Anticancer Drugs Practice Questions

Q: Which of the following anticancer agents has specific activity in a subset of female breast cancers?

Trastuzumab. **Explanation:** **Trastuzumab** is the correct answer because it is a recombinant DNA-derived humanized monoclonal antibody specifically designed to target the **HER2/neu (ErbB2) receptor**. This receptor is overexpressed in approximately 15–25% of female breast cancers. Trastuzumab inhibits the proliferation of tumor cells that overexpress HER2, making its activity specific to this molecular subset. **Analysis of Incorrect Options:** * **Anastrozole:** While used in breast cancer, it is a non-steroidal **Aromatase Inhibitor**. It works by blocking the peripheral conversion of androgens to estrogens. It is used in postmenopausal women with estrogen receptor-positive (ER+) cancer, but it is not considered "subset-specific" in the same targeted molecular context as Trastuzumab. * **Doxorubicin:** An anthracycline antibiotic that acts via DNA intercalation and inhibition of Topoisomerase II. It is a **broad-spectrum** cytotoxic agent used in many cancers (including breast cancer) regardless of specific receptor subsets. * **Fluoxymesterone:** An oral androgen occasionally used as palliative therapy in breast cancer, but it lacks the targeted specificity for a modern molecular subset. **High-Yield Clinical Pearls for NEET-PG:** * **Mechanism of Trastuzumab:** Binds to the extracellular domain of HER2; induces cell cycle arrest and antibody-dependent cellular cytotoxicity (ADCC). * **Key Side Effect:** **Cardiotoxicity** (manifests as a decrease in LVEF/congestive heart failure). Unlike Doxorubicin, Trastuzumab-induced cardiotoxicity is usually **reversible** and not dose-dependent. * **Monitoring:** Baseline and periodic Echocardiography/MUGA scans are mandatory. * **Combination Warning:** Never combine Trastuzumab with Anthracyclines (like Doxorubicin) due to synergistic cardiotoxicity.

Q: All of the following anticancer drugs act on the G2 phase except?

Paclitaxel. **Explanation:** The cell cycle consists of specific phases (G1, S, G2, M), and many anticancer drugs are **cell-cycle specific**. To answer this question, one must distinguish between drugs acting on the **G2 phase** (pre-mitotic interval) and the **M phase** (mitosis). **1. Why Paclitaxel is the correct answer:** **Paclitaxel** (a Taxane) acts specifically on the **M phase**. Its mechanism involves stabilizing microtubules and inhibiting their depolymerization. This prevents the formation of the mitotic spindle, leading to mitotic arrest. Since it acts on the M phase and not the G2 phase, it is the "except" in this list. **2. Analysis of incorrect options (Drugs acting on G2):** * **Bleomycin:** This is a classic G2-specific drug. It causes DNA fragmentation by generating free radicals, arresting cells in the **G2 phase**. * **Etoposide:** A Topoisomerase II inhibitor. While it has some activity in the S phase, its primary lethal effect occurs in the **late S and G2 phases**. * **Irinotecan:** A Topoisomerase I inhibitor. These drugs typically cause arrest in the **S and G2 phases** by preventing the religation of DNA strands. **High-Yield Clinical Pearls for NEET-PG:** * **M-Phase Specific:** Vinca alkaloids (Vincristine/Vinblastine) and Taxanes (Paclitaxel/Docetaxel). * **S-Phase Specific:** Antimetabolites (Methotrexate, 5-FU, Cytarabine). * **G2-Phase Specific:** Bleomycin and Etoposide. * **Cell-Cycle Non-Specific (CCNS):** Alkylating agents (Cyclophosphamide) and Platinum compounds (Cisplatin). * **Side Effect Tip:** Bleomycin is notorious for **Pulmonary Fibrosis**, while Paclitaxel is known for **Peripheral Neuropathy** and hypersensitivity reactions.

Q: All of the following statements about vincristine are true EXCEPT?

