Anticancer Drugs — MCQs

Anticancer Drugs Indian Medical PG Practice Questions and MCQs

Question 11: 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].

Question 12: Tamoxifen is useful in which of the following conditions?

A. Carcinoma of the prostate
B. Carcinoma of the ovary
C. Estrogen receptor-positive breast carcinoma (Correct Answer)
D. Seminoma

Explanation: **Explanation:** **Tamoxifen** is the prototype **Selective Estrogen Receptor Modulator (SERM)**. Its therapeutic utility depends on its tissue-specific action: it acts as an **antagonist** in the breast but as a partial **agonist** in the endometrium and bone. 1. **Why Option C is Correct:** In breast tissue, Tamoxifen competitively binds to estrogen receptors (ER), blocking the proliferative effects of endogenous estrogen. Since approximately 70% of breast cancers are hormone-dependent, Tamoxifen is the gold standard for the treatment and prophylaxis of **ER-positive breast carcinoma** in both pre- and post-menopausal women. 2. **Why Other Options are Incorrect:** * **Carcinoma of the Prostate (A):** This is an androgen-dependent malignancy. Treatment typically involves androgen deprivation therapy (e.g., GnRH agonists like Leuprolide or anti-androgens like Flutamide), not anti-estrogens. * **Carcinoma of the Ovary (B):** While some ovarian cancers express ER, Tamoxifen is not a primary treatment modality. Standard care involves platinum-based chemotherapy (e.g., Carboplatin and Paclitaxel). * **Seminoma (D):** This is a germ cell tumor of the testis. It is highly radiosensitive and chemosensitive (e.g., BEP regimen: Bleomycin, Etoposide, Cisplatin), but not responsive to SERMs. **High-Yield NEET-PG Pearls:** * **Side Effects:** Increased risk of **endometrial carcinoma** (due to agonist action on the uterus) and **thromboembolism** (DVT/PE). * **Beneficial Side Effect:** It prevents post-menopausal bone loss (agonist action on bone). * **Drug Interaction:** It is a prodrug activated by **CYP2D6**. Potent inhibitors like Fluoxetine or Paroxetine can decrease its efficacy. * **Alternative:** For post-menopausal women, **Aromatase Inhibitors** (e.g., Letrozole, Anastrozole) are often preferred over Tamoxifen.

Question 13: Which phase of the cell cycle is resistant to most chemotherapeutic agents that are classified as phase-specific?

A. G0 (Correct Answer)
B. G1
C. G2
D. M

Explanation: ### Explanation **Correct Option: A (G0 Phase)** The **G0 phase (Resting Phase)** is the period where cells are quiescent and have exited the replicative cycle. Most cell cycle-specific (CCS) chemotherapeutic agents target metabolic processes active during DNA synthesis or cell division. Since cells in G0 are not actively dividing, they lack the targets (like topoisomerase, thymidylate synthase, or mitotic spindles) that these drugs attack. This makes G0 the most resistant phase and a major cause of tumor recurrence, as these "dormant" cells can re-enter the cycle after treatment ends. **Incorrect Options:** * **B (G1 Phase):** This is the pre-synthetic phase. While less sensitive than S or M, certain drugs like **Vinblastine** or **Asparaginase** can act here. * **C (G2 Phase):** This is the post-synthetic phase where proteins for mitosis are synthesized. It is specifically targeted by **Bleomycin** and **Etoposide**. * **D (M Phase):** The Mitotic phase is the most sensitive phase for **Vinca alkaloids** (inhibit microtubule assembly) and **Taxanes** (inhibit microtubule disassembly). **NEET-PG High-Yield Pearls:** 1. **Cell Cycle Specific (CCS) Drugs:** Act on dividing cells (e.g., Antimetabolites, Vincas, Taxanes). They are **schedule-dependent** (best given in divided doses or infusions). 2. **Cell Cycle Non-Specific (CCNS) Drugs:** Act on both resting and dividing cells (e.g., Alkylating agents like Cyclophosphamide, Cisplatin). They are **dose-dependent** (bolus doses). 3. **S-Phase Specific:** Most Antimetabolites (Methotrexate, 5-FU, Cytarabine). 4. **Growth Fraction:** Tumors with a high growth fraction (more cells in cycle, fewer in G0) respond better to chemotherapy (e.g., Burkitt’s Lymphoma).

Question 14: Hand-foot syndrome is a known side effect of which anticancer drug?

