Anticancer Drugs Practice Questions

Q: Which of the following parameters is not monitored in a patient on methotrexate therapy?

Eye examination. **Explanation:** Methotrexate (MTX) is a folate antimetabolite that inhibits the enzyme **dihydrofolate reductase (DHFR)**. While it is a cornerstone in treating malignancies and autoimmune conditions (like Rheumatoid Arthritis), it carries a significant profile of systemic toxicities. **Why Eye Examination is the Correct Answer:** Unlike drugs such as Hydroxychloroquine (which requires retinal monitoring) or Ethambutol (which causes optic neuritis), **Methotrexate does not typically cause ocular toxicity**. Therefore, routine eye examinations are not a standard part of MTX monitoring protocols. **Why other options are monitored:** * **Liver Function Tests (LFTs):** MTX is hepatotoxic. Chronic use can lead to elevated transaminases, steatosis, and eventually **hepatic fibrosis or cirrhosis**. Baseline and periodic LFTs are mandatory. * **Hemogram (CBC):** As a cytotoxic drug, MTX causes **bone marrow suppression** (myelosuppression), leading to leucopenia, thrombocytopenia, and anemia. Monitoring the CBC is critical to prevent life-threatening pancytopenia. * **Lung Function Tests:** MTX can induce **interstitial pneumonitis** (Methotrexate-induced lung injury) or pulmonary fibrosis. Patients presenting with a dry cough or dyspnea require urgent pulmonary evaluation. **High-Yield Clinical Pearls for NEET-PG:** * **Rescue Therapy:** **Leucovorin (Folinic acid)** is used to "rescue" normal cells from MTX toxicity by bypassing the inhibited DHFR enzyme. * **Nephrotoxicity:** High-dose MTX can precipitate in renal tubules; **vigorous hydration and urinary alkalinization** are required. * **Contraindication:** MTX is highly **teratogenic** (Category X) and must be avoided in pregnancy. * **Antidote for Overdose:** **Glucarpidase** (carboxypeptidase G2) can rapidly reduce toxic plasma MTX levels.

Q: Which of the following causes peripheral neuritis?

Vincristine. **Explanation:** **Vincristine** is a Vinca alkaloid that acts as a **microtubule inhibitor**. It binds to tubulin and inhibits its polymerization into microtubules, leading to mitotic arrest in the M-phase. Microtubules are not only essential for cell division but are also critical for **axonal transport** in neurons. By disrupting these microtubule tracks, Vincristine interferes with the transport of neurotransmitters and essential proteins along the long axons of peripheral nerves, leading to **dose-limiting peripheral neuropathy (neuritis)**. This typically manifests as symmetrical "glove and stocking" paresthesia, loss of deep tendon reflexes, and motor weakness. **Why other options are incorrect:** * **Methotrexate:** A folate antagonist (antimetabolite) primarily known for bone marrow suppression, mucositis, and hepatotoxicity. It can cause neurotoxicity (leukoencephalopathy) if given intrathecally, but peripheral neuritis is not its hallmark. * **Busulfan:** An alkylating agent (alkyl sulfonate) most famous for causing **pulmonary fibrosis** ("Busulfan lung") and hyperpigmentation (Addisonian-like syndrome). * **Cyclophosphamide:** An alkylating agent (nitrogen mustard) notorious for **hemorrhagic cystitis** due to the metabolite **Acrolein**. It is also highly emetogenic and causes alopecia. **High-Yield Clinical Pearls for NEET-PG:** * **Vincristine vs. Vinblastine:** Remember the mnemonic: **Vincristine** = **C**NS/Nerve toxicity (Peripheral neuropathy); **Vinblastine** = **B**last (Bone marrow suppression). * Vincristine is notably **bone marrow sparing**, making it ideal for combination regimens. * **Fatal Error:** Vincristine is for **Intravenous use ONLY**. Intrathecal administration is fatal due to ascending myeloencephalopathy. * Other anticancer drugs causing peripheral neuropathy: **Paclitaxel** (microtubule stabilizer) and **Cisplatin** (platinum compound).

Q: Which one of the following medications is most likely to be responsible for this appearance?

Doxorubicin. ***Doxorubicin*** - **Doxorubicin** (anthracycline) causes **dose-dependent cardiotoxicity** leading to **dilated cardiomyopathy** and reduced ejection fraction as shown in the image. - The mechanism involves **free radical damage** to cardiac myocytes with a cumulative dose limit of ~**550 mg/m²**; **dexrazoxane** can be used for cardioprotection. *Clarithromycin* - This **macrolide antibiotic** primarily causes **QT prolongation** and potential arrhythmias, not structural heart changes. - Does not cause **cardiomegaly** or **dilated cardiomyopathy** as seen in the image. *Dexamethasone* - This **corticosteroid** causes **Cushingoid features** including moon face, buffalo hump, and central obesity. - Cardiovascular effects include **hypertension** and **fluid retention**, but not dilated cardiomyopathy. *Efavirenz* - This **NNRTI antiretroviral** causes **CNS effects** (vivid dreams, dizziness) and **neuropsychiatric symptoms**. - Associated with **lipodystrophy** and metabolic changes, but not cardiac structural abnormalities.

