Anticancer Drugs — MCQs

Anticancer Drugs Indian Medical PG Practice Questions and MCQs

Question 341: Inotuzumab acts against which CD antigen?

A. CD11
B. CD19
C. CD22 (Correct Answer)
D. CD25

Explanation: **Inotuzumab ozogamicin** is an antibody-drug conjugate (ADC) consisting of a humanized monoclonal antibody targeting **CD22**, linked to a cytotoxic agent called calicheamicin . 1. **Why CD22 is correct:** CD22 is a cell surface antigen expressed on more than 90% of B-cell malignancies. When Inotuzumab binds to CD22, the complex is internalized, and calicheamicin is released, causing double-stranded DNA breaks and subsequent cell death. It is primarily used in the treatment of relapsed or refractory **B-cell precursor Acute Lymphoblastic Leukemia (ALL)**. 2. **Analysis of Incorrect Options:** * **CD11:** CD11c is a marker typically associated with Hairy Cell Leukemia and myeloid cells; no major monoclonal antibody used in ALL targets this. * **CD19:** This is the target for **Blinatumomab** (a BiTE - Bispecific T-cell Engager) and **Tisagenlecleucel** (CAR-T cell therapy). * **CD25:** This is the alpha chain of the IL-2 receptor, targeted by **Basiliximab** and **Daclizumab** (used in transplant medicine to prevent rejection). **High-Yield Clinical Pearls for NEET-PG:** * **Mnemonic:** Inotu-**ZZ**-umab targets CD-**22**. * **Black Box Warning:** Inotuzumab is associated with a high risk of **Hepatotoxicity**, specifically **Veno-Occlusive Disease (VOD)** or Sinusoidal Obstruction Syndrome, especially after hematopoietic stem cell transplant. * **Gemtuzumab ozogamicin:** A similar ADC that targets **CD33**, used in Acute Myeloid Leukemia (AML). Remember: **G**emtuzumab for **G**ranulocytes (Myeloid).

Question 342: Which of the following anticancer drugs causes nephrotoxicity as an adverse effect?

A. Imatinib
B. Irinotecan
C. Bleomycin
D. Cisplatin (Correct Answer)

Explanation: ### Explanation **Correct Answer: D. Cisplatin** **Mechanism and Nephrotoxicity:** Cisplatin is a potent platinum-based alkylating-like agent that inhibits DNA synthesis by forming intra-strand cross-links. Its most significant dose-limiting toxicity is **nephrotoxicity**, specifically causing **Acute Tubular Necrosis (ATN)**. It accumulates in the proximal convoluted tubule cells, leading to oxidative stress and apoptosis. To mitigate this, clinicians use **aggressive hydration** with normal saline and may administer **Amifostine** (a cytoprotective free-radical scavenger). **Analysis of Incorrect Options:** * **A. Imatinib:** A selective Tyrosine Kinase Inhibitor (TKI) targeting the BCR-ABL protein. Its hallmark side effect is **fluid retention**, typically manifesting as periorbital edema. * **B. Irinotecan:** A Topoisomerase I inhibitor used in colorectal cancer. Its classic adverse effect is **severe diarrhea** ("I run to the can"), which can be acute (cholinergic) or delayed. * **C. Bleomycin:** An antitumor antibiotic that causes DNA strand breaks. Its dose-limiting toxicity is **Pulmonary Fibrosis**, not renal damage. It is unique because it lacks significant bone marrow suppression. **High-Yield Clinical Pearls for NEET-PG:** * **Cisplatin Triad of Toxicity:** Nephrotoxicity, Ototoxicity (high-frequency hearing loss), and severe Emetogenicity (requires Aprepitant/Ondansetron). * **Electrolyte Imbalance:** Cisplatin frequently causes **Hypomagnesemia** due to renal wasting. * **Carboplatin:** A related drug that is less nephrotoxic but more myelosuppressive (causes thrombocytopenia).

Question 343: Which of the following drugs is used for Acute Myeloid Leukemia (AML)?