A. Cisplatin
B. 5-fluorouracil (Correct Answer)
C. Methotrexate
D. Imatinib

Explanation: **Explanation:** **Hand-foot syndrome (Palmar-Plantar Erythrodysesthesia)** is a distinctive dermatological toxicity characterized by redness, swelling, pain, and sometimes blistering on the palms of the hands and soles of the feet. **Why 5-fluorouracil (5-FU) is correct:** 5-FU and its oral prodrug, **Capecitabine**, are the most common causes of Hand-foot syndrome. The mechanism involves the leakage of the drug from small capillaries in the palms and soles due to high pressure and friction in these areas. Once leaked, the drug causes direct cytotoxic damage to the surrounding tissue. It is particularly associated with **continuous infusion** of 5-FU rather than bolus doses. **Analysis of Incorrect Options:** * **A. Cisplatin:** Primarily known for its "Cs": **C**ytotoxicity (Ototoxicity), **C**alculi (Nephrotoxicity), and severe **C**hemoreceptor trigger zone stimulation (highly emetogenic). * **C. Methotrexate:** Major side effects include **mucositis**, myelosuppression, and hepatotoxicity. It is also a potent teratogen. * **D. Imatinib:** A tyrosine kinase inhibitor commonly causing **periorbital edema**, fluid retention, and GI upset. **NEET-PG High-Yield Pearls:** * **Management:** Pyridoxine (Vitamin B6) is often used for prophylaxis/treatment, along with topical emollients and dose reduction. * **Other drugs causing HFS:** Cytarabine, Doxorubicin (especially liposomal), and Sorafenib. * **5-FU Antidote:** Uridine triacetate is used for life-threatening 5-FU or Capecitabine overdose/toxicity. * **Thymidylate Synthase:** 5-FU acts by inhibiting this enzyme, leading to "thymineless death" of cells.

Question 15: A 58-year-old woman with a history of myocardial infarction and congestive heart failure has been diagnosed with locally advanced breast cancer and recommended for chemotherapy. Which antineoplastic drug should be best avoided?

A. Anthracycline (Correct Answer)
B. Alkylating agent
C. Platinum compound
D. Bisphosphonates

Explanation: ### Explanation **Correct Option: A. Anthracyclines** Anthracyclines (e.g., **Doxorubicin, Daunorubicin**) are notorious for their **dose-dependent cardiotoxicity** [1]. The underlying mechanism involves the generation of iron-dependent free radicals (reactive oxygen species) that cause lipid peroxidation of the myocardial cell membrane [1]. Since the patient already has a history of myocardial infarction and congestive heart failure (CHF), using anthracyclines would significantly increase the risk of worsening her cardiac status or inducing irreversible dilated cardiomyopathy [1]. **Why other options are incorrect:** * **B. Alkylating agents:** While drugs like Cyclophosphamide can cause hemorrhagic cystitis (prevented by Mesna), they are generally not contraindicated in patients with pre-existing CHF, though high doses can occasionally cause acute myocarditis. * **C. Platinum compounds:** Cisplatin is primarily associated with nephrotoxicity, ototoxicity, and severe emesis. It does not have the same direct, cumulative cardiotoxic profile as anthracyclines. * **D. Bisphosphonates:** These are not antineoplastic drugs but are supportive therapies used to manage bone metastases or hypercalcemia of malignancy. Their primary side effects include osteonecrosis of the jaw and esophageal irritation. **High-Yield NEET-PG Pearls:** * **Dexrazoxane:** An iron-chelating agent used to prevent/reduce anthracycline-induced cardiotoxicity [1]. * **Monitoring:** Patients on Doxorubicin should be monitored via **ECHO or MUGA scans** to assess the Left Ventricular Ejection Fraction (LVEF) [1]. * **Liposomal Doxorubicin:** A formulation designed to reduce cardiac uptake and decrease toxicity. * **Trastuzumab:** Another breast cancer drug that causes cardiotoxicity, but unlike anthracyclines, its effect is usually **reversible** and not dose-dependent.

Question 16: Which of the following drugs is used for medical adrenalectomy?

A. Mitotane (Correct Answer)
B. Methotrexate
C. Doxorubicin
D. 5-Fluorouracil

Explanation: **Explanation:** **1. Why Mitotane is Correct:** Mitotane is a unique adrenolytic agent chemically related to the insecticide DDT. It acts as a selective cytotoxic agent for the adrenal cortex, specifically targeting the mitochondria of cells in the **zona fasciculata and zona reticularis**. By causing focal degeneration and atrophy of the adrenal cortex, it effectively suppresses cortisol production. This pharmacological destruction of adrenal tissue is termed **"medical adrenalectomy."** It is primarily indicated for the treatment of inoperable adrenocortical carcinoma and occasionally for refractory Cushing’s syndrome. **2. Why Other Options are Incorrect:** * **Methotrexate (B):** An antimetabolite that inhibits dihydrofolate reductase (DHFR). It is used for various cancers (leukemia, choriocarcinoma) and autoimmune diseases, but has no specific affinity for adrenal tissue. * **Doxorubicin (C):** An anthracycline antibiotic that works by intercalating DNA and inhibiting Topoisomerase II. It is a broad-spectrum cardiotoxic anticancer drug used in solid tumors and lymphomas. * **5-Fluorouracil (D):** A pyrimidine analog that inhibits thymidylate synthase. It is a mainstay for GI tract cancers and breast cancer, not adrenal suppression. **3. High-Yield Clinical Pearls for NEET-PG:** * **Mechanism:** Selective mitochondrial destruction in adrenal cortical cells. * **Drug of Choice:** Mitotane is the drug of choice for **Adrenocortical Carcinoma**. * **Side Effects:** Significant GI distress (nausea/vomiting) and neurological symptoms (lethargy/ataxia). * **Note:** Other drugs used to suppress adrenal function (but not via "adrenalectomy" or cell death) include **Ketoconazole** (inhibits 17α-hydroxylase) and **Metyrapone** (inhibits 11β-hydroxylase).