Q: Which of the following is/are used in the hormonal therapy of breast carcinoma?

All of the above. Hormonal therapy is a cornerstone in the management of hormone receptor-positive (ER/PR+) breast cancer. The goal is to either block estrogen receptors or decrease circulating estrogen levels. **Explanation of Options:** * **Tamoxifen (Option C):** This is a **Selective Estrogen Receptor Modulator (SERM)**. It acts as a competitive antagonist at estrogen receptors in breast tissue, making it the gold standard for pre-menopausal women. It also has agonist effects on the bone (preventing osteoporosis) and endometrium (increasing the risk of endometrial carcinoma). * **Letrozole and Anastrozole (Options A & B):** These are **Third-generation Aromatase Inhibitors (AIs)**. They inhibit the enzyme aromatase, which converts peripheral androgens into estrogens. Since they cannot stop ovarian estrogen production, they are primarily used in **post-menopausal women**. **Why "All of the above" is correct:** All three drugs are FDA-approved and standard-of-care agents used to treat or prevent the recurrence of breast carcinoma by targeting the estrogen signaling pathway. **High-Yield Clinical Pearls for NEET-PG:** 1. **Drug of Choice:** Tamoxifen is preferred in pre-menopausal women; Aromatase Inhibitors (Letrozole/Anastrozole) are preferred in post-menopausal women. 2. **Side Effects:** Tamoxifen increases the risk of **thromboembolism** and **endometrial cancer**. Aromatase inhibitors are associated with an increased risk of **osteoporosis** and joint pain. 3. **Fulvestrant:** A Selective Estrogen Receptor Downregulator (SERD) used in tamoxifen-resistant cases. 4. **Trastuzumab:** Not a hormonal agent, but a monoclonal antibody used for HER2/neu positive breast cancer.

Q: All of the following statements about methotrexate are true EXCEPT:

Folic acid reverses its toxic effects.. ### Explanation **1. Why Option C is the correct (False) statement:** Methotrexate (MTX) is a folate antagonist that works by inhibiting the enzyme **Dihydrofolate Reductase (DHFR)**. This prevents the conversion of dihydrofolate to tetrahydrofolate (THF). Once MTX binds to DHFR, the cell’s pool of active folate is depleted. Administering **Folic acid** is ineffective because it also requires DHFR to be converted into its active form. To reverse MTX toxicity, we must provide **Folinic acid (Leucovorin/Citrovorum factor)**, which is already a reduced form of folate (N5-formyl-THF) that bypasses the inhibited enzyme. This is known as **"Leucovorin Rescue."** **2. Analysis of other options:** * **Option A:** MTX is a classic **Antimetabolite**. These drugs are **Cell Cycle Specific (CCS)** and act specifically during the **S-phase** by inhibiting DNA synthesis. * **Option B:** Like most cytotoxic drugs, MTX targets rapidly dividing cells. Its primary dose-limiting toxicities include **Bone Marrow Suppression** (myelosuppression) and damage to **Epithelial structures** (leading to oral mucositis and GI ulceration). * **Option D:** MTX is highly effective against trophoblastic tumors and remains the **Drug of Choice for Choriocarcinoma**, often achieving a 100% cure rate in low-risk cases. **3. NEET-PG High-Yield Clinical Pearls:** * **Resistance:** Occurs via decreased drug uptake, decreased polyglutamation, or altered DHFR with lower affinity for MTX. * **Excretion:** MTX is primarily excreted renally. **Salicylates and Sulfonamides** can displace MTX from plasma proteins and inhibit its renal secretion, leading to fatal toxicity. * **Other Uses:** Low-dose MTX is a first-line **Disease-Modifying Antirheumatic Drug (DMARD)** for Rheumatoid Arthritis and is used in Ectopic Pregnancy. * **Specific Toxicity:** Long-term use can lead to **Hepatic Fibrosis/Cirrhosis**.

Q: Which of the following drugs cause metaphase arrest?