A. Bevacizumab
B. Rituximab
C. Ozogamicin (Correct Answer)
D. Trastuzumab

Explanation: ### **Explanation** **Correct Option: C. Ozogamicin** **Gemtuzumab ozogamicin** is a monoclonal antibody conjugated with a cytotoxic agent (calicheamicin). It specifically targets **CD33**, a cell surface antigen expressed on the blasts of approximately 90% of patients with **Acute Myeloid Leukemia (AML)**. Once bound, the complex is internalized, releasing calicheamicin to cause DNA double-strand breaks and cell death. It is FDA-approved for both newly diagnosed and relapsed/refractory CD33-positive AML. **Incorrect Options:** * **A. Bevacizumab:** This is a humanized monoclonal antibody against **VEGF** (Vascular Endothelial Growth Factor). It acts as an angiogenesis inhibitor and is primarily used in solid tumors like colorectal cancer, renal cell carcinoma, and glioblastoma. * **B. Rituximab:** This targets the **CD20** antigen found on B-cells. It is the cornerstone treatment for B-cell Non-Hodgkin Lymphomas (NHL), Chronic Lymphocytic Leukemia (CLL), and various autoimmune conditions, but not AML (which is of myeloid origin). * **D. Trastuzumab:** This is a monoclonal antibody against the **HER2/neu** receptor. It is used specifically in HER2-positive breast cancer and gastric adenocarcinoma. **High-Yield Clinical Pearls for NEET-PG:** * **Gemtuzumab ozogamicin Side Effect:** A significant and specific adverse effect is **Sinusoidal Obstruction Syndrome (SOS)**, formerly known as Veno-Occlusive Disease (VOD). * **Other "Mabs" in Hemat-Oncology:** * **Brentuximab vedotin:** Targets **CD30** (used in Hodgkin Lymphoma). * **Alemtuzumab:** Targets **CD52** (used in CLL). * **Blinatumomab:** A BiTE (Bispecific T-cell Engager) targeting **CD19** and **CD3** (used in ALL).

Question 344: What is the most important adverse effect of Bleomycin?

A. Myelosuppression
B. Hepatotoxicity
C. Pulmonary fibrosis (Correct Answer)
D. Peripheral neuropathy

Explanation: **Explanation:** **Bleomycin** is a unique cytotoxic antibiotic that acts by binding to DNA and causing single- and double-strand breaks through the generation of free radicals (ferrous iron oxidation). **Why Pulmonary Fibrosis is the correct answer:** The most serious and dose-limiting toxicity of Bleomycin is **Pulmonary Fibrosis**. This occurs because the enzyme responsible for inactivating Bleomycin (**Bleomycin hydrolase**) is significantly deficient in the lungs and skin. Consequently, the drug accumulates in pulmonary tissues, leading to oxidative stress, inflammation, and eventual fibrosis. It typically presents as dry cough and progressive dyspnea. **Analysis of Incorrect Options:** * **A. Myelosuppression:** Unlike most conventional anticancer drugs, Bleomycin is famously **"bone marrow sparing."** This makes it a vital component of combination regimens (like ABVD for Hodgkin’s Lymphoma) as it does not worsen leukopenia or thrombocytopenia. * **B. Hepatotoxicity:** While some chemotherapeutic agents (like Methotrexate or 6-Mercaptopurine) are hepatotoxic, it is not a characteristic or dose-limiting side effect of Bleomycin. * **D. Peripheral Neuropathy:** This is the classic dose-limiting toxicity of **Vinca alkaloids** (Vincristine) and **Taxanes** (Paclitaxel), not Bleomycin. **High-Yield Clinical Pearls for NEET-PG:** * **Monitoring:** Patients on Bleomycin should undergo periodic **Pulmonary Function Tests (PFTs)**; a decrease in DLCO (Diffusion Capacity of Carbon Monoxide) is an early sign of toxicity. * **Dermatological Toxicity:** Bleomycin can cause **Flagellate hyperpigmentation** (whip-like streaks on the skin). * **Cell Cycle:** It is a **G2-phase specific** drug. * **Cumulative Dose:** The risk of fibrosis increases significantly when the cumulative dose exceeds **400 units**.

Question 345: Which anticancer drug is known to cause lung fibrosis?