Question 17: Busulfan toxicity does not include which of the following?

A. Hyperpigmentation
B. Toxic carditis (Correct Answer)
C. Hyperuricemia
D. Pulmonary fibrosis

Explanation: **Explanation:** Busulfan is an alkylating agent (specifically an alkyl sulfonate) primarily used in the treatment of Chronic Myeloid Leukemia (CML) and as a conditioning agent before bone marrow transplantation. **Why "Toxic Carditis" is the correct answer:** Toxic carditis is not a recognized side effect of Busulfan. Cardiotoxicity (specifically hemorrhagic cystitis and cardiomyopathy) is more characteristically associated with high doses of **Cyclophosphamide**. Busulfan’s toxicity profile is primarily focused on the lungs, skin, and bone marrow. **Analysis of Incorrect Options:** * **A. Hyperpigmentation:** Busulfan frequently causes a "tan-like" skin hyperpigmentation. In some cases, this is part of **"Busulfan-induced Addison-like syndrome,"** characterized by wasting, hypotension, and skin darkening, though without actual adrenal insufficiency (normal cortisol levels). * **C. Hyperuricemia:** Like most cytotoxic drugs that cause rapid tumor cell lysis (Tumor Lysis Syndrome), Busulfan leads to increased purine catabolism, resulting in elevated uric acid levels. * **D. Pulmonary Fibrosis:** This is a classic, high-yield side effect known as **"Busulfan Lung."** It is a dose-dependent interstitial pulmonary fibrosis that can occur months to years after treatment. **High-Yield Clinical Pearls for NEET-PG:** * **Mnemonic for Busulfan:** **B**-**B**-**B** (Bone marrow suppression, Busulfan Lung, Bronze skin). * **Seizures:** At high doses (conditioning regimens), Busulfan crosses the blood-brain barrier and can cause seizures; prophylactic anticonvulsants (like Phenytoin) are often administered. * **Veno-occlusive disease (VOD):** Busulfan is a major risk factor for hepatic VOD (Sinusoidal Obstruction Syndrome) during transplant conditioning.

Question 18: A 40-year-old woman, who has been on chemotherapy for 6 months for ovarian carcinoma, presents with progressive bilateral sensorineural hearing loss. Which drug is responsible for this adverse effect?

A. Cisplatin (Correct Answer)
B. Doxorubicin
C. Cyclophosphamide
D. Paclitaxel

Explanation: **Explanation:** The correct answer is **Cisplatin**. **1. Why Cisplatin is correct:** Cisplatin is a potent platinum-based alkylating agent used frequently in ovarian, lung, and bladder cancers. Its most characteristic dose-limiting toxicities are **nephrotoxicity** and **ototoxicity**. The drug causes damage to the hair cells in the cochlea and the stria vascularis, leading to progressive, bilateral, and often irreversible **high-frequency sensorineural hearing loss** and tinnitus. Amifostine (a cytoprotective agent) is sometimes used to reduce cisplatin-induced nephrotoxicity, though its role in preventing ototoxicity is less established. **2. Why other options are incorrect:** * **Doxorubicin:** An anthracycline primarily known for **cardiotoxicity** (dilated cardiomyopathy) due to free radical generation. It does not cause hearing loss. * **Cyclophosphamide:** An alkylating agent (nitrogen mustard) most famous for causing **hemorrhagic cystitis** due to the metabolite acrolein. This can be prevented with aggressive hydration and **MESNA**. * **Paclitaxel:** A taxane that inhibits microtubule disassembly. Its hallmark toxicity is **peripheral neuropathy** (stocking-and-glove distribution) and myelosuppression, not ototoxicity. **High-Yield Clinical Pearls for NEET-PG:** * **Platinum Compounds:** Cisplatin (Ototoxicity/Nephrotoxicity), Carboplatin (Myelosuppression/Thrombocytopenia), Oxaliplatin (Cold-induced peripheral neuropathy). * **Ototoxic Drugs Mnemonic:** "A-C-E-L" (Aminoglycosides, Cisplatin, Erythromycin, Loop diuretics). * **Vincristine vs. Vinblastine:** Vincristine causes peripheral neuropathy (nerve damage); Vinblastine causes bone marrow suppression (blasts the marrow).

