Anticancer Drugs — MCQs

Anticancer Drugs Indian Medical PG Practice Questions and MCQs

Question 491: What is a known adverse effect of Tamoxifen?

A. Osteoporosis
B. Endometrial hyperplasia (Correct Answer)
C. Ovarian cancer
D. Decreased triglyceride level

Explanation: **Explanation:** Tamoxifen is a **Selective Estrogen Receptor Modulator (SERM)**. Its mechanism of action is tissue-specific, acting as an estrogen **antagonist** in the breast but as a partial **agonist** in the uterus and bone. 1. **Why Endometrial Hyperplasia is Correct:** In the uterus, Tamoxifen acts as an estrogen agonist. This stimulates the proliferation of the endometrial lining, leading to **endometrial hyperplasia**, which significantly increases the risk of **endometrial carcinoma**. This is why post-menopausal patients on Tamoxifen require regular monitoring for abnormal vaginal bleeding. 2. **Analysis of Incorrect Options:** * **A. Osteoporosis:** Incorrect. Because Tamoxifen acts as an estrogen **agonist in bone**, it actually prevents bone loss and decreases the risk of osteoporosis in post-menopausal women. * **C. Ovarian cancer:** Incorrect. Tamoxifen is not associated with an increased risk of ovarian cancer; its primary oncogenic risk is limited to the endometrium. * **D. Decreased triglyceride level:** Incorrect. As an estrogen agonist in the liver, Tamoxifen can actually **increase** serum triglyceride levels, though it may decrease LDL cholesterol. **High-Yield Clinical Pearls for NEET-PG:** * **Drug of Choice:** Tamoxifen is the DOC for ER-positive breast cancer in **pre-menopausal** women. * **Thromboembolism:** Like estrogen, Tamoxifen increases the risk of Deep Vein Thrombosis (DVT) and Pulmonary Embolism. * **Visual Disturbances:** It can cause cataracts and retinopathy. * **Raloxifene:** A related SERM that is an antagonist in both breast and uterus (no risk of endometrial cancer) but remains an agonist in bone (used for osteoporosis).

Question 492: Tyrosine kinase inhibitors are first-line treatment in which of the following conditions?

A. Gastrointestinal stromal tumors (Correct Answer)
B. Receptor-mediated neuroendocrine tumors
C. Breast cancer
D. Renal cell carcinoma

Explanation: ### Explanation **Correct Answer: A. Gastrointestinal stromal tumors (GIST)** **Mechanism and Rationale:** Gastrointestinal stromal tumors (GIST) are primarily driven by activating mutations in the **KIT (CD117)** proto-oncogene or the **PDGFRA** (Platelet-Derived Growth Factor Receptor Alpha) gene. Both are receptor tyrosine kinases. **Imatinib**, a selective tyrosine kinase inhibitor (TKI), specifically targets these proteins, inhibiting the downstream signaling pathways that lead to tumor cell proliferation. It is the established first-line therapy for unresectable, metastatic, or recurrent GIST. **Analysis of Incorrect Options:** * **B. Neuroendocrine tumors (NETs):** While some TKIs (like Sunitinib) are used in pancreatic NETs, they are generally second-line or used in specific subsets. Somatostatin analogs (Octreotide) or surgery remain the primary management. * **C. Breast cancer:** First-line treatments typically involve hormonal therapy (Tamoxifen/Aromatase inhibitors), chemotherapy, or monoclonal antibodies (Trastuzumab for HER2+). While Lapatinib is a TKI used in breast cancer, it is not the universal first-line agent. * **D. Renal cell carcinoma (RCC):** Although TKIs (Sunitinib, Pazopanib) are used in RCC, the current first-line standard of care often involves **Immune Checkpoint Inhibitors** (e.g., Pembrolizumab + Axitinib or Nivolumab + Cabozantinib) rather than TKI monotherapy alone. **High-Yield Clinical Pearls for NEET-PG:** * **Imatinib (The "Magic Bullet"):** Also the first-line treatment for **Chronic Myeloid Leukemia (CML)**, targeting the BCR-ABL fusion protein (Philadelphia chromosome). * **Side Effects of Imatinib:** Most characteristic is **periorbital edema** and fluid retention. * **Resistance:** Resistance to Imatinib in GIST is often managed by switching to second-generation TKIs like **Sunitinib** or **Regorafenib**. * **Diagnostic Marker:** CD117 is the most specific immunohistochemical marker for GIST.

