Anticancer Drugs Practice Questions

Q: Skin pigmentation is caused by:

Busulphan. **Explanation:** **Busulphan** is an alkylating agent primarily used in the treatment of Chronic Myeloid Leukemia (CML) and as a conditioning agent before bone marrow transplantation. A classic and high-yield side effect of Busulphan is **generalized hyperpigmentation**, which often mimics the bronze skin seen in Addison’s disease. This occurs due to increased melanin production and is frequently accompanied by other symptoms like pulmonary fibrosis ("Busulphan lung") and adrenal insufficiency-like syndrome. **Analysis of Incorrect Options:** * **A. Methotrexate:** This folate antagonist is more commonly associated with photosensitivity, alopecia, and mucosal ulcerations (stomatitis) rather than generalized skin pigmentation. * **B. Dactinomycin:** Also known as Actinomycin D, this drug is a potent vesicant. Its primary dermatological concern is severe soft tissue necrosis if extravasated and "radiation recall" phenomenon, but not systemic pigmentation. * **C. Cyclophosphamide:** While it can cause nail pigmentation (melanonychia) and occasionally pigmentation of the palms and soles, it is not the classic answer for generalized skin pigmentation compared to Busulphan. Its hallmark toxicity is hemorrhagic cystitis. **High-Yield Clinical Pearls for NEET-PG:** * **Busulphan Triad:** Hyperpigmentation, Pulmonary Fibrosis, and Adrenal Insufficiency (pseudo-Addison’s). * **Other drugs causing skin pigmentation:** Bleomycin (flagellate dermatosis), Clofazimine (reddish-brown discoloration), Chloroquine (bluish-grey), and Amiodarone (blue-grey "Smurf" skin). * **Mnemonic:** "Busulphan burns the skin (pigmentation) and the lungs (fibrosis)."

Q: Which of the following anticancer drugs causes hemolytic uremic syndrome?

Mitomycin. **Explanation:** **Mitomycin C** is a potent alkylating agent (specifically an antibiotic derived from *Streptomyces caespitosus*) that acts by cross-linking DNA. It is notorious for causing **delayed and cumulative myelosuppression** and a specific, life-threatening form of nephotoxicity known as **Mitomycin-induced Hemolytic Uremic Syndrome (HUS)**. This syndrome is characterized by microangiopathic hemolytic anemia, thrombocytopenia, and progressive renal failure, typically occurring at cumulative doses exceeding 40-50 mg/m². **Analysis of Incorrect Options:** * **Vincristine (A):** A Vinca alkaloid that inhibits microtubule assembly. Its dose-limiting toxicity is **peripheral neuropathy** (paresthesia, loss of reflexes) and autonomic dysfunction (constipation/paralytic ileus). It is notably bone marrow sparing. * **Vinblastine (B):** Also a Vinca alkaloid, but unlike Vincristine, its dose-limiting toxicity is **bone marrow suppression** (neutropenia). It does not cause HUS. * **Cisplatin (C):** A platinum compound known for significant **nephotoxicity** (specifically Acute Tubular Necrosis), ototoxicity, and severe emesis. While it affects the kidneys, it does not typically present as HUS. **High-Yield Clinical Pearls for NEET-PG:** * **Mitomycin C** is also used topically for superficial bladder cancer and in ophthalmic surgery (glaucoma) to prevent scarring. * **Vincristine** is famous for "stocking and glove" neuropathy. * **Cisplatin** nephotoxicity is minimized by aggressive **hydration** and **Amifostine** (a cytoprotective agent). * **Cyclophosphamide** is associated with hemorrhagic cystitis (prevented by **MESNA**).