Question 19: Which of the following chemotherapeutic agents is specific for the M phase of the cell cycle?

A. Cytarabine
B. Daunorubicin
C. Hydroxyurea
D. Vincristine (Correct Answer)

Explanation: ### Explanation **Correct Answer: D. Vincristine** **Mechanism and Cell Cycle Specificity:** Chemotherapeutic agents are classified as either **Cell Cycle-Specific (CCS)** or **Cell Cycle-Non-Specific (CCNS)**. Vincristine, a Vinca alkaloid, is a classic example of a CCS drug that acts specifically during the **M (Mitosis) phase**. It works by binding to tubulin and inhibiting its polymerization into microtubules. This prevents the formation of the mitotic spindle, leading to "mitotic arrest" in metaphase and subsequent apoptosis. **Analysis of Incorrect Options:** * **A. Cytarabine (Ara-C):** This is an antimetabolite (pyrimidine analog) that inhibits DNA polymerase. It is specific for the **S phase** (DNA synthesis). * **B. Daunorubicin:** This is an Anthracycline antibiotic. While it has some increased activity in the S phase, it is generally considered **Cell Cycle-Non-Specific (CCNS)** because it intercalates into DNA and inhibits Topoisomerase II, affecting cells regardless of their phase. * **C. Hydroxyurea:** This drug inhibits the enzyme ribonucleotide reductase, preventing the conversion of ribonucleotides to deoxyribonucleotides. It is highly specific for the **S phase**. **High-Yield NEET-PG Pearls:** * **M-Phase Specific Drugs:** Remember the mnemonic **"TV"** (Taxanes and Vincas). *Vincas* (Vincristine, Vinblastine) inhibit microtubule **assembly**, while *Taxanes* (Paclitaxel, Docetaxel) inhibit microtubule **disassembly** (stabilize them). * **S-Phase Specific Drugs:** Most antimetabolites (Methotrexate, 5-FU, 6-MP, Cytarabine) and Hydroxyurea. * **G2-Phase Specific Drugs:** Bleomycin and Etoposide. * **Vincristine Side Effect:** Distinctive for **peripheral neuropathy** (areflexia, foot drop) but notably **bone marrow sparing** (unlike Vinblastine).

Question 20: Which of the following monoclonal antibodies is used for the treatment of colorectal carcinoma?

A. Pembrolizumab
B. Cetuximab (Correct Answer)
C. Rituximab
D. Natalizumab

Explanation: **Explanation:** **Correct Answer: B. Cetuximab** Cetuximab is a recombinant human/mouse chimeric monoclonal antibody that targets the **Epidermal Growth Factor Receptor (EGFR)**. In colorectal carcinoma, EGFR is often overexpressed, leading to uncontrolled cell proliferation. By binding to the extracellular domain of EGFR, Cetuximab inhibits downstream signaling pathways (like KRAS/MAPK). * **High-Yield Note:** It is only effective in patients with **wild-type KRAS** genes. If a patient has a KRAS mutation, the pathway remains "on" regardless of EGFR inhibition, making the drug ineffective. **Incorrect Options:** * **A. Pembrolizumab:** This is a **PD-1 inhibitor** (checkpoint inhibitor). While used for various solid tumors, its specific indication in colorectal cancer is limited to cases with **Microsatellite Instability-High (MSI-H)** or mismatch repair deficiency (dMMR), rather than being the primary targeted therapy for general colorectal carcinoma. * **C. Rituximab:** This is a chimeric monoclonal antibody against **CD20**, primarily found on B-cells. It is used in the treatment of Non-Hodgkin Lymphoma (NHL), Chronic Lymphocytic Leukemia (CLL), and autoimmune conditions like Rheumatoid Arthritis. * **D. Natalizumab:** This antibody targets **α4-integrin**. It is used in the management of **Multiple Sclerosis** and Crohn’s disease by preventing leukocyte migration into inflamed tissues. **Clinical Pearls for NEET-PG:** 1. **Panitumumab** is another EGFR inhibitor used in colorectal cancer (fully humanized). 2. **Bevacizumab** (anti-VEGF) is also used in colorectal cancer to inhibit angiogenesis. 3. **Side Effect:** EGFR inhibitors like Cetuximab characteristically cause an **acneiform skin rash**; the presence of the rash often correlates with a positive therapeutic response.

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

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Immunotherapy

Practice Questions

Management of Chemotherapy Side Effects

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