Anticancer Drugs — MCQs
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Which drug is the best treatment for estrogen-positive breast cancer?
Cerebellar toxicity is commonly associated with which of the following anticancer drugs?
Panitumumab is used for which of the following conditions?
Flutamide is used in which type of cancer?
Methotrexate is used in all of the following conditions except?
A 65-year-old female with ovarian cancer is being treated with cisplatin-based chemotherapy. All of the following are used to limit the toxicity of cisplatin except?
Binimetinib was recently approved by the FDA for which condition?
Which immunostimulant is used for the treatment of malignant melanoma?
Methotrexate is used for the management of all of the following conditions except?
Which of the following is an approved drug for prostate cancer?
Anticancer Drugs Indian Medical PG Practice Questions and MCQs
Question 41: Which drug is the best treatment for estrogen-positive breast cancer?
- A. Tamoxifen (Correct Answer)
- B. Clomifene
- C. Glutethemide
- D. 5-FU
Explanation: **Explanation:** **Tamoxifen (Option A)** is the gold standard and first-line treatment for hormone receptor-positive (ER/PR+) breast cancer in both pre- and post-menopausal women. It belongs to the class of **Selective Estrogen Receptor Modulators (SERMs)**. Its mechanism involves competitive antagonism of estrogen receptors in breast tissue, thereby inhibiting the growth of estrogen-dependent cancer cells. **Analysis of Incorrect Options:** * **Clomifene (Option B):** While also a SERM, it acts primarily on the hypothalamus to block the feedback inhibition of estrogen. This increases GnRH, FSH, and LH, making it a drug of choice for **ovulation induction** in infertility, not cancer. * **Glutethimide (Option C):** This is an older sedative-hypnotic drug (similar to barbiturates) with no role in oncology. * **5-Fluorouracil (Option D):** An antimetabolite (pyrimidine analog) used in various chemotherapy regimens (e.g., CMF). While used in breast cancer, it is not specific to estrogen-positive status and is generally a second-line or adjuvant cytotoxic choice compared to targeted hormonal therapy. **High-Yield Clinical Pearls for NEET-PG:** * **Dual Action:** Tamoxifen is an **antagonist in the breast** but an **agonist in the endometrium and bone**. * **Side Effects:** Due to its agonist effect on the uterus, it increases the risk of **endometrial carcinoma** and thromboembolism (DVT/PE). However, it helps prevent osteoporosis. * **Drug of Choice:** For post-menopausal ER+ breast cancer, **Aromatase Inhibitors** (e.g., Anastrozole, Letrozole) are now often preferred over Tamoxifen, but Tamoxifen remains the classic correct answer for general ER+ management in exams.
Question 42: Cerebellar toxicity is commonly associated with which of the following anticancer drugs?
- A. Cisplatin
- B. Cytarabine (Correct Answer)
- C. Bleomycin
- D. Actinomycin D
Explanation: **Explanation:** **Cytarabine (Ara-C)** is the correct answer. It is a pyrimidine antimetabolite that inhibits DNA polymerase. **Cerebellar toxicity** (manifesting as ataxia, dysarthria, and nystagmus) is a classic, dose-limiting side effect specifically associated with **High-Dose Cytarabine (HiDAC)** therapy, often used in acute myeloid leukemia (AML). The mechanism involves the drug’s ability to cross the blood-brain barrier and cause direct damage to Purkinje cells in the cerebellum. **Analysis of Incorrect Options:** * **A. Cisplatin:** Primarily known for its "3 Os": **O**totoxicity (tinnitus/hearing loss), **O**nephrotoxicity (renal tubular damage), and severe **O**moting (highly emetogenic). It also causes peripheral neuropathy (glove-and-stocking anesthesia) rather than cerebellar symptoms. * **C. Bleomycin:** Its most dreaded complication is **Pulmonary Fibrosis**. It is also known for causing skin hyperpigmentation (flagellate dermatitis) but lacks significant neurotoxicity. * **D. Actinomycin D:** Primarily associated with bone marrow suppression and "radiation recall" phenomenon. It does not typically cause cerebellar dysfunction. **High-Yield Clinical Pearls for NEET-PG:** * **Cytarabine:** Apart from cerebellar ataxia, it causes **conjunctivitis** (prophylactic steroid eye drops are mandatory with high doses) and "Ara-C syndrome" (fever, rash, bone pain). * **5-Fluorouracil (5-FU):** Another pyrimidine analog that can also cause cerebellar ataxia, though it is more frequently tested for **Hand-Foot Syndrome**. * **Vincristine:** Most common anticancer drug causing **peripheral neuropathy** and paralytic ileus (autonomic neuropathy). * **Paclitaxel:** Known for peripheral neuropathy and hypersensitivity reactions.
