Anticancer Drugs — MCQs

Anticancer Drugs Indian Medical PG Practice Questions and MCQs

Question 31: Gemcitabine is effective in which of the following conditions?

A. Head and neck cancers
B. Pancreatic cancer (Correct Answer)
C. Small cell lung cancer
D. Soft tissue sarcoma

Explanation: **Explanation:** **Gemcitabine** is a pyrimidine antimetabolite and a deoxycytidine analog. It acts by inhibiting **ribonucleotide reductase**, thereby decreasing the pool of intracellular nucleotides, and by getting incorporated into DNA to cause chain termination (masked chain termination). **Why Pancreatic Cancer is Correct:** Gemcitabine is considered the **first-line chemotherapy** for locally advanced or metastatic **adenocarcinoma of the pancreas**. It was the first drug to show a "clinical benefit response" (improvement in pain, performance status, and weight) in pancreatic cancer patients, even when survival benefit was modest. It is also widely used in non-small cell lung cancer (NSCLC) and bladder cancer. **Analysis of Incorrect Options:** * **Head and Neck Cancers:** These are primarily treated with Cisplatin, 5-Fluorouracil (5-FU), and Taxanes (Docetaxel). Gemcitabine is not a standard first-line agent here. * **Small Cell Lung Cancer (SCLC):** The cornerstone of SCLC treatment is the combination of Etoposide and Cisplatin/Carboplatin. Gemcitabine is used in **Non-Small Cell Lung Cancer (NSCLC)**, not SCLC. * **Soft Tissue Sarcoma:** Standard treatments include Doxorubicin and Ifosfamide. While Gemcitabine (often with Docetaxel) can be used in specific subtypes like leiomyosarcoma, it is not the primary association tested for this drug. **High-Yield Clinical Pearls for NEET-PG:** * **Mechanism:** Deoxycytidine analog; inhibits ribonucleotide reductase. * **Major Indication:** Drug of choice for Pancreatic Cancer. * **Side Effects:** Myelosuppression (primarily neutropenia) and a characteristic **flu-like syndrome** (fever, malaise, myalgia) occurring in about 40% of patients. * **Metabolism:** It is rapidly inactivated by **cytidine deaminase** in the liver and blood.

Question 32: Which of the following are alkylating agents?

A. Cyclophosphamide
B. Ifosfamide
C. Paclitaxel (Correct Answer)
D. Methotrexate

Explanation: **Explanation:** The question asks to identify the **alkylating agent** among the given options. However, based on pharmacological classification, there is a discrepancy in the provided answer key. **1. Analysis of the Correct Answer (as per the key):** * **Paclitaxel (Option C):** This is a **Taxane**, not an alkylating agent. It acts as a **microtubule stabilizer** by binding to the β-subunit of tubulin, preventing depolymerization (the "frozen mitosis" effect). While it is a potent anticancer drug, it belongs to the **M-phase specific** plant alkaloid group. **2. Analysis of Other Options (The actual Alkylating Agents):** * **Cyclophosphamide (Option A) & Ifosfamide (Option B):** These are the **prototypical Nitrogen Mustards (Alkylating Agents)**. They work by attaching an alkyl group to the N7 position of guanine in DNA, leading to cross-linking and strand breakage. They are cell-cycle non-specific. * **Methotrexate (Option D):** This is an **Antimetabolite** (Folate antagonist). It inhibits the enzyme **Dihydrofolate Reductase (DHFR)**, preventing the synthesis of DNA, RNA, and proteins. It is S-phase specific. **Clinical Pearls for NEET-PG:** * **Cyclophosphamide/Ifosfamide:** Both can cause **Hemorrhagic Cystitis** due to the metabolite **Acrolein**. This is prevented by aggressive hydration and **MESNA** (a sulfhydryl compound that neutralizes acrolein). * **Paclitaxel:** Common side effects include peripheral neuropathy and hypersensitivity reactions (pre-medicate with steroids and antihistamines). * **High-Yield Mnemonic:** "Mustards, Nitrosoureas, and Platinum compounds" are the core alkylating/alkylating-like agents. *Note: In a standard exam, both A and B are correct examples of alkylating agents. If the key marks C as correct, it is likely an error in the question source or key.*

Question 33: Side-effects of cisplatin include all of the following except?