A. Bleomycin (Correct Answer)
B. Cisplatin
C. Fulvestrant
D. Tamoxifen

Explanation: **Bleomycin** is a cytotoxic antibiotic that acts by producing free radicals (superoxide and hydroxyl radicals) which cause DNA strand breaks. The primary reason it causes **pulmonary fibrosis** is the lack of the enzyme **bleomycin hydrolase** in the lungs and skin. While other tissues can metabolize the drug, the lungs are unable to inactivate it, leading to oxidative damage, inflammation, and subsequent irreversible fibrosis. This is a dose-dependent toxicity (cumulative dose >400 units). **Explanation of Incorrect Options:** * **B. Cisplatin:** A platinum compound primarily known for its **nephrotoxicity** (prevented by aggressive hydration and amifostine) and severe **ototoxicity**. It does not typically cause lung fibrosis. * **C. Fulvestrant:** A Selective Estrogen Receptor Degrader (SERD) used in breast cancer. Its side effects are hormonal (hot flashes, injection site pain) rather than organ-specific fibrosis. * **D. Tamoxifen:** A Selective Estrogen Receptor Modulator (SERM). Its high-yield side effects include an increased risk of **endometrial carcinoma** and thromboembolism. **Clinical Pearls for NEET-PG:** * **Monitoring:** Patients on Bleomycin must undergo periodic **Pulmonary Function Tests (PFTs)**; a decrease in DLCO (Diffusion Capacity of Carbon Monoxide) is an early sign of toxicity. * **Skin Toxicity:** Bleomycin also causes **flagellate hyperpigmentation** (whip-like streaks on the skin). * **Cell Cycle:** It is unique among antibiotics for being **G2 phase-specific**. * **Other drugs causing lung fibrosis:** Busulfan ("Busulfan lung"), Methotrexate, and Amiodarone.

Question 346: All of the following anticancer agents cause bone marrow suppression except?

A. Chlorambucil
B. Danorubicin
C. Doxorubicin
D. Flutamide (Correct Answer)

Explanation: **Explanation:** The correct answer is **Flutamide**. **1. Why Flutamide is the correct answer:** Bone marrow suppression (myelosuppression) is the most common dose-limiting toxicity of traditional cytotoxic chemotherapy. These drugs target rapidly dividing cells, including hematopoietic stem cells. **Flutamide**, however, is a **non-steroidal anti-androgen**. It works by competitively inhibiting androgen receptors in target tissues. Since it does not interfere with DNA synthesis or cell division in a non-specific manner, it lacks the typical cytotoxic profile and **does not cause bone marrow suppression**. Its primary side effects are related to androgen deprivation, such as gynecomastia and hepatotoxicity. **2. Why the other options are incorrect:** * **Chlorambucil:** An **Alkylating agent** (Nitrogen mustard). It cross-links DNA, leading to cell death. It is highly myelosuppressive and can cause cumulative bone marrow toxicity. * **Daunorubicin & Doxorubicin:** These are **Anthracycline antibiotics**. They inhibit Topoisomerase II, intercalate DNA, and generate free radicals. Significant, dose-limiting myelosuppression (neutropenia) is a hallmark of this class, alongside cardiotoxicity. **3. NEET-PG High-Yield Clinical Pearls:** * **"Marrow-Sparing" Anticancer Drugs:** Remember the mnemonic **"V-C-B-L-A"** for drugs with minimal/no bone marrow suppression: **V**incristine, **C**isplatin (more nephrotoxic), **B**leomycin (pulmonary fibrosis), **L**-Asparaginase (pancreatitis/clotting issues), and **A**ntihormones (like Flutamide, Tamoxifen). * **Flutamide** is frequently used in the treatment of metastatic prostatic carcinoma, often combined with GnRH agonists to prevent the "testosterone flare." * **Most common side effect of Flutamide:** Gynecomastia. * **Most serious side effect of Flutamide:** Hepatotoxicity (monitor LFTs).

Question 347: Which of the following drugs is used as an immunosuppressant but lacks anticancer activity?

