Anticancer Drugs — MCQs
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Which of the following anti-cancer drugs is known to cause nephrotoxicity?
Carmustine is a:
Capillary leak syndrome is caused by which of the following drugs?
Which of the following is NOT a treatment used for promyelocytic leukemia (M3)?
Long-term use of tamoxifen may cause which of the following?
What is the anti-CD25 monoclonal antibody used in the prophylaxis of acute organ rejection in adult patients?
Which drug is used in the treatment of carcinoma of the thyroid?
Which group of drugs is used as subsidiary medicines in cancer treatment?
Which single chemotherapeutic drug regimen, when used for carcinoma esophagus, shows a tumor size decrease of around 15-20%?
All of the following are examples of alkylating agents except?
Anticancer Drugs Indian Medical PG Practice Questions and MCQs
Question 301: Which of the following anti-cancer drugs is known to cause nephrotoxicity?
- A. Cyclophosphamide
- B. Busulfan
- C. Cisplatin (Correct Answer)
- D. Procarbazine
Explanation: **Explanation:** **Cisplatin** is a potent platinum-based alkylating agent. Its most significant dose-limiting toxicity is **nephrotoxicity**, specifically causing acute tubular necrosis (ATN) and damage to the proximal convoluted tubules. It accumulates in the renal tubular cells, leading to oxidative stress and apoptosis. To prevent this, patients are managed with aggressive **intravenous hydration** and the administration of **Amifostine** (a cytoprotective free-radical scavenger). **Analysis of Incorrect Options:** * **A. Cyclophosphamide:** While it is toxic to the urinary tract, its hallmark side effect is **Hemorrhagic Cystitis** (bladder toxicity) due to the metabolite **Acrolein**, not direct nephrotoxicity. This is prevented by **MESNA**. * **B. Busulfan:** This drug is primarily associated with **Pulmonary Fibrosis** ("Busulfan lung") and skin hyperpigmentation. * **C. Procarbazine:** It is known for causing disulfiram-like reactions and has MAO inhibitory activity, but it is not typically nephrotoxic. **High-Yield Clinical Pearls for NEET-PG:** * **Cisplatin Triad of Toxicity:** Nephrotoxicity, Ototoxicity (high-frequency hearing loss), and severe Emetogenicity (highly emetogenic). * **Electrolyte Imbalance:** Cisplatin frequently causes **Hypomagnesemia** due to renal wasting. * **Carboplatin:** A related drug that is significantly *less* nephrotoxic and ototoxic than Cisplatin but causes more dose-limiting **Myelosuppression** (specifically thrombocytopenia).
Question 302: Carmustine is a:
- A. Anti metabolite
- B. Nitrogen mustard
- C. Nitrosourea (Correct Answer)
- D. Taxane
Explanation: **Explanation:** **Carmustine (BCNU)** belongs to the **Nitrosourea** class of alkylating agents. Its primary mechanism involves the alkylation of DNA and the carbamoylation of proteins, which inhibits DNA repair and synthesis. **Why Nitrosourea is correct:** Nitrosoureas (including Carmustine, Lomustine, and Semustine) are highly **lipid-soluble** molecules. This property allows them to cross the **blood-brain barrier (BBB)** effectively. Consequently, Carmustine is a first-line treatment for primary brain tumors (e.g., Glioblastoma multiforme) and is often administered via biodegradable wafers (Gliadel) implanted directly into the tumor cavity. **Why other options are incorrect:** * **Anti-metabolites (e.g., Methotrexate, 5-FU):** These are S-phase specific drugs that interfere with nucleic acid synthesis. Carmustine is cell-cycle non-specific. * **Nitrogen mustards (e.g., Cyclophosphamide, Ifosfamide):** While also alkylating agents, they have a different chemical structure and generally lower CNS penetration compared to nitrosoureas. * **Taxanes (e.g., Paclitaxel, Docetaxel):** These are microtubule stabilizers that inhibit mitosis (M-phase). **High-Yield Clinical Pearls for NEET-PG:** * **CNS Penetration:** Always associate Nitrosoureas with brain tumors due to their lipophilicity. * **Toxicity:** The dose-limiting toxicity of Carmustine is **delayed myelosuppression** (occurring 4–6 weeks after treatment). * **Pulmonary Fibrosis:** Long-term use or high doses can lead to interstitial lung disease/fibrosis. * **Mnemonic:** Remember the **"Mustines"** (Car**mustine**, Lo**mustine**) are Nitrosoureas.