It is a drug of choice for solid tumors. **Explanation:** **1. Why Option D is the Correct Answer (The "Except" statement):** Vincristine is primarily used in the treatment of **hematological malignancies** (e.g., Acute Lymphoblastic Leukemia, Hodgkin’s and Non-Hodgkin’s Lymphoma) and specific pediatric tumors (e.g., Wilms' tumor). While it is part of combination regimens for some solid tumors, it is **not** considered a general "drug of choice" for the broad category of adult solid tumors (like breast, lung, or colon cancer), where drugs like taxanes, platinum compounds, or 5-FU are preferred. **2. Analysis of Other Options:** * **Option A (Inhibits Mitosis):** Vincristine is a **Vinca alkaloid** that binds to tubulin and prevents its polymerization into microtubules. This causes **mitotic arrest in the M-phase**, specifically preventing the formation of the mitotic spindle. * **Option B (Peripheral Neuropathy):** This is the **dose-limiting toxicity** of vincristine. It interferes with axonal microtubule transport, leading to symmetrical sensory-motor neuropathy, paresthesia, and loss of deep tendon reflexes. * **Option C (Does not suppress bone marrow):** Vincristine is unique among traditional cytotoxic drugs because it is **bone marrow sparing**. This makes it an ideal component for combination chemotherapy (e.g., the MOPP or CHOP regimens) as it does not add to the myelosuppression caused by other agents. **NEET-PG High-Yield Pearls:** * **Vincristine vs. Vinblastine:** Remember the mnemonic: **"B"** for Vin**b**lastine = **B**one marrow suppression; **"C"** for Vin**c**ristine = **C**onstipation (autonomic neuropathy) and **C**entral/Peripheral nerve damage. * **Fatal Route:** Vincristine is for **Intravenous (IV) use only**. Intrathecal administration is fatal due to progressive neurotoxicity. * **SIADH:** Vincristine is a well-known cause of the Syndrome of Inappropriate Antidiuretic Hormone secretion.

Q: What is the drug of choice for the T790M mutation of EGFR in Non-Small Cell Lung Cancer?

Osimertinib. **Explanation:** **Osimertinib** is the correct answer because it is a **third-generation irreversible EGFR Tyrosine Kinase Inhibitor (TKI)** specifically designed to target the **T790M resistance mutation**. In Non-Small Cell Lung Cancer (NSCLC), patients treated with first-generation TKIs (like Gefitinib or Erlotinib) often develop resistance via the T790M mutation, which increases the ATP affinity of the EGFR kinase domain. Osimertinib selectively inhibits both sensitizing mutations and the T790M resistance mutation while sparing wild-type EGFR, reducing skin and GI toxicity. **Analysis of Incorrect Options:** * **Lapatinib:** A dual TKI targeting both **EGFR (ErbB1) and HER2 (ErbB2)**. It is primarily used in HER2-positive breast cancer, not for T790M-mutated lung cancer. * **Crizotinib:** An inhibitor of **ALK (Anaplastic Lymphoma Kinase)**, ROS1, and MET. It is the drug of choice for ALK-positive NSCLC, but ineffective against EGFR mutations. * **Alemtuzumab:** A monoclonal antibody against **CD52**, used in Chronic Lymphocytic Leukemia (CLL) and Multiple Sclerosis, with no role in EGFR-mutated lung cancer. **High-Yield Clinical Pearls for NEET-PG:** * **Generations of EGFR TKIs:** * 1st Gen (Reversible): Gefitinib, Erlotinib. * 2nd Gen (Irreversible): Afatinib, Dacomitinib. * 3rd Gen (T790M specific): **Osimertinib**. * **Adverse Effect:** While Osimertinib has fewer skin rashes than 1st gen drugs, it can cause **QT interval prolongation** and cardiomyopathy. * **Blood-Brain Barrier:** Osimertinib has excellent CNS penetration, making it preferred for patients with brain metastases.

Q: Arsenic compounds are used for the treatment of which of the following cancers?