A. Nausea and vomiting
B. Nephrotoxicity
C. Blindness (Correct Answer)
D. Ototoxicity

Explanation: **Explanation:** Cisplatin is a potent platinum-based alkylating agent used for various solid tumors. While it has a significant side-effect profile, **blindness** is not a characteristic or common adverse effect. **1. Why Blindness is the Correct Answer:** Ocular toxicity with cisplatin is rare and usually limited to blurred vision or changes in color perception at very high doses. It does not typically cause blindness. In contrast, the other options represent the "classic triad" of cisplatin toxicity. **2. Analysis of Other Options:** * **Nausea and Vomiting (Option A):** Cisplatin is classified as a **highly emetogenic** drug. It triggers severe acute and delayed chemotherapy-induced nausea and vomiting (CINV) by stimulating the chemoreceptor trigger zone (CTZ). * **Nephrotoxicity (Option B):** This is the **dose-limiting toxicity**. It causes acute tubular necrosis (ATN). To prevent this, patients are managed with **aggressive intravenous hydration** and sometimes **Amifostine** (a cytoprotective free-radical scavenger). * **Ototoxicity (Option D):** Cisplatin causes high-frequency sensorineural hearing loss and tinnitus due to damage to the hair cells in the cochlea. This is often irreversible and more common in children. **Clinical Pearls for NEET-PG:** * **Mnemonic for Cisplatin:** Remember the **"3 N's"**: **N**ephrotoxicity, **N**eurotoxicity (peripheral neuropathy), and **N**ausea/vomiting, plus **Ototoxicity**. * **Electrolyte Imbalance:** Cisplatin frequently causes **hypomagnesemia** and hypokalemia due to renal tubular damage. * **Drug of Choice:** It is a cornerstone treatment for testicular, ovarian, and bladder cancers. * **Carboplatin:** A related drug that is less nephrotoxic and ototoxic but causes more significant **myelosuppression** (thrombocytopenia).

Question 34: Which is the most cardiotoxic anticancer drug class?

A. Anthracyclines (Correct Answer)
B. Alkylating agents
C. Platinum compounds
D. Bisphosphonates

Explanation: **Explanation:** **1. Why Anthracyclines are the correct answer:** Anthracyclines (e.g., **Doxorubicin, Daunorubicin**) are notorious for causing dose-dependent, cumulative cardiotoxicity. The underlying mechanism involves the generation of **reactive oxygen species (ROS)** and the formation of iron-anthracycline complexes. These lead to lipid peroxidation of the myocardial cell membrane and damage to the sarcoplasmic reticulum. Unlike other tissues, the heart is particularly vulnerable because it has low levels of antioxidant enzymes like catalase and superoxide dismutase. This can manifest as acute arrhythmias or, more commonly, chronic **congestive heart failure (CHF)**. **2. Why other options are incorrect:** * **Alkylating agents (e.g., Cyclophosphamide):** While high doses can cause hemorrhagic cystitis (prevented by Mesna) or acute myocarditis, they are primarily known for bone marrow suppression and secondary malignancies, not chronic cardiotoxicity. * **Platinum compounds (e.g., Cisplatin):** These are primarily associated with **nephrotoxicity** and **ototoxicity**. They do not typically cause significant cardiotoxicity. * **Bisphosphonates:** These are not primary anticancer drugs but are used to treat bone metastases and hypercalcemia. Their main side effects include osteonecrosis of the jaw and esophageal irritation. **3. NEET-PG High-Yield Clinical Pearls:** * **Dexrazoxane:** An iron chelator used to prevent/reduce doxorubicin-induced cardiotoxicity. * **Monitoring:** Patients on Anthracyclines should have regular **ECHO/MUGA scans** to monitor the Left Ventricular Ejection Fraction (LVEF). * **Trastuzumab (Herceptin):** Another cardiotoxic drug (monoclonal antibody), but unlike Anthracyclines, its toxicity is usually **reversible** and not dose-dependent. * **Lifetime Dose:** The risk of CHF increases significantly once the cumulative dose of Doxorubicin exceeds **450–550 mg/m²**.

Question 35: A patient with Non-Hodgkin's Lymphoma (NHL) is being treated with the CHOP chemotherapy regimen. Which of the listed agents is most likely to be protective against the cardiotoxicity associated with doxorubicin?