Question 43: Panitumumab is used for which of the following conditions?
- A. Multiple Sclerosis
- B. Osmotic diarrhea
- C. Ascites
- D. Colorectal Carcinoma (Correct Answer)
Explanation: **Explanation:** **Panitumumab** is a recombinant, fully humanized monoclonal antibody that targets the **Epidermal Growth Factor Receptor (EGFR)**. By binding to the extracellular domain of EGFR, it inhibits downstream signaling pathways (like RAS-RAF-MAPK) that promote cell proliferation and survival. * **Why Colorectal Carcinoma is correct:** Panitumumab is specifically indicated for the treatment of **metastatic Colorectal Carcinoma (mCRC)**. It is used in patients whose tumors express wild-type **KRAS** (non-mutated). If the KRAS gene is mutated, the signaling pathway remains "permanently on" regardless of EGFR inhibition, making the drug ineffective. **Analysis of Incorrect Options:** * **Multiple Sclerosis:** This is an autoimmune demyelinating disease. Drugs used here include Ocrelizumab (anti-CD20) or Natalizumab (anti-alpha-4 integrin), not EGFR inhibitors. * **Osmotic Diarrhea:** This is a physiological state caused by poorly absorbed solutes (e.g., lactulose or magnesium salts). It is not a clinical indication for monoclonal antibodies. * **Ascites:** This is a clinical sign of portal hypertension or malignancy. While treating the underlying cancer might reduce ascites, Panitumumab is not a direct treatment for the fluid accumulation itself. **High-Yield Clinical Pearls for NEET-PG:** * **Mechanism:** EGFR (ErbB1) Inhibitor. * **Genetic Testing:** Always check for **KRAS/NRAS mutations** before prescribing. It only works in **Wild-type** cases. * **Key Side Effect:** **Acneiform skin rash** (the severity of the rash often correlates with a better therapeutic response). * **Comparison:** **Cetuximab** is another EGFR inhibitor used for mCRC, but it is a chimeric antibody, whereas Panitumumab is fully humanized (lower risk of infusion reactions).
Question 44: Flutamide is used in which type of cancer?
- A. Cervix
- B. Prostate (Correct Answer)
- C. Kidneys
- D. Liver
Explanation: **Explanation:** **Flutamide** is a non-steroidal, competitive **androgen receptor antagonist**. Its primary mechanism involves blocking the binding of dihydrotestosterone (DHT) and testosterone to their receptors in target tissues. Since prostate cancer cells are typically androgen-dependent for growth and proliferation, blocking these receptors inhibits tumor progression. * **Why Prostate is Correct:** Prostate cancer is the classic indication for anti-androgens. Flutamide is frequently used in "Combined Androgen Blockade" (CAB) alongside GnRH agonists (like Leuprolide). This combination prevents the "testosterone flare" (a transient rise in testosterone) that occurs when GnRH agonists are first initiated. * **Why other options are incorrect:** * **Cervix:** Cervical cancer is primarily associated with HPV infection and is treated with surgery, radiation, or platinum-based chemotherapy (e.g., Cisplatin), not hormonal therapy. * **Kidneys:** Renal Cell Carcinoma (RCC) is managed with surgery, tyrosine kinase inhibitors (e.g., Sunitinib), or immunotherapy. * **Liver:** Hepatocellular carcinoma is treated with multi-kinase inhibitors like Sorafenib. **High-Yield Clinical Pearls for NEET-PG:** 1. **Side Effects:** The most characteristic side effect of Flutamide is **gynecomastia** (due to increased peripheral conversion of androgens to estrogen) and potential **hepatotoxicity** (requires monitoring of LFTs). 2. **Bicalutamide:** A newer congener of Flutamide, preferred nowadays due to its once-daily dosing and lower risk of hepatotoxicity. 3. **Cyproterone Acetate:** Another anti-androgen, but unlike Flutamide, it also has progestational activity and inhibits LH secretion.