Acute Promyelocytic Leukemia (APML). **Explanation:** **Arsenic Trioxide ($As_2O_3$)** is a highly effective treatment for **Acute Promyelocytic Leukemia (APML)**, specifically for patients who are refractory to or have relapsed after treatment with All-Trans Retinoic Acid (ATRA). **Why the correct answer is right:** APML (FAB M3 subtype) is characterized by the $t(15;17)$ translocation, which creates the **PML-RARα fusion protein**. This protein arrests myeloid differentiation at the promyelocyte stage. Arsenic Trioxide works through a dual mechanism: 1. **Degradation of the PML-RARα protein:** It binds directly to the PML moiety, inducing its degradation and allowing the cells to differentiate. 2. **Induction of Apoptosis:** It triggers the mitochondrial pathway of programmed cell death in leukemic cells. **Why incorrect options are wrong:** * **CLL (B):** Primarily treated with BTK inhibitors (Ibrutinib), BCL-2 inhibitors (Venetoclax), or anti-CD20 monoclonal antibodies (Rituximab). * **ALL (C):** Managed with a combination of Vincristine, L-Asparaginase, Corticosteroids, and Anthracyclines. * **CML (D):** The mainstay of treatment is Tyrosine Kinase Inhibitors (TKIs) like **Imatinib**, which target the BCR-ABL fusion protein. **High-Yield Clinical Pearls for NEET-PG:** * **Side Effects:** The most critical side effect of Arsenic Trioxide is **QT interval prolongation**, which can lead to Torsades de Pointes. Regular ECG monitoring is mandatory. * **Differentiation Syndrome:** Similar to ATRA, Arsenic can cause "Differentiation Syndrome" (fever, dyspnea, weight gain, pulmonary infiltrates), treated with high-dose **Dexamethasone**. * **Historical Context:** Arsenic was historically used as "Fowler’s Solution," but its modern use is strictly limited to APML.

Q: Which chemotherapeutic agent is used in brain tumors?

Nitrosoureas. **Explanation:** The primary challenge in treating brain tumors is the **Blood-Brain Barrier (BBB)**, a highly selective semipermeable border that prevents most hydrophilic and large-molecular-weight drugs from entering the central nervous system (CNS). **Why Nitrosoureas are correct:** Nitrosoureas (such as **Lomustine (CCNU), Carmustine (BCNU), and Semustine**) are the drugs of choice for primary brain tumors (e.g., Glioblastoma Multiforme). Their efficacy stems from their **high lipid solubility** and non-ionized state, which allows them to readily cross the BBB. They act by alkylating DNA and inhibiting DNA repair enzymes. **Analysis of Incorrect Options:** * **Cisplatin:** While it is a potent platinum-based alkylating agent used for various solid tumors (lung, ovary, bladder), it has **poor CNS penetration** and is not a primary choice for brain tumors. * **Bleomycin:** This is a glycopeptide antibiotic that causes DNA strand scission. It is a large, polar molecule with **negligible BBB penetration**. Its major dose-limiting toxicity is pulmonary fibrosis. * **Vincristine:** A Vinca alkaloid that inhibits microtubule polymerization. It has **very poor CNS entry** and is primarily used in leukemias and lymphomas. Interestingly, it is notorious for causing peripheral neuropathy but lacks central neurotoxicity because it cannot cross the BBB. **High-Yield Clinical Pearls for NEET-PG:** * **Temozolomide:** An oral alkylating agent that also crosses the BBB; it is currently the first-line standard of care for Glioblastoma. * **Carmustine Wafers (Gliadel):** These are biodegradable polymers implanted directly into the tumor cavity after surgical resection to bypass the BBB. * **Procarbazine:** Another lipid-soluble drug used in the PCV regimen (Procarbazine, CCNU, Vincristine) for brain tumors.