Question 303: Capillary leak syndrome is caused by which of the following drugs?
- A. Fligrastim
- B. Sargramostim (Correct Answer)
- C. Pegfilgrastim
- D. Darbepoetin
Explanation: **Explanation:** **Sargramostim** is a recombinant **Granulocyte-Macrophage Colony-Stimulating Factor (GM-CSF)**. Unlike G-CSF, which acts specifically on neutrophil lineages, GM-CSF stimulates a broader range of cells, including monocytes and macrophages. These activated cells release pro-inflammatory cytokines (such as TNF-α and IL-1), which increase vascular permeability. At higher doses, this leads to **Capillary Leak Syndrome**, characterized by peripheral edema, pleural and pericardial effusions, and "First-dose reaction" (hypotension and tachycardia). **Analysis of Incorrect Options:** * **Filgrastim (A) & Pegfilgrastim (C):** These are recombinant **G-CSF** (Granulocyte Colony-Stimulating Factors). They are more lineage-specific than GM-CSF and do not typically cause cytokine-mediated capillary leak. Their most common side effect is **bone pain** due to marrow expansion. * **Darbepoetin (D):** This is a long-acting erythropoiesis-stimulating agent (ESA). Its primary side effects are **hypertension** and an increased risk of thromboembolic events, not capillary leak. **High-Yield Clinical Pearls for NEET-PG:** * **Sargramostim (GM-CSF):** Associated with "First-dose reaction" and Capillary Leak Syndrome. * **Filgrastim (G-CSF):** Most common side effect is medullary bone pain; used to reduce the duration of neutropenia after chemotherapy. * **Other drugs causing Capillary Leak Syndrome:** **Interleukin-2 (Aldesleukin)** is the most classic cause (often more severe than Sargramostim). * **Distinction:** G-CSF (Filgrastim) is generally preferred over GM-CSF (Sargramostim) in clinical practice because it is better tolerated and more specific for treating neutropenia.
Question 304: Which of the following is NOT a treatment used for promyelocytic leukemia (M3)?
- A. Arsenic
- B. Tretinoin
- C. Retinoic acid
- D. Cisplatin (Correct Answer)
Explanation: **Explanation:** Acute Promyelocytic Leukemia (APL), the M3 subtype of AML, is characterized by a specific chromosomal translocation **t(15;17)**. This translocation creates the **PML-RARα** fusion protein, which blocks myeloid differentiation at the promyelocyte stage. **Why Cisplatin is the Correct Answer:** **Cisplatin** is a platinum-based alkylating-like agent that causes DNA cross-linking. It is primarily used for solid tumors (e.g., testicular, ovarian, and lung cancers). It has **no role** in the management of APL, as the treatment of M3 focuses on "differentiation therapy" rather than traditional cytotoxic DNA damage. **Why the other options are incorrect:** * **Tretinoin & Retinoic Acid (ATRA):** All-trans retinoic acid (ATRA) is the cornerstone of APL treatment. It binds to the altered retinoic acid receptor (RARα), inducing the malignant promyelocytes to differentiate into mature neutrophils, thereby inducing remission. * **Arsenic (Arsenic Trioxide):** This is used for both induction and consolidation in APL. It works by promoting the degradation of the PML-RARα fusion protein and inducing apoptosis in leukemia cells. **High-Yield Clinical Pearls for NEET-PG:** * **Differentiation Syndrome:** A life-threatening complication of ATRA/Arsenic therapy characterized by fever, dyspnea, and pulmonary infiltrates. It is treated with **high-dose Dexamethasone**. * **DIC Risk:** APL is highly associated with Disseminated Intravascular Coagulation (DIC) due to the release of procoagulants from promyelocyte granules. * **Molecular Marker:** The presence of the **PML-RARα** gene is diagnostic and used to monitor minimal residual disease (MRD).