A. Amifostine
B. Leucovorin
C. Vitamin C
D. Dexrazoxane (Correct Answer)

Explanation: **Explanation:** **1. Why Dexrazoxane is the correct answer:** Doxorubicin (the ‘H’ or Hydroxydaunorubicin in the CHOP regimen) causes dose-dependent cardiotoxicity. The underlying mechanism involves the formation of **iron-anthracycline complexes** that generate reactive oxygen species (ROS), leading to lipid peroxidation and cardiomyocyte death [1]. **Dexrazoxane** is an iron-chelating agent that enters cardiac cells and interferes with iron-mediated free radical formation [1]. It also inhibits Topoisomerase IIβ, further protecting the heart. It is specifically FDA-approved to reduce the incidence and severity of cardiomyopathy associated with doxorubicin administration. **2. Why the other options are incorrect:** * **Amifostine:** A cytoprotective agent (free radical scavenger) used primarily to reduce nephrotoxicity associated with **Cisplatin** and xerostomia in radiotherapy. * **Leucovorin (Folinic Acid):** Used as a "rescue" therapy to prevent bone marrow toxicity after high-dose **Methotrexate** or to potentiate the action of 5-Fluorouracil. * **Vitamin C:** While an antioxidant, it has no proven clinical role in preventing anthracycline-induced cardiotoxicity and is not used in standard oncological protocols for this purpose. **3. NEET-PG High-Yield Pearls:** * **Doxorubicin Toxicity:** Look for "Dilated Cardiomyopathy" or "Congestive Heart Failure" in clinical vignettes [1]. * **Monitoring:** Periodic **ECHO or MUGA scans** are mandatory to monitor the Left Ventricular Ejection Fraction (LVEF) [1]. * **Cumulative Dose:** Risk increases significantly when the cumulative dose of Doxorubicin exceeds **450–550 mg/m²** [1]. * **Mnemonic for CHOP:** **C**yclophosphamide, **H**ydroxydaunorubicin (Doxorubicin), **O**ncovin (Vincristine), **P**rednisolone.

Question 36: Which of the following is a common side effect of cisplatin?

A. Diarrhea
B. Vomiting (Correct Answer)
C. Pulmonary fibrosis
D. Alopecia

Explanation: **Explanation:** **Cisplatin** is a potent platinum-based alkylating agent used for various solid tumors. It is classified as a **highly emetogenic** drug. 1. **Why Vomiting is Correct:** Cisplatin is notorious for causing severe nausea and vomiting. It triggers the release of serotonin from enterochromaffin cells in the GI tract and directly stimulates the **Chemoreceptor Trigger Zone (CTZ)** in the medulla. It causes both acute (within 24 hours) and delayed emesis. Management typically requires a combination of 5-HT3 antagonists (e.g., Ondansetron), NK1 receptor antagonists (e.g., Aprepitant), and Dexamethasone. 2. **Why Other Options are Incorrect:** * **Diarrhea:** While some chemotherapeutic agents (like Irinotecan or 5-Fluorouracil) are known for causing severe diarrhea, it is not the hallmark side effect of Cisplatin. * **Pulmonary Fibrosis:** This is the classic dose-limiting toxicity of **Bleomycin** and **Busulfan**, not Cisplatin. * **Alopecia:** While many anticancer drugs cause hair loss, it is relatively less common or less severe with Cisplatin compared to Taxanes, Doxorubicin, or Cyclophosphamide. **High-Yield Clinical Pearls for NEET-PG:** * **Dose-limiting toxicity:** Nephrotoxicity (prevented by aggressive **Amifostine** and hydration). * **Ototoxicity:** High-frequency hearing loss and tinnitus (often irreversible). * **Peripheral Neuropathy:** "Glove and stocking" distribution. * **Mnemonic:** Remember the **"3 N's"** of Cisplatin: **N**ausea/Vomiting, **N**ephrotoxicity, and **N**eurotoxicity (including Ototoxicity).

Question 37: What is the effect of parenteral administration of streptokinase?

A. Increases the formation of plasminogen.
B. Is less effective following a myocardial infarct than t-PA.
C. Causes a high incidence of thrombocytopenia.
D. May cause bleeding reversible by aminocaproic acid. (Correct Answer)

Explanation: **Explanation:** Streptokinase is a first-generation fibrinolytic agent derived from Beta-hemolytic Streptococci. It acts by forming a non-covalent 1:1 complex with **plasminogen**, which then undergoes a conformational change to become an active complex that converts free plasminogen into **plasmin**. Plasmin subsequently degrades fibrin clots. **Why Option D is Correct:** The primary adverse effect of all thrombolytics is systemic bleeding due to the depletion of circulating fibrinogen (systemic lytic state). **Aminocaproic acid** (and Tranexamic acid) acts as a specific antidote by competitively inhibiting plasminogen activation and plasmin activity, thereby reversing the bleeding caused by streptokinase. **Analysis of Incorrect Options:** * **Option A:** Streptokinase does not increase the *formation* of plasminogen; it *activates* existing plasminogen into plasmin. * **Option B:** In the management of ST-elevation myocardial infarction (STEMI), large trials (like GISSI-2 and ISIS-3) showed that streptokinase is **equally effective** as t-PA (Alteplase) in terms of overall mortality reduction, although t-PA has a slight edge in early vessel patency. * **Option C:** Thrombocytopenia is a classic side effect of **Heparin** (HIT), not streptokinase. The main non-bleeding side effect of streptokinase is **hypersensitivity/anaphylaxis** due to its bacterial origin. **NEET-PG High-Yield Pearls:** * **Mechanism:** It is a non-enzymatic activator (unlike t-PA/Urokinase which are enzymes). * **Antigenicity:** Because it is antigenic, it should not be repeated within 6–12 months of prior use due to the risk of neutralization by antibodies or anaphylaxis. * **Specificity:** It is **non-fibrin specific**, meaning it acts on both clot-bound and circulating plasminogen (increasing bleeding risk compared to Tenecteplase).