Q: All of the following is true about hydroxyurea except:

Oral bioavailability is very low.. **Explanation:** **Hydroxyurea** is an antimetabolite that inhibits the enzyme **ribonucleotide reductase**, thereby depleting intracellular deoxynucleotide pools and arresting cells in the **S-phase** of the cell cycle. 1. **Why Option B is the Correct Answer (The False Statement):** Contrary to the option, Hydroxyurea has **excellent oral bioavailability** (nearly 100%). It is rapidly absorbed from the gastrointestinal tract, reaches peak plasma levels within 1–4 hours, and readily crosses the blood-brain barrier. This high oral efficacy makes it a convenient long-term maintenance therapy. 2. **Analysis of Other Options:** * **A. Causes myelosuppression:** This is the **dose-limiting toxicity** of hydroxyurea. It primarily causes leukopenia, though anemia and thrombocytopenia can also occur. * **C. Used in CML:** Hydroxyurea was historically the first-line agent for Chronic Myeloid Leukemia (CML) to rapidly reduce high white blood cell counts (cytoreduction) before the advent of Imatinib. It is still used for rapid debulking in blast crises. * **D. Acts as a radiosensitizer:** By arresting cells in the G1-S phase (the most radiation-sensitive phase) and inhibiting DNA repair, it enhances the effectiveness of radiotherapy, particularly in head and neck or cervical cancers. **High-Yield Clinical Pearls for NEET-PG:** * **Sickle Cell Anemia:** Hydroxyurea is a mainstay treatment because it increases the production of **Fetal Hemoglobin (HbF)**, which inhibits the polymerization of HbS. * **Other Uses:** Polycythemia Vera and Essential Thrombocytosis (to reduce hematocrit/platelet counts). * **Side Effects:** Apart from myelosuppression, it can cause **macrocytic anemia**, cutaneous ulcers, and hyperpigmentation of nails.

Q: Practically all antineoplastic drugs can produce the following toxic effects except?

Cardiomyopathy. ### Explanation The core principle of traditional antineoplastic chemotherapy is the targeting of **rapidly dividing cells**. Most cytotoxic drugs are non-selective, affecting both malignant cells and normal tissues with high turnover rates. **Why Cardiomyopathy is the Correct Answer:** Cardiomyopathy is **not** a universal side effect of all anticancer drugs. It is a **drug-specific toxicity**, most notably associated with **Anthracyclines** (e.g., Doxorubicin, Daunorubicin) due to the generation of free radicals and lipid peroxidation in cardiac myocytes. Other examples of drug-specific toxicities include nephrotoxicity (Cisplatin), pulmonary fibrosis (Bleomycin), and hemorrhagic cystitis (Cyclophosphamide). **Analysis of Incorrect Options (Common Toxicities):** * **Depression of Leucocyte Count (Bone Marrow Suppression):** This is the most common dose-limiting toxicity. Since hematopoietic stem cells divide rapidly, they are highly susceptible to DNA-damaging agents. * **Mucositis:** The epithelial lining of the gastrointestinal tract (from the mouth to the anus) has a high turnover rate. Damage to these cells leads to painful inflammation and ulceration. * **Oligozoospermia:** Germinal epithelium in the testes is highly proliferative. Most cytotoxic drugs cause a decrease in sperm count, often leading to temporary or permanent sterility. **High-Yield Clinical Pearls for NEET-PG:** * **Exceptions to Bone Marrow Suppression:** Most drugs cause it, but **Vincristine, Bleomycin, and L-Asparaginase** are notable for being "bone marrow sparing." * **Doxorubicin Toxicity:** Acute toxicity presents as arrhythmias; chronic toxicity presents as **congestive heart failure (CHF)**. Dexrazoxane (an iron chelator) is used to prevent this. * **Emetic Potential:** Cisplatin is the drug with the highest emetic potential among anticancer agents.

Q: Which of the following agents acts as a proteasome inhibitor?

Bortezomib. **Explanation:** **Bortezomib** is the correct answer. It is a reversible inhibitor of the **26S proteasome**, a large protein complex responsible for degrading ubiquitinated proteins. By inhibiting the proteasome, Bortezomib prevents the degradation of pro-apoptotic proteins and inhibits the activation of **NF-κB** (Nuclear Factor kappa B). In normal cells, NF-κB promotes survival; its inhibition leads to apoptosis, particularly in plasma cells. This makes it a first-line agent for **Multiple Myeloma** and Mantle Cell Lymphoma. **Analysis of Incorrect Options:** * **A. Fludarabine:** A purine antimetabolite (analog of adenosine). it inhibits DNA polymerase and ribonucleotide reductase. It is primarily used in Chronic Lymphocytic Leukemia (CLL). * **B. Thioguanine:** A purine antimetabolite (6-TG) that incorporates into DNA/RNA to inhibit synthesis. It is used in Acute Myeloid Leukemia (AML). * **D. Rivaroxaban:** Not an anticancer drug. It is a **Direct Factor Xa inhibitor** (Oral Anticoagulant) used to prevent DVT and stroke in atrial fibrillation. **High-Yield Clinical Pearls for NEET-PG:** * **Mechanism:** Bortezomib contains **Boron**, which binds to the catalytic site of the proteasome. * **Adverse Effects:** The most characteristic side effect is **Peripheral Neuropathy** (often painful). It can also cause reactivation of Herpes Zoster (prophylactic acyclovir is often given). * **Other Proteasome Inhibitors:** Carfilzomib (irreversible) and Ixazomib (oral). * **Mnemonic:** Remember **"Bort-Myeloma"** – Bortezomib is the "gold standard" for Multiple Myeloma.