Question 305: Long-term use of tamoxifen may cause which of the following?
- A. Endometrial carcinoma (Correct Answer)
- B. Cervical carcinoma
- C. Vaginal carcinoma
- D. Ovarian carcinoma
Explanation: **Explanation:** Tamoxifen is a **Selective Estrogen Receptor Modulator (SERM)**. Its clinical effects are unique because it acts as an antagonist in some tissues and an agonist in others. 1. **Why Endometrial Carcinoma is correct:** In the breast, tamoxifen acts as an **antagonist**, making it effective for ER-positive breast cancer. However, in the **uterus**, it acts as a **partial agonist**. This estrogenic stimulation leads to endometrial hyperplasia, which significantly increases the risk of developing **endometrial carcinoma** with long-term use. 2. **Why other options are incorrect:** * **Cervical Carcinoma:** This is primarily associated with High-Risk Human Papillomavirus (HPV) infection, not hormonal stimulation by SERMs. * **Vaginal Carcinoma:** Clear cell adenocarcinoma of the vagina is classically linked to *in utero* exposure to Diethylstilbestrol (DES), not tamoxifen. * **Ovarian Carcinoma:** Tamoxifen does not have a significant stimulatory effect on the ovarian epithelium; in fact, it is sometimes studied as a treatment for certain ovarian cancers. **High-Yield Clinical Pearls for NEET-PG:** * **Bone & Lipids:** Tamoxifen acts as an **agonist** in bone (preventing osteoporosis) and on liver lipids (lowering LDL). * **Thromboembolism:** Due to its estrogenic effect in the liver, it increases the synthesis of clotting factors, leading to an increased risk of **Deep Vein Thrombosis (DVT)** and pulmonary embolism. * **Raloxifene:** Unlike tamoxifen, raloxifene is an **antagonist** at the endometrium, so it does **not** increase the risk of endometrial cancer. * **Monitoring:** Patients on tamoxifen should undergo regular gynecological check-ups to monitor for abnormal vaginal bleeding.
Question 306: What is the anti-CD25 monoclonal antibody used in the prophylaxis of acute organ rejection in adult patients?
- A. Basiliximab (Correct Answer)
- B. Muromonab
- C. Efalizumab
- D. Eculizumab
Explanation: **Explanation:** **Basiliximab** is a chimeric monoclonal antibody that acts as an **IL-2 receptor antagonist**. It specifically binds to the **α-chain (CD25)** of the IL-2 receptor expressed on the surface of activated T-lymphocytes. By blocking this receptor, it inhibits IL-2-mediated T-cell proliferation, which is a critical step in the immune response leading to graft rejection. It is primarily used for the **prophylaxis of acute organ rejection** in renal transplantation, often as part of an induction regimen. **Analysis of Incorrect Options:** * **Muromonab (OKT3):** This is a murine monoclonal antibody against the **CD3** receptor on T-cells. While used for transplant rejection, it is associated with "cytokine release syndrome" and has largely been replaced by newer agents. * **Efalizumab:** This is an anti-**CD11a** antibody (targeting LFA-1) formerly used for plaque psoriasis. It was withdrawn from the market due to the risk of progressive multifocal leukoencephalopathy (PML). * **Eculizumab:** This is a monoclonal antibody against the **C5 complement protein**. It is used in the treatment of Paroxysmal Nocturnal Hemoglobinuria (PNH) and Atypical Hemolytic Uremic Syndrome (aHUS). **High-Yield Pearls for NEET-PG:** * **Daclizumab** is another anti-CD25 antibody (humanized), though it was primarily used for Multiple Sclerosis before being withdrawn. * **Basiliximab** is "chimeric" (suffix **-ximab**), meaning it is ~75% human and 25% murine, which reduces its immunogenicity compared to Muromonab. * Unlike general immunosuppressants, Basiliximab does not cause significant myelosuppression, making it ideal for induction therapy.