A. Methotrexate
B. 6-Mercaptopurine
C. Azathioprine (Correct Answer)
D. 5-Fluorouracil

Explanation: **Explanation** The correct answer is **Azathioprine**. **Why Azathioprine is correct:** Azathioprine is a prodrug of **6-Mercaptopurine (6-MP)**. While 6-MP is used in the treatment of acute leukemias (anticancer), Azathioprine is specifically designed to release 6-MP slowly. This slow release results in a sustained suppression of T-lymphocyte proliferation, making it an excellent **immunosuppressant** for organ transplantation and autoimmune diseases (like Rheumatoid Arthritis or SLE). However, because it does not achieve the rapid, high peak concentrations required to kill rapidly dividing malignant cells, it **lacks significant anticancer activity**. **Analysis of Incorrect Options:** * **Methotrexate:** A folate antagonist that inhibits dihydrofolate reductase (DHFR). It is used both as an anticancer agent (choriocarcinoma, osteosarcoma) and as an immunosuppressant (RA, Psoriasis). * **6-Mercaptopurine:** A purine analog that inhibits de novo purine synthesis. It is a potent anticancer drug used primarily in Acute Lymphoblastic Leukemia (ALL). * **5-Fluorouracil:** A pyrimidine analog that inhibits thymidylate synthase. It is a mainstay in the treatment of solid tumors, particularly colorectal and breast cancers, but is not used as a systemic immunosuppressant. **High-Yield Clinical Pearls for NEET-PG:** * **Drug Interaction:** Both Azathioprine and 6-MP are metabolized by **Xanthine Oxidase**. If a patient is also taking **Allopurinol** (a xanthine oxidase inhibitor), the dose of Azathioprine/6-MP must be reduced by **75%** to avoid life-threatening bone marrow toxicity. * **Pharmacogenomics:** Patients with a genetic deficiency of the enzyme **TPMT** (Thiopurine Methyltransferase) are at high risk of severe myelosuppression when taking these drugs. * **Leflunomide** is another example of a drug used as an immunosuppressant (DMARD) that lacks anticancer activity.

Question 348: What is the mechanism of action of Bevacizumab?

A. Acts on Vascular Endothelial Growth Factor (VEGF) (Correct Answer)
B. Epidermal Growth Factor Receptor (EGFR) antagonist
C. Platelet-Derived Growth Factor (PDGF) monoclonal antibody
D. Tyrosine kinase inhibitor

Explanation: **Explanation:** **Mechanism of Action:** Bevacizumab is a recombinant humanized monoclonal antibody that binds directly to **Vascular Endothelial Growth Factor (VEGF-A)**. By binding to the circulating VEGF ligand, it prevents the growth factor from interacting with its receptors (VEGFR-1 and VEGFR-2) on the surface of endothelial cells. This inhibits **angiogenesis** (the formation of new blood vessels), thereby "starving" the tumor of the blood supply and nutrients required for growth and metastasis. **Analysis of Options:** * **Option B (EGFR antagonist):** Drugs like **Cetuximab** and **Panitumumab** are monoclonal antibodies against EGFR, while **Erlotinib** and **Gefitinib** are small molecule inhibitors. These are used primarily in colorectal and lung cancers. * **Option C (PDGF antibody):** While PDGF is involved in angiogenesis, Bevacizumab specifically targets VEGF. **Olaratumab** is an example of a monoclonal antibody targeting PDGF receptors. * **Option D (Tyrosine kinase inhibitor):** Bevacizumab is a monoclonal antibody (large molecule) that acts extracellularly. In contrast, TKIs like **Sunitinib** or **Sorafenib** are small molecules that act intracellularly to inhibit the signaling cascade of VEGF and other receptors. **Clinical Pearls for NEET-PG:** * **Indications:** Metastatic colorectal cancer (first-line), renal cell carcinoma, and wet Age-related Macular Degeneration (AMD) – though Ranibizumab is more specific for ophthalmic use. * **Specific Side Effects:** The most high-yield side effects are **hypertension**, **proteinuria**, and **impaired wound healing** (it must be stopped 4-6 weeks before surgery). It also increases the risk of gastrointestinal perforation and thromboembolism.