Question 493: Mercaptopurine is:

A. Purine analogue (Correct Answer)
B. Nucleoside analogue
C. Pyrimidine analogue
D. Antitumor antibiotic

Explanation: **Explanation:** **Mercaptopurine (6-MP)** is a classic antimetabolite used in cancer chemotherapy. It is a **thiol analogue of the purine bases hypoxanthine and adenine**. 1. **Why Option A is correct:** 6-MP acts as a **purine analogue**. Once inside the cell, it is converted by the enzyme **Hypoxanthine-guanine phosphoribosyltransferase (HGPRT)** into 6-thioinosinic acid (TIMP). TIMP inhibits the de novo synthesis of purine nucleotides and prevents the conversion of inosinic acid to adenine and guanine nucleotides, thereby disrupting DNA and RNA synthesis (S-phase specific). 2. **Why other options are incorrect:** * **Option B:** While some purine analogues are nucleosides (e.g., Cladribine), 6-MP is technically a **base analogue**. * **Option C:** Pyrimidine analogues include drugs like 5-Fluorouracil, Cytarabine, and Capecitabine, which mimic cytosine, thymine, or uracil. * **Option D:** Antitumor antibiotics (e.g., Doxorubicin, Bleomycin) are derived from *Streptomyces* and work via intercalation or free radical production, not as base mimics. **High-Yield Clinical Pearls for NEET-PG:** * **Drug Interaction:** 6-MP is metabolized by **Xanthine Oxidase**. If co-administered with **Allopurinol** (a xanthine oxidase inhibitor), the dose of 6-MP must be reduced by **75%** to avoid life-threatening toxicity. * **Pharmacogenomics:** Patients with a genetic deficiency of the enzyme **TPMT (Thiopurine Methyltransferase)** are at high risk for severe bone marrow suppression when taking 6-MP. * **Clinical Use:** Primarily used for the maintenance therapy of **Acute Lymphoblastic Leukemia (ALL)**.

Question 494: Which of the following anticancer drugs can be administered orally?

A. Cytosine arabinoside
B. Actinomycin D
C. Doxorubicin
D. Mesna (Correct Answer)

Explanation: **Explanation:** The correct answer is **Mesna**. While traditionally administered intravenously alongside high-dose chemotherapy, Mesna (2-mercaptoethane sulfonate) is also available in an **oral formulation**. It is a cytoprotective adjuvant used to prevent **hemorrhagic cystitis** caused by the metabolites of oxazaphosphorines (Cyclophosphamide and Ifosfamide). It works by providing a free sulfhydryl group that binds to and neutralizes **Acrolein**, the toxic metabolite excreted in the urine. **Analysis of Incorrect Options:** * **Cytosine arabinoside (Ara-C):** An antimetabolite used primarily in leukemias. It has very poor oral bioavailability due to extensive deamination by cytidine deaminase in the gastrointestinal tract and liver; hence, it is given IV or intrathecally. * **Actinomycin D (Dactinomycin):** An antitumor antibiotic that is highly corrosive to tissues. It must be administered intravenously; oral administration is ineffective and would cause severe GI toxicity. * **Doxorubicin:** An anthracycline that is not absorbed orally and is a potent vesicant. It is administered strictly via the intravenous route to avoid severe local tissue necrosis. **High-Yield Clinical Pearls for NEET-PG:** * **Oral Anticancer Drugs (Commonly tested):** Methotrexate, Capecitabine (prodrug of 5-FU), Busulfan, Cyclophosphamide, Chlorambucil, and most Tyrosine Kinase Inhibitors (e.g., Imatinib). * **Mesna Protocol:** In oral administration, the dose is typically 40% of the Ifosfamide dose, given at 0, 4, and 8 hours. * **Vesicants:** Doxorubicin and Actinomycin D are notorious vesicants; if extravasation occurs, **Dexrazoxane** is the specific antidote for Doxorubicin.

