Anticancer Drugs — MCQs
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Which of the following drugs causes hemorrhagic cystitis?
Which of the following drugs is known to cause hemorrhagic cystitis as a side effect?
Which of the following is a VEGF inhibitor?
Which is a glycoprotein, produced by many mammalian cells, and used in the treatment of hepatitis, papillomaviruses, hairy-cell leukemia, and AIDS-related Kaposi's sarcoma?
Which of the following is a cytoprotectant?
Which drug is used exclusively in organ transplantation and autoimmune diseases, but not in cancers?
Arsenic is useful in the treatment of which of the following conditions?
Which of the following therapies is known to stimulate progenitor megakaryocytes and is used in the treatment of cancer chemotherapy-induced thrombocytopenia?
Baezomib is:
Which drug is NOT effective in Multiple Myeloma?
Anticancer Drugs Indian Medical PG Practice Questions and MCQs
Question 1: Which of the following drugs causes hemorrhagic cystitis?
- A. Cyclophosphamide (Correct Answer)
- B. Cycloserine
- C. Ciprofloxacin
- D. Cyclosporine
Explanation: **Explanation:** **Cyclophosphamide** 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 **hemorrhagic cystitis**. This condition is characterized by gross hematuria and bladder pain. **Analysis of Options:** * **Cycloserine (B):** An antitubercular drug (second-line) primarily known for its neurotoxic side effects, such as seizures and psychosis. * **Ciprofloxacin (C):** A fluoroquinolone antibiotic. Common side effects include tendon rupture and QT prolongation, but not bladder toxicity. * **Cyclosporine (D):** An immunosuppressant (calcineurin inhibitor). Its dose-limiting toxicity is **nephrotoxicity** (afferent arteriolar vasoconstriction), not cystitis. **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). MESNA contains a thiol group that binds to and neutralizes acrolein in the bladder. * **Other Drug:** **Ifosfamide** is another alkylating agent that produces acrolein and carries an even higher risk of hemorrhagic cystitis than cyclophosphamide. * **Long-term Risk:** Chronic irritation from cyclophosphamide can increase the risk of **transitional cell carcinoma** of the bladder. * **Other Side Effects:** Cyclophosphamide is also associated with SIADH and infertility (premature ovarian failure/azoospermia).
Question 2: Which of the following drugs is known to cause hemorrhagic cystitis as a side effect?
- A. 5-Fluorouracil
- B. Methotrexate
- C. Bleomycin
- D. Cyclophosphamide (Correct Answer)
Explanation: **Explanation:** **Cyclophosphamide** is an alkylating agent (nitrogen mustard) that is metabolized in the liver to form two active metabolites: phosphoramide mustard (the therapeutic moiety) and **acrolein**. Acrolein is a toxic byproduct that accumulates in the urinary bladder, causing direct irritation and sloughing of the bladder mucosa, leading to **hemorrhagic cystitis**. **Why the other options are incorrect:** * **A. 5-Fluorouracil (5-FU):** An antimetabolite (pyrimidine analog) primarily known for causing gastrointestinal toxicity (mucositis, diarrhea) and **Hand-Foot Syndrome** (palmar-plantar erythrodysesthesia). * **B. Methotrexate:** A folate antagonist known for bone marrow suppression, hepatotoxicity, and **nephrotoxicity** (due to crystalluria), but not hemorrhagic cystitis. * **C. Bleomycin:** A cytotoxic antibiotic famous for causing **pulmonary fibrosis** and skin hyperpigmentation. It is "bone marrow sparing." **High-Yield Clinical Pearls for NEET-PG:** 1. **Prevention:** Hemorrhagic cystitis can be prevented by aggressive hydration and the administration of **MESNA** (2-Mercaptoethane Sulfonate Na). 2. **Mechanism of MESNA:** It contains a thiol (-SH) group that binds to and neutralizes acrolein in the bladder to form a non-toxic compound. 3. **Other Drugs:** **Ifosfamide** (an analog of cyclophosphamide) is even more likely to cause hemorrhagic cystitis and always requires MESNA prophylaxis. 4. **Long-term Risk:** Chronic irritation from acrolein increases the risk of **transitional cell carcinoma** of the bladder.