Question 45: Methotrexate is used in all of the following conditions except?
- A. Sickle cell anemia (Correct Answer)
- B. Psoriasis
- C. Rheumatoid arthritis
- D. Ankylosing spondylitis
Explanation: **Explanation:** **1. Why Sickle Cell Anemia is the Correct Answer:** Methotrexate is a **folate antagonist** that inhibits the enzyme **dihydrofolate reductase (DHFR)**, leading to a decrease in DNA synthesis. In **Sickle Cell Anemia**, the drug of choice is **Hydroxyurea**, which works by increasing the levels of Fetal Hemoglobin (HbF). Methotrexate has no therapeutic role in sickle cell disease; in fact, its bone marrow suppressive effects could worsen the anemia. **2. Why the other options are incorrect:** * **Psoriasis:** Methotrexate is a first-line systemic therapy for severe psoriasis. It acts by inhibiting the rapid proliferation of epidermal keratinocytes and providing systemic anti-inflammatory effects. * **Rheumatoid Arthritis (RA):** It is the **"Gold Standard" Disease-Modifying Antirheumatic Drug (DMARD)**. It acts as an immunosuppressant by increasing extracellular adenosine, which inhibits T-cell activation and inflammation. * **Ankylosing Spondylitis:** While TNF-inhibitors are preferred for axial disease, Methotrexate is frequently used as a DMARD to manage peripheral joint involvement in patients with spondyloarthropathies. **Clinical Pearls for NEET-PG:** * **Mechanism:** Competitive inhibition of DHFR. * **Rescue Therapy:** **Leucovorin (Folinic acid)** is used to "rescue" normal cells from methotrexate toxicity (it bypasses the blocked DHFR enzyme). * **Toxicity:** Most common side effect is mucosal ulceration (stomatitis). Most serious are hepatotoxicity (cirrhosis) and pulmonary fibrosis. * **Contraindication:** It is highly **teratogenic** (causes neural tube defects) and contraindicated in pregnancy. * **Other Uses:** Ectopic pregnancy, Choriocarcinoma, and Acute Lymphoblastic Leukemia (ALL).
Question 46: A 65-year-old female with ovarian cancer is being treated with cisplatin-based chemotherapy. All of the following are used to limit the toxicity of cisplatin except?
- A. N-acetylcysteine (Correct Answer)
- B. Slow rate of infusion
- C. Chloride diuresis
- D. Amifostine
Explanation: **Explanation:** The correct answer is **A. N-acetylcysteine**. Cisplatin is a potent platinum-based alkylating agent known for its significant dose-limiting **nephrotoxicity**. N-acetylcysteine (NAC) is primarily used as an antidote for acetaminophen (paracetamol) toxicity and as a mucolytic agent; it has no established clinical role in preventing cisplatin-induced nephrotoxicity. **Why the other options are incorrect (Mechanisms of Protection):** * **Chloride Diuresis:** This is the most critical preventive measure. Cisplatin is less toxic in high-chloride environments. Maintaining high chloride concentration in the renal tubules (via 0.9% Normal Saline) keeps the drug in its non-reactive, neutral form, preventing it from converting into the toxic aquated species that damages tubular cells. * **Slow rate of infusion:** Administering cisplatin slowly (over several hours) reduces the peak plasma concentration, thereby decreasing the intensity of acute renal tubular damage. * **Amifostine:** This is a cytoprotective organic thiophosphate. It is a prodrug that is dephosphorylated by alkaline phosphatase (more active in normal tissues) to a free thiol that scavenges reactive metabolites of cisplatin, specifically reducing nephrotoxicity. **High-Yield Clinical Pearls for NEET-PG:** * **Cisplatin Toxicities:** Remember the mnemonic **"3 N's"**: **N**ephrotoxicity, **N**eurotoxicity (peripheral neuropathy), and **N**ausea/vomiting (highly emetogenic). It is also famously **Ototoxic**. * **Drug of Choice for Vomiting:** Palonosetron (5-HT3 antagonist) + Dexamethasone + Aprepitant (NK1 antagonist) is the standard regimen for cisplatin-induced emesis. * **Alternative:** **Carboplatin** is often preferred over cisplatin as it is less nephrotoxic and ototoxic, though it causes more myelosuppression (thrombocytopenia).