Vincristine, Paclitaxel, Colchicine. ### Explanation **1. Mechanism of Metaphase Arrest** Metaphase arrest occurs when drugs interfere with the **mitotic spindle apparatus**, preventing the separation of sister chromatids. This triggers the "spindle assembly checkpoint," halting the cell cycle in the **M-phase (Metaphase)**. * **Vinca Alkaloids (Vincristine/Vinblastine):** These bind to tubulin and **inhibit polymerization**, preventing the formation of microtubules ("Spindle poisons"). * **Taxanes (Paclitaxel/Docetaxel):** These bind to tubulin and **enhance polymerization**, stabilizing microtubules and preventing their disassembly ("Spindle stabilizers"). * **Colchicine:** Primarily used in gout, it also inhibits microtubule polymerization, leading to metaphase arrest. **2. Analysis of Incorrect Options** * **Option B & C (Griseofulvin):** While Griseofulvin is an antifungal that interferes with microtubule function, it is **not** classified as a standard anticancer drug. Furthermore, Option C includes Etoposide. * **Option C & D (Etoposide):** Etoposide is a **Topoisomerase II inhibitor**. It acts primarily in the **S and G2 phases** of the cell cycle, not the M-phase. It causes DNA strand breaks rather than spindle interference. **3. NEET-PG High-Yield Pearls** * **Cell Cycle Specificity:** Vincas and Taxanes are **M-phase specific**. * **Dose-Limiting Toxicities:** * **Vincristine:** Peripheral neuropathy (Areflexia, paralytic ileus). Note: It is relatively bone marrow sparing. * **Vinblastine:** Bone marrow suppression ("Blast" the marrow). * **Paclitaxel:** Hypersensitivity reactions (pre-treat with dexamethasone/antihistamines) and neuropathy. * **Other M-phase inhibitors:** Ixabepilone (Epothilones) and Eribulin.

Q: Which of the following agents is not a proliferation-independent agent?

Vincristine. ### Explanation Anticancer drugs are classified based on their relationship to the cell cycle into two categories: **Cell Cycle-Specific (CCS)** and **Cell Cycle-Nonspecific (CCNS)**. **1. Why Vincristine is the Correct Answer:** Vincristine is a **Cell Cycle-Specific (CCS)** agent. It belongs to the Vinca alkaloid class, which acts specifically during the **M-phase (Mitosis)** of the cell cycle. It binds to tubulin and inhibits its polymerization into microtubules, preventing the formation of the mitotic spindle. Because its efficacy is strictly dependent on the cell being in the process of division (proliferation), it is a **proliferation-dependent** agent. **2. Why the other options are incorrect:** * **Cyclophosphamide, Melphalan, and Carmustine:** These are all **Alkylating Agents**. Alkylating agents work by covalently bonding alkyl groups to DNA, leading to cross-linking and DNA strand breaks. This damage occurs regardless of whether the cell is actively dividing or in a resting state ($G_0$ phase). Therefore, they are classified as **Cell Cycle-Nonspecific (CCNS)** or **proliferation-independent** agents. ### NEET-PG High-Yield Pearls: * **M-Phase Specific Drugs:** Vinca alkaloids (Vincristine, Vinblastine) and Taxanes (Paclitaxel, Docetaxel). *Mnemonic: Vinca prevents assembly; Taxanes prevent disassembly.* * **S-Phase Specific Drugs:** Antimetabolites (Methotrexate, 5-FU, Cytarabine). * **$G_2$-Phase Specific Drugs:** Bleomycin. * **Dose-limiting toxicity of Vincristine:** Peripheral neuropathy (unlike Vinblastine, which is Bone Marrow Suppression). * **Carmustine/Lomustine:** Highly lipid-soluble nitrosoureas used primarily for brain tumors because they cross the blood-brain barrier.

Q: Which of the following is an inhibitor of DNA synthesis?

Actinomycin. The correct answer is Actinomycin (Dactinomycin) [2]. **Mechanism of Action:** Actinomycin acts by binding to the guanine residues of DNA, forming a stable complex. This intercalates between the DNA base pairs, which inhibits the movement of RNA polymerase, thereby preventing transcription [2]. At higher concentrations, it also interferes with **DNA replication (DNA synthesis)** by inhibiting DNA-dependent DNA polymerase [1]. **Analysis of Incorrect Options:** * **A. Penicillin:** This is a Beta-lactam antibiotic that inhibits **cell wall synthesis** by binding to Penicillin-Binding Proteins (PBPs) and preventing the cross-linking of peptidoglycan chains. * **B. Polymyxin:** These are cationic detergents that disrupt the **cell membrane** integrity of Gram-negative bacteria, leading to leakage of intracellular contents. * **C. Chloramphenicol:** This is a bacteriostatic antibiotic that inhibits **protein synthesis** by binding to the 50S ribosomal subunit and preventing peptidyl transferase activity. **High-Yield Clinical Pearls for NEET-PG:** * **Actinomycin D** is primarily used as a chemotherapy agent for pediatric tumors like **Wilms’ tumor**, Ewing’s sarcoma, and Rhabdomyosarcoma. * **Other DNA Synthesis Inhibitors:** Fluoroquinolones (inhibit DNA Gyrase/Topoisomerase), Metronidazole (causes DNA strand breakage), and Acyclovir (inhibits viral DNA polymerase) [1]. * **Mnemonic for Protein Synthesis Inhibitors:** **"Buy AT 30, CELL at 50"** (Aminoglycosides/Tetracyclines at 30S; Chloramphenicol/Erythromycin/Linezolid/Lincosamides at 50S).