Question 3: Which of the following is a VEGF inhibitor?
- A. Bevacizumab (Correct Answer)
- B. Omalizumab
- C. Adalizumab
- D. Abciximab
Explanation: **Explanation:** **1. Correct Answer: A. Bevacizumab** Bevacizumab is a recombinant humanized monoclonal antibody that acts as a **VEGF (Vascular Endothelial Growth Factor) inhibitor**. It binds directly to circulating VEGF-A, preventing it 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 required for growth and metastasis. It is clinically used in colorectal cancer, renal cell carcinoma, and age-related macular degeneration (AMD). **2. Analysis of Incorrect Options:** * **B. Omalizumab:** This is a monoclonal antibody against **IgE**. It is used in the management of moderate-to-severe persistent allergic asthma and chronic urticaria. * **C. Adalizumab:** This is a **TNF-α (Tumor Necrosis Factor) inhibitor**. It is used in chronic inflammatory conditions such as Rheumatoid Arthritis, Psoriasis, and Crohn’s disease. * **D. Abciximab:** This is a **Glycoprotein IIb/IIIa receptor antagonist**. It inhibits platelet aggregation and is used during percutaneous coronary intervention (PCI) to prevent ischemic complications. **3. NEET-PG High-Yield Pearls:** * **Side Effects of Bevacizumab:** The most characteristic side effect is **Hypertension**. Other risks include GI perforation, impaired wound healing (should be stopped before surgery), and proteinuria. * **Nomenclature Tip:** Monoclonal antibodies ending in **"-umab"** are human; **"-ximab"** are chimeric; **"-zumab"** are humanized. * **Other VEGF Inhibitors:** **Ranibizumab** and **Pegaptanib** (used intravitreally for wet AMD) and **Ziv-aflibercept** (a "VEGF trap").
Question 4: Which is a glycoprotein, produced by many mammalian cells, and used in the treatment of hepatitis, papillomaviruses, hairy-cell leukemia, and AIDS-related Kaposi's sarcoma?
- A. Interferon (Correct Answer)
- B. Idoxuridine
- C. Zidovudine
- D. Zalcitabine
Explanation: **Explanation:** **Correct Answer: A. Interferon** Interferons (IFNs) are endogenous **glycoproteins** produced by host cells in response to viral infections, tumors, and other biological inducers. They act by binding to specific cell surface receptors, triggering the synthesis of enzymes (like 2’,5’-oligoadenylate synthetase) that inhibit viral protein synthesis and degrade viral RNA. * **Clinical Utility:** Interferon-alpha (IFN-α) is the specific subtype used for the conditions mentioned. It has potent antiviral and antiproliferative properties, making it the drug of choice for **Hairy-cell leukemia**, **Kaposi’s sarcoma** (in AIDS patients), **Chronic Hepatitis B and C**, and **Condyloma acuminatum** (caused by Papillomaviruses). **Why other options are incorrect:** * **B. Idoxuridine:** A pyrimidine analogue used primarily as a topical antiviral for Herpes Simplex Keratitis. It is not a glycoprotein and is too toxic for systemic use. * **C. Zidovudine (AZT):** A nucleoside reverse transcriptase inhibitor (NRTI). While used in AIDS, it is a synthetic drug, not a glycoprotein, and is not used for Hairy-cell leukemia or Hepatitis. * **D. Zalcitabine:** Another NRTI used in HIV treatment. Like Zidovudine, it lacks the broad-spectrum anticancer and glycoprotein properties of Interferons. **NEET-PG High-Yield Pearls:** * **Interferon-alpha:** Used in Hairy-cell leukemia, Kaposi’s sarcoma, and Hepatitis B/C. * **Interferon-beta:** Used primarily in **Multiple Sclerosis** to reduce the frequency of relapses. * **Interferon-gamma:** Used in **Chronic Granulomatous Disease** to reduce infections. * **Side Effects:** The most common side effect is a **"Flu-like syndrome"** (fever, chills, myalgia) and dose-limiting bone marrow suppression.