Question 307: Which drug is used in the treatment of carcinoma of the thyroid?
- A. Doxorubicin (Correct Answer)
- B. 5-Fluorouracil
- C. Methotrexate
- D. Vinblastine
Explanation: **Explanation:** **Doxorubicin** (an anthracycline antibiotic) is the correct answer because it is historically the most effective and commonly used cytotoxic chemotherapy agent for advanced **thyroid carcinoma**, particularly for **Anaplastic Thyroid Cancer** and metastatic Differentiated Thyroid Cancer (DTC) that is refractory to radioactive iodine. It works by inhibiting Topoisomerase II, intercalating DNA, and generating free radicals. **Analysis of Incorrect Options:** * **5-Fluorouracil (5-FU):** This is an antimetabolite primarily used for "solid" GI tract tumors (colorectal, gastric, pancreatic) and breast cancer. It has no significant role in thyroid cancer management. * **Methotrexate:** A folate antagonist used for leukemias, lymphomas, choriocarcinoma, and osteosarcoma. It is not a standard treatment for thyroid malignancies. * **Vinblastine:** A vinca alkaloid that inhibits microtubule assembly. While used in Hodgkin’s lymphoma and testicular cancer, it is not indicated for thyroid carcinoma. **High-Yield Clinical Pearls for NEET-PG:** * **Cardiotoxicity:** Doxorubicin is notorious for dose-dependent cardiotoxicity (dilated cardiomyopathy). Dexrazoxane is used to prevent this. * **Targeted Therapy:** While Doxorubicin is the classic cytotoxic choice, the current "Gold Standard" for advanced thyroid cancer has shifted toward Tyrosine Kinase Inhibitors (TKIs) like **Lenvatinib** and **Sorafenib**. * **Medullary Thyroid Cancer:** The drugs of choice are **Vandetanib** and **Cabozantinib**. * **Red Urine:** Patients should be warned that Doxorubicin can cause harmless red discoloration of urine.
Question 308: Which group of drugs is used as subsidiary medicines in cancer treatment?
- A. Amefostine
- B. Filgrastim
- C. Cytochalasin
- D. All of the above (Correct Answer)
Explanation: **Explanation:** In oncology, **subsidiary medicines** (also known as supportive or adjuvant care drugs) are not used to kill cancer cells directly but to manage the side effects of chemotherapy, protect healthy tissues, or enhance the efficacy of the primary treatment. **Breakdown of Options:** * **Amifostine:** This is a **cytoprotective agent** (free radical scavenger). It is specifically used to reduce renal toxicity associated with Cisplatin and to prevent xerostomia (dry mouth) in patients undergoing radiation therapy for head and neck cancers. * **Filgrastim:** This is a **Granulocyte Colony-Stimulating Factor (G-CSF)**. It is used to treat or prevent chemotherapy-induced neutropenia. By stimulating the bone marrow to produce neutrophils, it reduces the risk of life-threatening infections and allows patients to maintain their chemotherapy schedule. * **Cytochalasin:** While less commonly used in routine clinical practice compared to the others, cytochalasins are fungal metabolites that inhibit actin polymerization. In a research and subsidiary context, they are studied for their ability to alter cell permeability and enhance the uptake of other chemotherapeutic agents into resistant tumor cells. **Conclusion:** Since all three agents serve supportive roles—protecting organs, managing hematological toxicity, or modulating cell response—the correct answer is **All of the above.** **High-Yield Clinical Pearls for NEET-PG:** * **Mesna:** Always remember Mesna is the subsidiary drug used to prevent **hemorrhagic cystitis** caused by Cyclophosphamide and Ifosfamide. * **Dexrazoxane:** Used to prevent **cardiotoxicity** (dilated cardiomyopathy) caused by Doxorubicin/Anthracyclines. * **Leucovorin (Folinic Acid):** Used as a "rescue" therapy for high-dose Methotrexate toxicity and to enhance the activity of 5-Fluorouracil.
Question 309: Which single chemotherapeutic drug regimen, when used for carcinoma esophagus, shows a tumor size decrease of around 15-20%?
