome (RRS)** is an inflammatory skin reaction that occurs in a previously irradiated area after the administration of certain cytotoxic drugs. It represents a "latent" radiation injury triggered by chemotherapy, even months or years after radiotherapy. **Why Bleomycin is the correct answer:** While **Bleomycin** is notorious for causing pulmonary fibrosis and skin hyperpigmentation (flagellate dermatitis), it is **not** typically associated with Radiation Recall Syndrome. In contrast, the other options are classic triggers for this phenomenon. **Analysis of other options:** * **Actinomycin D (Dactinomycin):** This is the most common and potent inducer of radiation recall. It is frequently tested in exams as the classic cause. * **Doxorubicin & Daunorubicin:** These Anthracyclines are well-documented triggers for RRS. They are potent radiosensitizers and can cause severe inflammatory reactions in previously treated skin or internal organs (like the esophagus or lungs). **Clinical Pearls for NEET-PG:** * **Common Triggers:** The "Big Three" for RRS are **Actinomycin D, Anthracyclines (Doxorubicin), and Taxanes (Paclitaxel).** Other triggers include Methotrexate and Gemcitabine. * **Clinical Presentation:** It mimics a severe sunburn (erythema, edema, blistering) localized strictly to the previous radiation field. * **Management:** Treatment involves stopping the offending drug and administering corticosteroids. * **High-Yield Distinction:** Do not confuse *Radiation Recall* (occurs after radiation) with *Radiosensitization* (occurs when drug and radiation are given concurrently). Bleomycin is a radiosensitizer but not a recall agent.

Q: Which of the following is used in the treatment of urinary bladder carcinoma?

Bacillus Calmette-Guérin (BCG). **Explanation:** The correct answer is **Bacillus Calmette-Guérin (BCG)**. **Why BCG is correct:** BCG is a live-attenuated strain of *Mycobacterium bovis*. In oncology, it is the gold standard for **intravesical immunotherapy** in patients with non-muscle invasive bladder cancer (NMIBC), particularly high-grade tumors and Carcinoma in situ (CIS). When instilled into the bladder, BCG triggers a local inflammatory response and a robust T-cell mediated immune reaction (Th1 response). This immune activation leads to the destruction of malignant cells by cytotoxic T lymphocytes and natural killer (NK) cells. **Why the other options are incorrect:** * **5-Fluorouracil (5FU):** An antimetabolite (pyrimidine analog) primarily used for colorectal, breast, and head/neck cancers. While used topically for actinic keratosis, it is not a standard treatment for bladder carcinoma. * **Cyclophosphamide:** An alkylating agent used for various malignancies (lymphomas, leukemia). Paradoxically, it is a **risk factor** for bladder cancer because its metabolite, **Acrolein**, causes hemorrhagic cystitis and chronic urothelial irritation. * **6-Mercaptopurine:** A purine analog used mainly in the maintenance therapy of Acute Lymphoblastic Leukemia (ALL). It has no role in bladder cancer management. **High-Yield Clinical Pearls for NEET-PG:** * **Acrolein Toxicity:** To prevent hemorrhagic cystitis caused by Cyclophosphamide, patients are given **MESNA** (2-Mercaptoethane sulfonate Na) and aggressive hydration. * **BCG Contraindications:** It should not be used in patients with gross hematuria, traumatic catheterization, or immunosuppression due to the risk of systemic BCG-osis (sepsis). * **Other Intravesical Agents:** If BCG fails or is unavailable, **Mitomycin C** or **Gemcitabine** are alternative intravesical chemotherapeutic agents used for bladder cancer.

Q: Which one of the following drugs is a Topoisomerase 1 inhibitor?

Irinotecan. **Explanation:** The correct answer is **Irinotecan**. **1. Mechanism of Action (Topoisomerase I Inhibitors):** Topoisomerase I is an enzyme responsible for creating single-strand breaks in DNA to relieve torsional strain during replication. Drugs like **Irinotecan** and **Topotecan** (derivatives of Camptothecin) bind to the DNA-topoisomerase I complex, preventing the religation of these single-strand breaks. This leads to lethal double-strand DNA damage and cell death. **2. Analysis of Incorrect Options:** * **Doxorubicin:** An anthracycline antibiotic that inhibits **Topoisomerase II**, intercalates DNA, and generates free radicals. * **Etoposide:** A podophyllotoxin derivative that specifically inhibits **Topoisomerase II**, leading to double-strand DNA breaks. * **Vincristine:** A Vinca alkaloid that inhibits **microtubule polymerization** by binding to tubulin, causing mitotic arrest in the M-phase. **3. High-Yield Clinical Pearls for NEET-PG:** * **Irinotecan Side Effects:** Known for causing severe **diarrhea**. * *Early-onset:* Occurs within 24 hours (cholinergic crisis); treated with **Atropine**. * *Late-onset:* Occurs after 24 hours; treated with **Loperamide**. * **Pharmacogenomics:** Patients with **UGT1A1*28 polymorphism** (Gilbert syndrome) are at a higher risk of severe toxicity from Irinotecan due to impaired glucuronidation of its active metabolite, SN-38. * **Mnemonic:** Remember **"I"** for **I**rinotecan and Topoisomerase **I**. Remember **"E"**toposide and **"D"**oxorubicin for Topoisomerase **II** (Two).

Question 1

Trastuzumab is directed against which of the following targets?

Accepted Answer

Human epidermal growth factor receptor 2

Answer

Vascular endothelial growth factor A

Answer

Platelet derived growth factor

Answer

Fibroblast growth factor 23

Question 2

Ipilimumab is a:

Accepted Answer

CTLA4 inhibitor

Answer

Anti CD30 Monoclonal Antibody

Answer

PDL1 receptor inhibitor

Answer

PTPN22 inhibitor

Question 3

Methotrexate is used for the management of all of the following conditions except?

Accepted Answer

Sickle cell anemia

Answer

Rheumatoid arthritis

Answer

Psoriasis

Answer

Organ transplantation

Question 4

Which chemotherapeutic agent is most commonly administered by continuous infusion?

Accepted Answer

Cytarabine (Ara-C)

Answer

5-Fluorouracil (5-FU)

Answer

Cisplatin

Answer

Etoposide

Question 5

Paclitaxel acts on which phase of the cell cycle?

Accepted Answer

M

Answer

G1

Answer

S

Answer

G2

Question 6

Methotrexate blocks the synthesis of thymidine monophosphate by inhibiting the activity of which enzyme?

Accepted Answer

Dihydrofolate reductase

Answer

Orotate phosphoribosyl transferase

Answer

Ribonucleotide reductase

Answer

Dihydroorotase

Question 7

Which of the following drugs is not categorized under anti-VEGF agents?

Accepted Answer

5-Fluorouracil

Answer

Sunitinib

Answer

Ranibizumab

Answer

Bevacizumab

Question 8

"Radiation recall syndrome" is seen with all of the following except?

Accepted Answer

Bleomycin

Answer

Actinomycin

Answer

Doxorubicin

Answer

Daunorubicin

Question 9

Which of the following is used in the treatment of urinary bladder carcinoma?

Accepted Answer

Bacillus Calmette-Guérin (BCG)

Answer

5-Fluorouracil (5FU)

Answer

Cyclophosphamide

Answer

6-Mercaptopurine

Question 10

Which one of the following drugs is a Topoisomerase 1 inhibitor?

Accepted Answer

Irinotecan

Answer

Doxorubicin

Answer

Etoposide

Answer

Vincristine

Anticancer Drugs — MCQs

Anticancer Drugs — MCQs

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