Question 5: Which of the following is a cytoprotectant?
- A. Minocycline
- B. Oxytetracycline
- C. Amifostine (Correct Answer)
- D. Doxycycline
Explanation: **Explanation:**Amifostine is the correct answer because it is a pharmacological cytoprotectant specifically designed to reduce the toxic effects of chemotherapy and radiotherapy. It is a prodrug that is converted by alkaline phosphatase in tissues to an active free thiol metabolite. This metabolite acts as a scavenger for free radicals generated by cisplatin or radiation, thereby protecting normal tissues without compromising the anti-tumor efficacy of the treatment. * **Clinical Use:** It is primarily used to reduce cumulative renal toxicity from **cisplatin** in patients with advanced ovarian cancer and to reduce the incidence of **xerostomia** (dry mouth) in patients undergoing radiotherapy for head and neck cancer. **Why the other options are incorrect:** * **Minocycline, Oxytetracycline, and Doxycycline (Options A, B, D):** These are all members of the **Tetracycline** class of broad-spectrum antibiotics. They work by inhibiting protein synthesis (binding to the 30S ribosomal subunit) and have no role as cytoprotectants in oncology [1]. **High-Yield Clinical Pearls for NEET-PG:** * **Mesna:** Another vital cytoprotectant used to prevent hemorrhagic cystitis caused by **Cyclophosphamide** and **Ifosfamide** [1]. * **Dexrazoxane:** An iron-chelating cytoprotectant used to prevent anthracycline-induced (e.g., **Doxorubicin**) cardiotoxicity. * **Leucovorin (Folinic Acid):** Used as a
Question 6: Which drug is used exclusively in organ transplantation and autoimmune diseases, but not in cancers?
- A. Cyclophosphamide
- B. Cyclosporine (Correct Answer)
- C. Methotrexate
- D. 6-Mercaptopurine
Explanation: **Explanation:** The correct answer is **Cyclosporine**. **1. Why Cyclosporine is correct:** Cyclosporine is a **calcineurin inhibitor** that selectively inhibits T-cell activation by blocking the production of Interleukin-2 (IL-2). Unlike traditional cytotoxic drugs, it does not interfere with DNA synthesis or cause bone marrow suppression. Because it lacks direct anti-proliferative activity against malignant cells, it has **no role in cancer chemotherapy**. Its clinical utility is strictly limited to preventing graft rejection in organ transplantation and managing severe autoimmune conditions (e.g., Psoriasis, Rheumatoid Arthritis). **2. Why other options are incorrect:** * **Cyclophosphamide (Option A):** An alkylating agent used for both cancers (Lymphomas, Breast cancer) and autoimmune diseases (SLE, Wegener’s). * **Methotrexate (Option B):** A folate antagonist used in high doses for malignancies (Osteosarcoma, ALL) and in low doses for autoimmune conditions (RA, Psoriasis). * **6-Mercaptopurine (Option D):** A purine analogue primarily used in the maintenance therapy of Acute Lymphoblastic Leukemia (ALL) and also in Inflammatory Bowel Disease (IBD). **3. High-Yield Clinical Pearls for NEET-PG:** * **Mechanism:** Cyclosporine binds to **Cyclophilin**, forming a complex that inhibits Calcineurin. * **Side Effects:** "The 4 H's" — **H**ypertension, **H**irsutism, **H**yperplasia of gums (Gingival Hyperplasia), and **H**yperlipidemia. * **Dose-limiting toxicity:** Nephrotoxicity (afferent arteriolar vasoconstriction). * **Metabolism:** Metabolized by **CYP3A4**; avoid grapefruit juice as it increases drug levels. * **Tacrolimus:** Another calcineurin inhibitor (binds to FKBP-12) that is more potent than Cyclosporine but does *not* cause hirsutism or gingival hyperplasia.
Question 7: Arsenic is useful in the treatment of which of the following conditions?