Question 47: Binimetinib was recently approved by the FDA for which condition?
- A. Prostate cancer
- B. Melanoma (Correct Answer)
- C. Smallpox
- D. Chickenpox
Explanation: **Explanation:** **Binimetinib** is a potent and selective oral inhibitor of **MEK1 and MEK2** (Mitogen-activated protein Kinase). These enzymes are key components of the MAPK/ERK pathway, which regulates cell proliferation and survival. In many cancers, particularly melanoma, this pathway is constitutively active due to mutations. 1. **Why Melanoma is Correct:** In 2018, the FDA approved the combination of **Binimetinib and Encorafenib** (a BRAF inhibitor) for the treatment of patients with unresectable or metastatic **melanoma** harboring a **BRAF V600E or V600K mutation**. Using a MEK inhibitor alongside a BRAF inhibitor helps delay the development of drug resistance and reduces specific side effects like cutaneous squamous cell carcinomas. 2. **Why Incorrect Options are Wrong:** * **Prostate Cancer:** Standard treatments include androgen deprivation therapy (e.g., Leuprolide), anti-androgens (e.g., Enzalutamide), or taxanes (e.g., Docetaxel). MEK inhibitors are not currently first-line FDA-approved treatments here. * **Smallpox & Chickenpox:** These are viral infections caused by Variola and Varicella-zoster viruses, respectively. They are treated with antivirals (e.g., Tecovirimat for smallpox; Acyclovir for chickenpox), not targeted antineoplastic kinase inhibitors. **High-Yield Clinical Pearls for NEET-PG:** * **Mechanism:** Binimetinib = MEK 1/2 Inhibitor. * **The "Nib" Suffix:** Indicates a small-molecule kinase inhibitor. * **Combination Therapy:** Always remember the pair: **Encorafenib + Binimetinib**. (Similar to Dabrafenib + Trametinib or Vemurafenib + Cobimetinib). * **Side Effects:** Common toxicities include diarrhea, fatigue, and uniquely, **retinal pigment epithelial detachment (RPED)** and increased Creatine Phosphokinase (CPK).
Question 48: Which immunostimulant is used for the treatment of malignant melanoma?
- A. Levamisole
- B. BCG
- C. Aldesleukin (Correct Answer)
- D. Methotrexate
Explanation: **Explanation:** **Aldesleukin (Option C)** is a recombinant form of **Interleukin-2 (IL-2)**. It acts as an immunostimulant by promoting the proliferation and activation of T-cells and Natural Killer (NK) cells, enhancing the body’s immune response against tumor cells. It is specifically FDA-approved and clinically indicated for the treatment of **metastatic renal cell carcinoma** and **metastatic malignant melanoma**. **Analysis of Incorrect Options:** * **Levamisole (Option A):** Historically used as an adjuvant in colorectal cancer (with 5-FU) and for its anthelmintic properties. It is no longer a primary choice for melanoma. * **BCG (Option B):** While an immunostimulant, its primary oncological use is intravesical therapy for **superficial bladder cancer**. It is not the systemic treatment of choice for malignant melanoma. * **Methotrexate (Option D):** This is an antimetabolite (folic acid antagonist) and an **immunosuppressant/cytotoxic** drug, not an immunostimulant. **High-Yield Clinical Pearls for NEET-PG:** 1. **Capillary Leak Syndrome:** The most characteristic and life-threatening side effect of Aldesleukin (IL-2). It leads to hypotension, edema, and multiorgan failure. 2. **Other Melanoma Drugs:** Modern management also includes BRAF inhibitors (**Vemurafenib**) for BRAF V600E mutations and Immune Checkpoint Inhibitors like **Ipilimumab** (CTLA-4 inhibitor) and **Pembrolizumab** (PD-1 inhibitor). 3. **Interferon-alpha:** Another cytokine used in melanoma, primarily for adjuvant therapy in high-risk cases.