- A. Bleomycin
- B. Cisplatin (Correct Answer)
- C. Doxorubicin
- D. Vincristine
Explanation: Cisplatin is considered the most active single-agent chemotherapeutic drug for the treatment of esophageal carcinoma (both squamous cell carcinoma and adenocarcinoma) [1]. When used as monotherapy, it typically yields an objective response rate (reduction in tumor size) of approximately 15–20% [1]. In clinical practice, it is rarely used alone; it serves as the backbone for combination regimens (e.g., with 5-Fluorouracil or Paclitaxel), which significantly increase response rates to 40–50%. Analysis of Incorrect Options: * Bleomycin (Option A): While it has some activity against squamous cell carcinomas, its single-agent efficacy in esophageal cancer is lower than Cisplatin, and its use is limited by the risk of pulmonary fibrosis. * Doxorubicin (Option C): This anthracycline is primarily used in breast cancer, lymphomas, and sarcomas. Its activity in esophageal cancer is minimal and inconsistent compared to platinum-based agents. * Vincristine (Option D): This vinca alkaloid is a microtubule inhibitor used mainly in hematological malignancies (leukemias/lymphomas) and pediatric tumors. It has no significant role or documented efficacy in the management of esophageal carcinoma. High-Yield Clinical Pearls for NEET-PG: * Mechanism of Action: Cisplatin is an alkylating-like agent that causes intra-strand cross-linking of DNA, inhibiting replication [1]. * Dose-Limiting Toxicity: Nephrotoxicity (prevented by aggressive hydration and amifostine) and Ototoxicity. * Highly Emetogenic: Cisplatin is the prototype for drugs with high emetic potential; it requires prophylaxis with 5-HT3 antagonists (e.g., Ondansetron) and Aprepitant. * Standard of Care: The current "Gold Standard" for esophageal cancer is the CROSS regimen (Carboplatin + Paclitaxel with concurrent radiotherapy).
Question 310: All of the following are examples of alkylating agents except?
- A. Procarbazine
- B. Melphalan
- C. Busulfan
- D. Bleomycin (Correct Answer)
Explanation: ### Explanation **Correct Answer: D. Bleomycin** **Mechanism and Classification:** Alkylating agents work by forming covalent bonds with DNA, specifically by attaching an alkyl group to the guanine base (usually at the N-7 position). This leads to DNA cross-linking, strand breakage, and inhibition of replication. **Bleomycin**, however, is classified as a **Cytotoxic Antibiotic**. It acts by binding to DNA and chelation of ferrous ions, leading to the formation of free radicals (superoxide and hydroxyl radicals) that cause single- and double-stranded DNA breaks. **Analysis of Options:** * **A. Procarbazine:** A methylhydrazine derivative that functions as a non-classic alkylating agent. It is metabolized to produce reactive intermediates that alkylate DNA. It is notably used in the MOPP regimen for Hodgkin’s Lymphoma. * **B. Melphalan:** A nitrogen mustard derivative (classic alkylating agent) primarily used in the treatment of Multiple Myeloma. * **C. Busulfan:** An alkyl sulfonate that cross-links DNA. It is a cell-cycle non-specific alkylating agent frequently used in chronic myeloid leukemia (CML) and as a conditioning agent before bone marrow transplantation. **High-Yield Clinical Pearls for NEET-PG:** * **Bleomycin Toxicity:** The most significant dose-limiting toxicity is **Pulmonary Fibrosis**. Unlike most anticancer drugs, it is **"Bone Marrow Sparing"** (minimal myelosuppression). * **Busulfan Toxicity:** Associated with "Busulfan Tan" (skin hyperpigmentation) and pulmonary fibrosis. * **Cyclophosphamide:** An alkylating agent known for causing **Hemorrhagic Cystitis**, which can be prevented by administering **MESNA** and adequate hydration. * **Procarbazine:** Has a unique side effect profile including **Disulfiram-like reactions** with alcohol and MAO inhibition (hypertensive crisis with tyramine-rich foods).
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
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Immunotherapy
Practice Questions
Management of Chemotherapy Side Effects
Practice Questions
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