- A. Acute promyelocytic leukemia (Correct Answer)
- B. Myelodysplastic syndrome
- C. Transient myeloproliferative disorder
- D. All of the above
Explanation: **Arsenic Trioxide ($As_2O_3$)** is a highly effective agent specifically used for the treatment of **Acute Promyelocytic Leukemia (APL)**, particularly in patients who are refractory to or have relapsed after treatment with All-Trans Retinoic Acid (ATRA). [1] **1. Why Option A is Correct:** APL (FAB M3 subtype) is characterized by a specific chromosomal translocation **t(15;17)**, which creates the **PML-RARα** fusion protein. This protein arrests myeloid differentiation at the promyelocyte stage. Arsenic trioxide works by: * **Degrading the PML-RARα fusion protein:** It binds to the PML moiety, leading to its degradation. * **Inducing Differentiation and Apoptosis:** This allows the malignant promyelocytes to differentiate into mature cells or undergo programmed cell death. **2. Why Other Options are Incorrect:** * **Myelodysplastic Syndrome (MDS):** While some studies have explored arsenic in MDS, it is not a standard or first-line treatment. Standard therapies include hypomethylating agents like Azacitidine or Decitabine. * **Transient Myeloproliferative Disorder (TMD):** This is a self-limiting condition typically seen in neonates with Down Syndrome. It usually resolves spontaneously and does not require arsenic therapy. **Clinical Pearls for NEET-PG:** * **Side Effects:** The most characteristic side effect of Arsenic Trioxide is **QT interval prolongation**, which can lead to Torsades de Pointes. Regular ECG monitoring is mandatory. [2] * **Differentiation Syndrome:** Like ATRA, arsenic can cause "Retinoic Acid Syndrome" (fever, dyspnea, weight gain, pulmonary infiltrates), treated with high-dose **Dexamethasone**. [1] * **First-line Therapy:** Current guidelines often combine Arsenic Trioxide with ATRA as a non-chemotherapy induction regimen for low-to-intermediate risk APL. [1]
Question 8: Which of the following therapies is known to stimulate progenitor megakaryocytes and is used in the treatment of cancer chemotherapy-induced thrombocytopenia?
- A. IL-2
- B. IL-6
- C. IL-8
- D. IL-11 (Correct Answer)
Explanation: **Explanation:** **Correct Option: D (IL-11)** Interleukin-11 (Oprelvekin) is a recombinant cytokine that acts directly on the **progenitor megakaryocytes** in the bone marrow. It stimulates their proliferation and maturation, leading to increased platelet production. It is the only FDA-approved cytokine specifically indicated for the prevention of severe **chemotherapy-induced thrombocytopenia (CIT)** in patients with non-myeloid malignancies. **Incorrect Options:** * **A (IL-2):** Also known as Aldesleukin, it primarily stimulates T-cell proliferation and NK cell activity. It is used in the treatment of metastatic renal cell carcinoma and malignant melanoma, not for platelet stimulation. * **B (IL-6):** While IL-6 does have some thrombopoietic activity, it is a potent pro-inflammatory cytokine. Its clinical use is limited by systemic toxicity (fever, acute phase response). Clinically, we use IL-6 *antagonists* (e.g., Tocilizumab) for Rheumatoid Arthritis and Cytokine Release Syndrome. * **C (IL-8):** This is a potent chemotactic factor for neutrophils. It plays a role in inflammation and angiogenesis but has no role in megakaryocytopoiesis. **High-Yield Clinical Pearls for NEET-PG:** * **Oprelvekin (IL-11) Side Effects:** The most characteristic side effect is **fluid retention** (leading to peripheral edema, dyspnea, and pleural effusion) and transient atrial arrhythmias. * **Romiplostim & Eltrombopag:** These are newer **Thrombopoietin (TPO) receptor agonists**. Romiplostim is a "peptibody" (SC route), while Eltrombopag is an oral non-peptide. They are primarily used for Chronic ITP. * **Filgrastim (G-CSF):** Used for chemotherapy-induced **neutropenia**, not thrombocytopenia.