Q: Skin pigmentation is caused by:

Busulphan. **Explanation:** **Busulphan** is an alkylating agent primarily used in the treatment of Chronic Myeloid Leukemia (CML) and as a conditioning agent before bone marrow transplantation. A classic and high-yield side effect of Busulphan is **generalized hyperpigmentation**, which often mimics the bronze skin seen in Addison’s disease. This occurs due to increased melanin production and is frequently accompanied by other symptoms like pulmonary fibrosis ("Busulphan lung") and adrenal insufficiency-like syndrome. **Analysis of Incorrect Options:** * **A. Methotrexate:** This folate antagonist is more commonly associated with photosensitivity, alopecia, and mucosal ulcerations (stomatitis) rather than generalized skin pigmentation. * **B. Dactinomycin:** Also known as Actinomycin D, this drug is a potent vesicant. Its primary dermatological concern is severe soft tissue necrosis if extravasated and "radiation recall" phenomenon, but not systemic pigmentation. * **C. Cyclophosphamide:** While it can cause nail pigmentation (melanonychia) and occasionally pigmentation of the palms and soles, it is not the classic answer for generalized skin pigmentation compared to Busulphan. Its hallmark toxicity is hemorrhagic cystitis. **High-Yield Clinical Pearls for NEET-PG:** * **Busulphan Triad:** Hyperpigmentation, Pulmonary Fibrosis, and Adrenal Insufficiency (pseudo-Addison’s). * **Other drugs causing skin pigmentation:** Bleomycin (flagellate dermatosis), Clofazimine (reddish-brown discoloration), Chloroquine (bluish-grey), and Amiodarone (blue-grey "Smurf" skin). * **Mnemonic:** "Busulphan burns the skin (pigmentation) and the lungs (fibrosis)."

Q: Which of the following anticancer drugs causes hemolytic uremic syndrome?

Mitomycin. **Explanation:** **Mitomycin C** is a potent alkylating agent (specifically an antibiotic derived from *Streptomyces caespitosus*) that acts by cross-linking DNA. It is notorious for causing **delayed and cumulative myelosuppression** and a specific, life-threatening form of nephotoxicity known as **Mitomycin-induced Hemolytic Uremic Syndrome (HUS)**. This syndrome is characterized by microangiopathic hemolytic anemia, thrombocytopenia, and progressive renal failure, typically occurring at cumulative doses exceeding 40-50 mg/m². **Analysis of Incorrect Options:** * **Vincristine (A):** A Vinca alkaloid that inhibits microtubule assembly. Its dose-limiting toxicity is **peripheral neuropathy** (paresthesia, loss of reflexes) and autonomic dysfunction (constipation/paralytic ileus). It is notably bone marrow sparing. * **Vinblastine (B):** Also a Vinca alkaloid, but unlike Vincristine, its dose-limiting toxicity is **bone marrow suppression** (neutropenia). It does not cause HUS. * **Cisplatin (C):** A platinum compound known for significant **nephotoxicity** (specifically Acute Tubular Necrosis), ototoxicity, and severe emesis. While it affects the kidneys, it does not typically present as HUS. **High-Yield Clinical Pearls for NEET-PG:** * **Mitomycin C** is also used topically for superficial bladder cancer and in ophthalmic surgery (glaucoma) to prevent scarring. * **Vincristine** is famous for "stocking and glove" neuropathy. * **Cisplatin** nephotoxicity is minimized by aggressive **hydration** and **Amifostine** (a cytoprotective agent). * **Cyclophosphamide** is associated with hemorrhagic cystitis (prevented by **MESNA**).

Q: All of the following is true about hydroxyurea except:

Oral bioavailability is very low.. **Explanation:** **Hydroxyurea** is an antimetabolite that inhibits the enzyme **ribonucleotide reductase**, thereby depleting intracellular deoxynucleotide pools and arresting cells in the **S-phase** of the cell cycle. 1. **Why Option B is the Correct Answer (The False Statement):** Contrary to the option, Hydroxyurea has **excellent oral bioavailability** (nearly 100%). It is rapidly absorbed from the gastrointestinal tract, reaches peak plasma levels within 1–4 hours, and readily crosses the blood-brain barrier. This high oral efficacy makes it a convenient long-term maintenance therapy. 2. **Analysis of Other Options:** * **A. Causes myelosuppression:** This is the **dose-limiting toxicity** of hydroxyurea. It primarily causes leukopenia, though anemia and thrombocytopenia can also occur. * **C. Used in CML:** Hydroxyurea was historically the first-line agent for Chronic Myeloid Leukemia (CML) to rapidly reduce high white blood cell counts (cytoreduction) before the advent of Imatinib. It is still used for rapid debulking in blast crises. * **D. Acts as a radiosensitizer:** By arresting cells in the G1-S phase (the most radiation-sensitive phase) and inhibiting DNA repair, it enhances the effectiveness of radiotherapy, particularly in head and neck or cervical cancers. **High-Yield Clinical Pearls for NEET-PG:** * **Sickle Cell Anemia:** Hydroxyurea is a mainstay treatment because it increases the production of **Fetal Hemoglobin (HbF)**, which inhibits the polymerization of HbS. * **Other Uses:** Polycythemia Vera and Essential Thrombocytosis (to reduce hematocrit/platelet counts). * **Side Effects:** Apart from myelosuppression, it can cause **macrocytic anemia**, cutaneous ulcers, and hyperpigmentation of nails.

Question 1

A 23-year-old female presented with palpable lumps in the axilla and supra-clavicular region. Following investigations including X-ray, USG-guided biopsy, and HPE, a diagnosis was made. Flow cytometry revealed CD15 and CD30 positivity. She was started on chemotherapy. Later, the patient developed fatigue, dyspnea, and orthopnea, with ECG showing left ventricular hypertrophy. Which of the following chemotherapeutic agents is most likely responsible for these manifestations?

Accepted Answer

Bleomycin

Answer

Daunorubicin

Answer

Capecitabine

Answer

Cyclophosphamide

Question 2

Which of the following anticancer agents has specific activity in a subset of female breast cancers?

Accepted Answer

Trastuzumab

Answer

Anastrozole

Answer

Doxorubicin

Answer

Fluoxymesterone

Question 3

All of the following anticancer drugs act on the G2 phase except?

Accepted Answer

Paclitaxel

Answer

Etoposide

Answer

Irinotecan

Answer

Bleomycin

Question 4

All of the following statements about vincristine are true EXCEPT?

Accepted Answer

It is a drug of choice for solid tumors

Answer

It acts by inhibiting mitosis

Answer

Its prominent adverse effect is peripheral neuropathy

Answer

It does not suppress bone marrow

Question 5

What is the drug of choice for the T790M mutation of EGFR in Non-Small Cell Lung Cancer?

Accepted Answer

Osimertinib

Answer

Lapatinib

Answer

Crizotinib

Answer

Alemtuzumab

Question 6

Arsenic compounds are used for the treatment of which of the following cancers?

Accepted Answer

Acute Promyelocytic Leukemia (APML)

Answer

Chronic Lymphocytic Leukemia (CLL)

Answer

Acute Lymphoblastic Leukemia (ALL)

Answer

Chronic Myeloid Leukemia (CML)

Question 7

Which chemotherapeutic agent is used in brain tumors?

Accepted Answer

Nitrosoureas

Answer

Cisplatin

Answer

Bleomycin

Answer

Vincristine

Question 8

Skin pigmentation is caused by:

Accepted Answer

Busulphan

Answer

Methotrexate

Answer

Dactinomycin

Answer

Cyclophosphamide

Question 9

Which of the following anticancer drugs causes hemolytic uremic syndrome?

Accepted Answer

Mitomycin

Answer

Vincristine

Answer

Vinblastine

Answer

Cisplatin

Question 10

All of the following is true about hydroxyurea except:

Accepted Answer

Oral bioavailability is very low.

Answer

Causes myelosuppression.

Answer

Used in CML.

Answer

Acts as a radiosensitizer.

Anticancer Drugs — MCQs

Anticancer Drugs — MCQs

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