Q: Which antineoplastic drug is associated with very high cardiac toxicity?

Doxorubicin. **Explanation:** **Doxorubicin** (an Anthracycline antibiotic) is the correct answer because its most notorious dose-limiting toxicity is **cardiotoxicity**. This occurs via two mechanisms: the generation of iron-dependent **free radicals** (superoxide anions) that cause oxidative stress to myocytes, and the inhibition of **Topoisomerase IIβ**, leading to mitochondrial dysfunction and cell death. * **Acute toxicity:** Presents as arrhythmias or ECG changes (transient). * **Chronic toxicity:** Leads to irreversible, dose-dependent **Dilated Cardiomyopathy** and congestive heart failure. The risk increases significantly once the cumulative dose exceeds **550 mg/m²**. **Analysis of Incorrect Options:** * **A. Bleomycin:** Primarily associated with **Pulmonary Fibrosis** (due to lack of bleomycin hydrolase in lungs) and skin hyperpigmentation. It is "heart-friendly" but "lung-toxic." * **B. Actinomycin–D (Dactinomycin):** Mainly causes significant bone marrow suppression and is used primarily in pediatric tumors (Wilms tumor, Ewing sarcoma). * **C. Mitomycin–C:** Known for causing **Hemolytic Uremic Syndrome (HUS)** and delayed bone marrow suppression. **High-Yield Clinical Pearls for NEET-PG:** 1. **Dexrazoxane:** An iron-chelating agent administered to prevent/reduce Doxorubicin-induced cardiotoxicity. 2. **Monitoring:** Periodic **ECHO or MUGA scans** are mandatory to monitor the Left Ventricular Ejection Fraction (LVEF) in patients on Anthracyclines. 3. **Liposomal Doxorubicin:** Formulated to reduce cardiac uptake and decrease toxicity.

Question 1

Which of the following parameters is not monitored in a patient on methotrexate therapy?

Accepted Answer

Eye examination

Answer

Liver function tests

Answer

Lung function tests

Answer

Hemogram

Question 2

Which of the following causes peripheral neuritis?

Accepted Answer

Vincristine

Answer

Methotrexate

Answer

Busulfan

Answer

Cyclophosphamide

Question 3

Which one of the following medications is most likely to be responsible for this appearance?

Accepted Answer

Doxorubicin

Answer

Clarithromycin

Answer

Dexamethasone

Answer

Efavirenz

Question 4

Which of the following is/are used in the hormonal therapy of breast carcinoma?

Accepted Answer

All of the above

Answer

Letrozole

Answer

Anastrozole

Answer

Tamoxifen

Question 5

Which of the following is the main mechanism by which mechlorethamine exerts its cell killing?

Accepted Answer

Alkylating DNA, causing cross-links between parallel DNA strands

Answer

Blocking microtubular assembly and mitosis during M-phase

Answer

Inhibiting topoisomerase, preventing repair of DNA strand breaks

Answer

Intercalating in DNA strands, thereby preventing DNA replication by mRNA

Question 6

All of the following statements about methotrexate are true EXCEPT:

Accepted Answer

Folic acid reverses its toxic effects.

Answer

It is cell cycle specific and kills cells in the S phase.

Answer

Its toxicity primarily affects bone marrow and epithelial structures.

Answer

It is the drug of choice for choriocarcinoma.

Question 7

Which of the following drugs cause metaphase arrest?

Accepted Answer

Vincristine, Paclitaxel, Colchicine

Answer

Griseofulvin, Vincristine, Paclitaxel

Answer

Griseofulvin, Paclitaxel, Etoposide

Answer

Vincristine, Etoposide, Colchicine

Question 8

Which of the following agents is not a proliferation-independent agent?

Accepted Answer

Vincristine

Answer

Carmustine

Answer

Melphalan

Answer

Cyclophosphamide

Question 9

Which of the following is an inhibitor of DNA synthesis?

Accepted Answer

Actinomycin

Answer

Penicillin

Answer

Polymyxin

Answer

Chloramphenicol

Question 10

Which antineoplastic drug is associated with very high cardiac toxicity?

Accepted Answer

Doxorubicin

Answer

Bleomycin

Answer

Actinomycin–D

Answer

Mitomycin–C

Anticancer Drugs — MCQs

Anticancer Drugs — MCQs

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