Question 9: Baezomib is:
- A. Proteasome inhibitor (Correct Answer)
- B. DNA methyl transferase inhibitor
- C. Tyrosine kinase inhibitor
- D. Histone deacetylase inhibitor
Explanation: **Explanation:** **Bortezomib** (often referred to in exams as Baezomib/Bortezomib) is a first-in-class **proteasome inhibitor**. It specifically binds to the 26S proteasome, inhibiting its ability to degrade intracellular proteins. In cancer cells (particularly plasma cells), this leads to the accumulation of pro-apoptotic proteins and the inhibition of **NF-κB**, a transcription factor that normally promotes cell survival and resistance to chemotherapy. By blocking NF-κB, Bortezomib induces apoptosis in malignant cells. **Analysis of Incorrect Options:** * **B. DNA Methyltransferase Inhibitors:** These are "hypomethylating agents" like **Azacitidine** and **Decitabine**, used primarily in Myelodysplastic Syndrome (MDS). * **C. Tyrosine Kinase Inhibitors (TKIs):** This is a broad class including **Imatinib** (BCR-ABL), **Erlotinib** (EGFR), and **Sorafenib** (VEGF). They work by blocking signal transduction pathways. * **D. Histone Deacetylase (HDAC) Inhibitors:** These include drugs like **Vorinostat** and **Romidepsin**, which increase histone acetylation to promote gene expression that halts tumor growth. **High-Yield Clinical Pearls for NEET-PG:** * **Primary Indication:** It is the drug of choice for **Multiple Myeloma** and is also used in Mantle Cell Lymphoma. * **Route of Administration:** Can be given Intravenously (IV) or Subcutaneously (SC). SC administration is preferred as it reduces the risk of neuropathy. * **Key Side Effect:** **Peripheral Neuropathy** (stocking-glove pattern) is the most characteristic dose-limiting toxicity. * **Other Proteasome Inhibitors:** Carfilzomib and Ixazomib (the first oral proteasome inhibitor).
Question 10: Which drug is NOT effective in Multiple Myeloma?
- A. Bortezomib
- B. Hydroxyurea (Correct Answer)
- C. Melphalan
- D. Cyclophosphamide
Explanation: **Explanation:** Multiple Myeloma (MM) is a plasma cell dyscrasia characterized by the malignant proliferation of plasma cells in the bone marrow. Treatment strategies focus on proteasome inhibitors, alkylating agents, and immunomodulators. **Why Hydroxyurea is the correct answer:** **Hydroxyurea** is an antimetabolite that inhibits the enzyme **ribonucleotide reductase**, thereby blocking the conversion of ribonucleotides to deoxyribonucleotides (inhibiting DNA synthesis). Its primary clinical utility is in **Myeloproliferative Neoplasms (MPNs)** such as Polycythemia Vera, Essential Thrombocythemia, and Chronic Myeloid Leukemia (CML), as well as in Sickle Cell Anemia (to increase HbF) [1, 2]. It has no significant efficacy against plasma cell malignancies like Multiple Myeloma. **Analysis of Incorrect Options:** * **Bortezomib:** A reversible inhibitor of the **26S proteasome**. It is a cornerstone of modern MM therapy (part of the VRd regimen) because plasma cells are highly dependent on proteasomes to degrade the excess monoclonal proteins they produce [3]. * **Melphalan:** An **alkylating agent** (nitrogen mustard). Historically, it was the gold standard for MM and remains a key component of "conditioning" regimens prior to Autologous Stem Cell Transplantation (ASCT). * **Cyclophosphamide:** Another potent alkylating agent often used in combination therapies (e.g., CyBorD regimen) for patients with MM, especially those with renal impairment. **High-Yield Clinical Pearls for NEET-PG:** * **Mnemonic for MM Drugs:** **M**elphalan, **I**mmunomodulators (Thalidomide/Lenalidomide), **P**roteasome inhibitors (Bortezomib), **S**teroids (Dexamethasone). * **Bortezomib Side Effect:** Peripheral neuropathy (shingles reactivation is also common; prophylaxis with Acyclovir is required). * **Thalidomide:** Used in MM but notorious for **phocomelia** (teratogenicity) and increased risk of thromboembolism [3].
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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