Question 495: Maintenance of high urinary pH is important during methotrexate treatment because:

A. Bladder irritation is reduced
B. It decreases renal tubular secretion of methotrexate
C. Leucovorin toxicity is increased in a dehydrated patient
D. Methotrexate is a weak acid (Correct Answer)

Explanation: ### Explanation **1. Why the Correct Answer is Right:** Methotrexate (MTX) is a **weak organic acid** ($pK_a$ ≈ 4.8). In an acidic environment (low pH), it remains in its non-ionized, lipid-soluble form, which is poorly soluble in water. This leads to the precipitation of MTX and its metabolite (7-OH-methotrexate) in the renal tubules, causing **crystalluria and acute kidney injury (AKI)**. By maintaining a **high urinary pH** (alkalinization, usually with Sodium Bicarbonate), the drug is converted into its **ionized (salt) form**. Ionized molecules are highly water-soluble and cannot be easily reabsorbed by the renal tubules, thereby enhancing excretion and preventing crystal-induced nephrotoxicity. **2. Analysis of Incorrect Options:** * **Option A:** While hydration helps, bladder irritation (hemorrhagic cystitis) is specifically associated with Cyclophosphamide/Ifosfamide (due to Acrolein), not MTX. * **Option B:** Alkalinization actually *increases* the clearance of MTX. Decreasing tubular secretion would increase systemic toxicity, which is the opposite of the goal. * **Option C:** Leucovorin (Folinic acid) is the *rescue agent* used to bypass the metabolic block; it does not become "toxic" in dehydrated patients, though its efficacy depends on adequate MTX clearance. **3. High-Yield Clinical Pearls for NEET-PG:** * **The "Rescue" Protocol:** High-dose MTX requires **vigorous hydration, urinary alkalinization (pH >7.0), and Leucovorin rescue** (to provide a source of reduced folate for healthy cells). * **Drug Interactions:** Avoid **NSAIDs, Salicylates, and Sulfonamides** with MTX, as they compete for renal tubular secretion and displace MTX from albumin, increasing toxicity. * **Antidote for Toxicity:** In cases of MTX-induced renal failure where clearance is stalled, **Glucarpidase** (carboxypeptidase G2) is used to rapidly break down extracellular MTX.

Question 496: Hand and foot syndrome is associated with which of the following medications?

A. Vincristine
B. Cisplatin
C. 5-fluorouracil (Correct Answer)
D. Azathioprine

Explanation: **Explanation:** **Hand-Foot Syndrome (Palmar-Plantar Erythrodysesthesia)** is a distinct dermatological toxicity characterized by redness, swelling, pain, and sometimes blistering or peeling of the palms and soles. It occurs due to the leakage of the drug from capillaries into the surrounding tissue under mechanical stress (friction/pressure). **1. Why 5-Fluorouracil (5-FU) is correct:** 5-FU and its oral prodrug, **Capecitabine**, are the most classic causes of Hand-Foot Syndrome. The mechanism involves the accumulation of the drug or its metabolites in the eccrine sweat glands, leading to local tissue damage. It is a dose-limiting toxicity for these antimetabolites. **2. Why the other options are incorrect:** * **Vincristine:** Primarily known for **Peripheral Neuropathy** (stocking-and-glove pattern) and paralytic ileus. It is a "M-phase" specific spindle poison that does not cause skin peeling. * **Cisplatin:** Its hallmark toxicities are **Nephrotoxicity** (prevented by aggressive hydration/Amifostine) and **Ototoxicity**. It is also highly emetogenic. * **Azathioprine:** An immunosuppressant whose main side effect is **Bone Marrow Suppression**, particularly in patients with TPMT deficiency. It is not associated with Hand-Foot Syndrome. **High-Yield Clinical Pearls for NEET-PG:** * **Other drugs causing Hand-Foot Syndrome:** Cytarabine, Doxorubicin (especially liposomal), and Multikinase inhibitors like **Sorafenib** and **Sunitinib**. * **Management:** Dose reduction, topical urea/corticosteroids, and avoiding heat or friction. * **5-FU Toxicity:** Often exacerbated in patients with **DPD (Dihydropyrimidine dehydrogenase) deficiency**. * **Antidote for 5-FU overdose:** Uridine Triacetate.