Question 49: Methotrexate is used for the management of all of the following conditions except?
- A. Rheumatoid arthritis
- B. Psoriasis
- C. Sickle cell anemia (Correct Answer)
- D. Organ transplantation
Explanation: **Explanation:** **Methotrexate (MTX)** is a folate antagonist that inhibits the enzyme **dihydrofolate reductase (DHFR)**. This inhibition prevents the conversion of dihydrofolate to tetrahydrofolate, leading to a deficiency in thymidylate and purine synthesis, which ultimately halts DNA synthesis and cell proliferation. **Why Sickle Cell Anemia is the Correct Answer:** Methotrexate 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**, which works by increasing the production of fetal hemoglobin (HbF). **Analysis of Other Options:** * **Rheumatoid Arthritis (RA):** MTX is the **"Anchor Drug"** and the first-line Disease-Modifying Antirheumatic Drug (DMARD) for RA. It acts via adenosine accumulation, which has potent anti-inflammatory effects. * **Psoriasis:** MTX is used in severe, recalcitrant psoriasis and psoriatic arthritis due to its ability to inhibit the rapid turnover of epidermal cells (keratinocytes). * **Organ Transplantation:** MTX is used as an immunosuppressant to prevent **Graft-versus-Host Disease (GVHD)** and organ rejection by suppressing T-cell activation and proliferation. **High-Yield Clinical Pearls for NEET-PG:** * **Rescue Therapy:** **Leucovorin (Folinic acid)** is used to "rescue" normal cells from MTX toxicity (Leucovorin Rescue). * **Toxicity:** The most common side effect is mucosal ulceration (stomatitis). Long-term use can lead to **hepatic fibrosis** and **pneumonitis**. * **Contraindication:** It is highly **teratogenic** (Category X) and must be avoided in pregnancy. * **Monitoring:** Periodic Liver Function Tests (LFTs) and Complete Blood Counts (CBC) are mandatory.
Question 50: Which of the following is an approved drug for prostate cancer?
- A. Bicalutamide
- B. Apalutamide (Correct Answer)
- C. Ibalizumab
- D. Ivacaftor
Explanation: **Explanation:** **Apalutamide** is a potent, second-generation **androgen receptor (AR) antagonist**. It works by binding directly to the ligand-binding domain of the AR, preventing androgen binding, nuclear translocation, and DNA binding. It is FDA-approved for the treatment of non-metastatic castration-resistant prostate cancer (nmCRPC) and metastatic castration-sensitive prostate cancer (mCSPC). **Analysis of Options:** * **Bicalutamide (Option A):** While this is a first-generation anti-androgen used in prostate cancer, the question asks for the "approved drug" in a context where modern oncology exams prioritize newer, high-potency agents. In clinical practice, second-generation agents like Apalutamide or Enzalutamide are preferred due to their superior efficacy and lack of partial agonist activity. * **Ibalizumab (Option C):** This is a **CD4-directed post-attachment inhibitor** used in the management of multidrug-resistant HIV-1 infection. It is a monoclonal antibody, not an anticancer drug. * **Ivacaftor (Option D):** This is a **CFTR potentiator** used in the treatment of Cystic Fibrosis (specifically for patients with the G551D mutation). **NEET-PG High-Yield Pearls:** * **Second-generation AR Antagonists:** Apalutamide, Enzalutamide, and Darolutamide. Unlike Bicalutamide, these do not exhibit agonist activity when AR is overexpressed. * **Side Effects of Apalutamide:** Notable for causing skin rash, hypothyroidism, and an increased risk of seizures (due to GABA-A inhibition). * **Mechanism of Prostate Cancer Drugs:** * GnRH Agonists (Leuprolide) – Initial flare, then down-regulation. * GnRH Antagonists (Degarelix) – No flare. * CYP17 Inhibitor (Abiraterone) – Blocks androgen synthesis.
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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