Question 349: Sterile hemorrhagic cystitis is caused by:

A. Busulfan
B. Ketoprofen
C. Methicillin
D. Cyclophosphamide (Correct Answer)

Explanation: **Explanation:** **Cyclophosphamide** (and its analog Ifosfamide) is a nitrogen mustard alkylating agent. Its metabolism in the liver produces a toxic metabolite called **Acrolein**. Acrolein is excreted in the urine, where it causes direct irritation and sloughing of the bladder mucosa, leading to **sterile hemorrhagic cystitis** (characterized by hematuria without evidence of infection). **Why the other options are incorrect:** * **Busulfan:** An alkylating agent primarily used in CML. Its classic side effects include pulmonary fibrosis ("Busulfan lung"), skin hyperpigmentation, and adrenal insufficiency-like syndrome. * **Ketoprofen:** An NSAID. While it can cause renal impairment (interstitial nephritis or papillary necrosis), it is not associated with hemorrhagic cystitis. * **Methicillin:** A penicillinase-resistant penicillin. Its classic renal side effect is **Acute Interstitial Nephritis (AIN)**, often presenting with fever, rash, and eosinophiluria. **High-Yield Clinical Pearls for NEET-PG:** * **Prevention:** Hemorrhagic cystitis can be prevented by aggressive hydration and the administration of **MESNA** (2-Mercaptoethane Sulfonate Na). * **Mechanism of MESNA:** It contains a sulfhydryl group that binds to and neutralizes acrolein in the bladder to form a non-toxic compound. * **Other Side Effects of Cyclophosphamide:** Bone marrow suppression, alopecia, and increased risk of transitional cell carcinoma of the bladder. * **Specific Toxicity:** While Cyclophosphamide causes cystitis, **Busulfan** is notorious for causing **Veno-occlusive disease (VOD)** of the liver.

Question 350: Which of the following drugs are used in the treatment of multiple myeloma?

A. Bortezomib, Melphalan, Hydroxyurea
B. Bortezomib, Melphalan, Cyclophosphamide (Correct Answer)
C. Hydroxyurea, Ketoconazole, Cyclophosphamide
D. Bortezomib, Hydroxyurea, Ketoconazole

Explanation: Multiple myeloma is a plasma cell dyscrasia characterized by the malignant proliferation of plasma cells in the bone marrow. The management involves a combination of proteasome inhibitors, alkylating agents, immunomodulators, and steroids. **Why Option B is Correct:** * **Bortezomib:** A reversible inhibitor of the **26S proteasome**. It prevents the degradation of pro-apoptotic proteins, leading to apoptosis of malignant plasma cells. It is a cornerstone of modern myeloma therapy. * **Melphalan:** A nitrogen mustard **alkylating agent**. It has been a standard treatment for myeloma for decades, often used in high doses prior to autologous stem cell transplantation. * **Cyclophosphamide:** Another **alkylating agent** frequently used in combination regimens (e.g., CyBorD: Cyclophosphamide, Bortezomib, Dexamethasone) for patients who may not tolerate melphalan or as part of salvage therapy. **Why Other Options are Incorrect:** * **Hydroxyurea:** Primarily used in myeloproliferative neoplasms (like Polycythemia Vera) and Sickle Cell Anemia (to increase HbF). It is not a standard treatment for multiple myeloma. * **Ketoconazole:** An antifungal that also inhibits steroidogenesis. While used in Cushing’s syndrome or advanced prostate cancer (to reduce androgens), it has no role in treating multiple myeloma. **High-Yield Clinical Pearls for NEET-PG:** * **Bortezomib Side Effect:** Peripheral neuropathy is a major dose-limiting toxicity. * **Thalidomide/Lenalidomide:** These immunomodulators (IMiDs) are also first-line agents for myeloma. Remember: Thalidomide causes **phocomelia** (teratogenicity). * **Mnemonic for Myeloma Clinical Features:** **CRAB** (Calcium elevation, Renal insufficiency, Anemia, Bone lesions). * **Drug of Choice for Hypercalcemia in Myeloma:** IV Bisphosphonates (e.g., Zoledronic acid).

Practice by Chapter

Principles of Cancer Chemotherapy

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Alkylating Agents

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Antimetabolites

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Antitumor Antibiotics

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Plant Alkaloids

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Topoisomerase Inhibitors

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Hormonal Agents

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Targeted Therapy

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Immunotherapy

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Management of Chemotherapy Side Effects

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