Question 497: Rituximab is a targeted antibody against which antigen?

A. CD 20 (Correct Answer)
B. CD 22
C. CD 34
D. CD 55

Explanation: **Explanation:** **Rituximab** is a chimeric monoclonal antibody that specifically targets the **CD20 antigen**. CD20 is a transmembrane protein expressed primarily on the surface of pre-B and mature B-lymphocytes, but not on hematopoietic stem cells or plasma cells. When Rituximab binds to CD20, it triggers B-cell lysis through antibody-dependent cellular cytotoxicity (ADCC), complement-dependent cytotoxicity (CDC), and induction of apoptosis. **Analysis of Options:** * **CD 20 (Correct):** The hallmark target for Rituximab. It is used clinically in B-cell Non-Hodgkin Lymphomas (e.g., Diffuse Large B-cell Lymphoma, Follicular Lymphoma), Chronic Lymphocytic Leukemia (CLL), and autoimmune conditions like Rheumatoid Arthritis and Wegener's Granulomatosis. * **CD 22:** This is the target for drugs like **Epratuzumab** and **Inotuzumab ozogamicin**. It is also expressed on B-cells but is distinct from the Rituximab binding site. * **CD 34:** This is a marker for **hematopoietic stem cells**. Targeting this would lead to bone marrow aplasia; it is primarily used in pathology to identify precursors in acute leukemias. * **CD 55:** Also known as Decay-Accelerating Factor (DAF). It protects cells from complement-mediated lysis. Deficiency of CD55 (and CD59) is seen in **Paroxysmal Nocturnal Hemoglobinuria (PNH)**. **High-Yield Clinical Pearls for NEET-PG:** * **Infusion Reaction:** The most common side effect of Rituximab is a cytokine release syndrome during the first infusion (pre-medicate with paracetamol and antihistamines). * **HBV Reactivation:** Always screen for Hepatitis B before starting Rituximab, as it can cause fatal viral reactivation. * **PML:** Rituximab is associated with Progressive Multifocal Leukoencephalopathy (JC virus reactivation).

Question 498: All of the following are true regarding Erlotinib except:

A. Used in non-small cell carcinoma of the lung.
B. It is a small molecule tyrosine kinase inhibitor acting as an EGFR antagonist.
C. Food decreases absorption. (Correct Answer)
D. It causes skin rashes and diarrhea.

Explanation: **Explanation:** **Erlotinib** is a targeted anticancer therapy belonging to the class of small-molecule **Tyrosine Kinase Inhibitors (TKIs)**. 1. **Why Option C is the correct answer (The Exception):** The statement "Food decreases absorption" is incorrect. In fact, **food significantly increases the bioavailability** of Erlotinib (potentially up to 100%). To ensure consistent drug levels and avoid increased toxicity, it must be taken on an empty stomach (at least 1 hour before or 2 hours after a meal). 2. **Analysis of Incorrect Options:** * **Option A:** Erlotinib is a standard first-line treatment for **Non-Small Cell Lung Carcinoma (NSCLC)**, particularly in patients with activating mutations in the EGFR gene (Exon 19 deletions or Exon 21 L858R mutations). * **Option B:** It acts by competitively inhibiting the ATP-binding site of the intracellular tyrosine kinase domain of the **Epidermal Growth Factor Receptor (EGFR/ErbB1)**, preventing downstream signaling. * **Option D:** The most common adverse effects of EGFR inhibitors are **acneiform skin rashes** (seen in >75% of patients) and **diarrhea**. Interestingly, the severity of the rash often correlates with a better therapeutic response. **High-Yield Clinical Pearls for NEET-PG:** * **Drug Interactions:** Solubility of Erlotinib is pH-dependent. **Proton Pump Inhibitors (PPIs)** and H2 blockers decrease its absorption by increasing gastric pH. * **Smoking:** Cigarette smoking induces CYP1A2, which increases the clearance of Erlotinib, necessitating higher doses in smokers. * **Resistance:** The most common mechanism of acquired resistance to Erlotinib is the **T790M mutation**, for which **Osimertinib** (a 3rd generation TKI) is used.