Question 38: Hemorrhagic cystitis is caused by which of the following agents?

A. Cyclophosphamide (Correct Answer)
B. 6-Mercaptopurine
C. 5-Fluorouracil
D. Busulfan

Explanation: **Explanation:** **Cyclophosphamide** (and its analog Ifosfamide) are nitrogen mustard alkylating agents. The correct answer is A because these drugs are metabolized into two active components: phosphoramide mustard (the cytotoxic moiety) and **Acrolein**. Acrolein is a toxic metabolite that accumulates in the urinary bladder, causing direct irritation and sloughing of the bladder mucosa, leading to **hemorrhagic cystitis**. **Analysis of Incorrect Options:** * **B. 6-Mercaptopurine:** A purine antimetabolite primarily associated with myelosuppression and hepatotoxicity. Its metabolism is inhibited by Allopurinol (via Xanthine Oxidase). * **C. 5-Fluorouracil:** A pyrimidine antimetabolite (Thymidylate Synthase inhibitor). Common side effects include hand-foot syndrome, mucositis, and diarrhea. * **D. Busulfan:** An alkylating agent used in CML and bone marrow transplants. Its classic "high-yield" side effects are **pulmonary fibrosis** ("Busulfan lung"), hyperpigmentation, and adrenal insufficiency-like syndrome. **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 conjugate. 3. **Other Side Effects:** Cyclophosphamide is also notorious for causing SIADH and increased risk of transitional cell carcinoma of the bladder in the long term.

Question 39: Which of the following is a known side effect associated with the chemotherapeutic agent Cisplatin?

A. Hemorrhagic cystitis
B. Renal failure (Correct Answer)
C. Tympanic membrane fibrosis
D. Necrotizing enterocolitis

Explanation: **Cisplatin** is a platinum-based alkylating agent widely used for solid tumors. Its most significant dose-limiting toxicity is **Nephrotoxicity (Renal Failure)**. ### 1. Why Renal Failure is Correct Cisplatin accumulates in the proximal convoluted tubule (PCT) cells of the kidney, leading to oxidative stress and apoptosis. This manifests as a decrease in GFR and an increase in serum creatinine. To prevent this, clinicians use **aggressive hydration with normal saline** and the administration of **Amifostine** (a cytoprotective free-radical scavenger). ### 2. Analysis of Incorrect Options * **A. Hemorrhagic cystitis:** This is the classic side effect of **Cyclophosphamide** and **Ifosfamide** due to the metabolite **Acrolein**. It is prevented by **MESNA**. * **C. Tympanic membrane fibrosis:** While Cisplatin causes **Ototoxicity** (high-frequency hearing loss and tinnitus), it is due to damage to the **hair cells in the Organ of Corti**, not fibrosis of the tympanic membrane. * **D. Necrotizing enterocolitis:** This is primarily a neonatal gastrointestinal emergency, not a recognized specific side effect of Cisplatin therapy. ### 3. High-Yield Clinical Pearls for NEET-PG * **Mnemonic for Cisplatin Side Effects:** "3 N's" — **N**ephrotoxicity, **N**eurotoxicity (peripheral neuropathy), and **N**ausea/vomiting (it is highly emetogenic). * **Electrolyte Imbalance:** Cisplatin frequently causes **Hypomagnesemia** and hypokalemia due to renal tubular damage. * **Drug of Choice for Vomiting:** For Cisplatin-induced emesis, the regimen of choice is a **5-HT3 antagonist (Ondansetron) + Dexamethasone + NK1 antagonist (Aprepitant).** * **Carboplatin:** A related drug that is less nephrotoxic but more **myelosuppressive** (causes thrombocytopenia).

Question 40: 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.

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

Practice Questions

Immunotherapy

Practice Questions

Management of Chemotherapy Side Effects

Practice Questions

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