Question 499: Which of the following is a radiation protector drug in clinical use?

A. Amifostine (Correct Answer)
B. Cisplatin
C. Mesna
D. Tirapazamine

Explanation: **Explanation:** **Amifostine (Option A)** is the correct answer. It is a cytoprotective adjuvant known as a **radioprotector**. It is a prodrug that is converted by alkaline phosphatase in tissues to an active thiol metabolite (WR-1065). This metabolite acts as a potent scavenger of free radicals generated by ionizing radiation and certain chemotherapeutic agents. It is selectively taken up by normal cells rather than tumor cells (due to higher alkaline phosphatase activity and better vascularity in normal tissue), thereby reducing xerostomia (dry mouth) in patients undergoing radiotherapy for head and neck cancer. **Incorrect Options:** * **Cisplatin (Option B):** This is a platinum-based cytotoxic drug that acts as a **radiosensitizer**. It makes tumor cells more sensitive to the effects of radiation, the opposite of a protector. * **Mesna (Option C):** While it is a cytoprotective agent, it is specifically used to prevent **hemorrhagic cystitis** caused by Cyclophosphamide or Ifosfamide by neutralizing acrolein in the bladder. It is not a radiation protector. * **Tirapazamine (Option D):** This is an experimental **hypoxic cytotoxin** that becomes toxic only in low-oxygen environments (common in solid tumors), specifically targeting radioresistant hypoxic tumor cells. **High-Yield NEET-PG Pearls:** * **Amifostine** also reduces cumulative nephrotoxicity associated with **Cisplatin**. * **Dexrazoxane** is another important cytoprotective agent used to prevent **Anthracycline-induced cardiotoxicity** (by chelating iron). * **Palifermin** (Keratinocyte Growth Factor) is used to reduce the incidence of severe **mucositis** in patients receiving high-dose chemo-radiotherapy.

Question 500: Which of the following anti-cancer drugs is NOT S-phase specific?

A. Methotrexate
B. Mercaptopurine
C. Ifosfamide (Correct Answer)
D. Thioguanine

Explanation: **Explanation:** The cell cycle specificity of anticancer drugs is a high-yield concept for NEET-PG. Anticancer agents are broadly classified into **Cell Cycle-Specific (CCS)** and **Cell Cycle-Non-Specific (CCNS)** drugs. **Why Ifosfamide is the correct answer:** Ifosfamide is an **alkylating agent** (a nitrogen mustard derivative). Alkylating agents work by covalently bonding alkyl groups to DNA bases (primarily Guanine), leading to DNA cross-linking and strand breaks. This mechanism occurs regardless of whether the cell is actively dividing or resting. Therefore, Ifosfamide is **Cell Cycle-Non-Specific (CCNS)**. While it is most toxic to cells in the late G1 or S phase, it does not target a specific phase to exert its action. **Why the other options are incorrect:** * **Methotrexate:** An antimetabolite that inhibits *Dihydrofolate Reductase (DHFR)*. It prevents the synthesis of tetrahydrofolate, which is essential for thymidylate and purine synthesis. This process is strictly required during DNA synthesis, making it **S-phase specific**. * **Mercaptopurine (6-MP) & Thioguanine (6-TG):** These are purine analogues. They act as "fraudulent nucleotides" that incorporate into DNA/RNA or inhibit *de novo* purine synthesis. Since DNA replication occurs during the **S-phase**, these drugs are phase-specific. **High-Yield Clinical Pearls for NEET-PG:** 1. **Acrolein Toxicity:** Both Ifosfamide and Cyclophosphamide produce a toxic metabolite called **Acrolein**, which causes **Hemorrhagic Cystitis**. 2. **Prevention:** Hemorrhagic cystitis is prevented by aggressive hydration and **MESNA** (2-Mercaptoethane sulfonate Na), which neutralizes acrolein in the bladder. 3. **Mnemonic for S-phase drugs:** "It’s **S**mart to **MET** at the **PUR**ine **PYR**amid" (**MET**hotrexate, **PUR**ines like 6-MP/6-TG, **PYR**imidines like 5-FU/Cytarabine).

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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