Q: Vismodegib is a new anticancer drug approved for the treatment of Basal Cell Carcinoma. It acts as an inhibitor of which pathway?

Hedgehog pathway. **Explanation:** **Vismodegib** is a first-in-class small molecule inhibitor specifically targeting the **Hedgehog (Hh) signaling pathway**. In normal physiology, this pathway is crucial for embryonic development, but its aberrant reactivation in adults is a primary driver of **Basal Cell Carcinoma (BCC)**. Vismodegib works by binding to and inhibiting **SMO (Smoothened)**, a transmembrane protein. By blocking SMO, the drug prevents the activation of GLI transcription factors, thereby halting the proliferation of tumor cells. It is primarily indicated for metastatic or locally advanced BCC where surgery or radiation is not feasible. **Analysis of Incorrect Options:** * **B. Poly ADP Ribose Polymerase (PARP):** Inhibitors like **Olaparib** and Niraparib are used for BRCA-mutated ovarian and breast cancers. They work by blocking DNA repair, leading to "synthetic lethality." * **C. Cyclin Dependent Kinase-4 (CDK4):** Inhibitors like **Palbociclib** and Ribociclib target the cell cycle (G1-S transition) and are used in HR-positive, HER2-negative breast cancer. * **D. Her-2/neu:** This is a receptor tyrosine kinase targeted by monoclonal antibodies like **Trastuzumab** or tyrosine kinase inhibitors like Lapatinib, primarily in breast and gastric cancers. **High-Yield Clinical Pearls for NEET-PG:** * **Mechanism:** SMO Inhibitor (Hedgehog pathway). * **Key Indication:** Advanced/Metastatic Basal Cell Carcinoma (BCC). * **Gorlin Syndrome:** Also known as Nevoid BCC syndrome, it involves a mutation in the *PTCH1* gene (part of the Hh pathway), making these patients highly responsive to Vismodegib. * **Teratogenicity:** It is highly teratogenic (Category X); pregnancy must be strictly avoided. * **Common Side Effects:** Muscle spasms, dysgeusia (taste disturbance), and alopecia.

Q: A patient receiving cisplatin, vinblastine, and bleomycin for a testicular neoplasm develops renal impairment. This is the effect of which drug(s)?

Cisplatin only. **Explanation:** The correct answer is **Cisplatin only**. **1. Why Cisplatin is the correct answer:** Cisplatin is a platinum-based alkylating agent [1] notorious for its dose-limiting **nephrotoxicity**. It causes damage primarily to the proximal convoluted tubules (PCT) through oxidative stress and the formation of reactive oxygen species. This leads to a decrease in GFR and an increase in serum creatinine. To prevent this, patients are typically managed with aggressive **pre-treatment hydration** and the administration of **Amifostine** (a cytoprotective free-radical scavenger). **2. Why the other options are incorrect:** * **Bleomycin:** Its primary dose-limiting toxicity is **pulmonary fibrosis** (interstitial pneumonitis) [2]. It is unique among anticancer drugs for having minimal bone marrow suppression and no significant renal toxicity. * **Vinblastine:** As a microtubule inhibitor (Vinca alkaloid), its major dose-limiting toxicity is **bone marrow suppression** (specifically leukopenia). Its sister drug, Vincristine, is more associated with peripheral neuropathy. Neither causes renal impairment. **3. High-Yield Clinical Pearls for NEET-PG:** * **Cisplatin Toxicities (Mnemonic: 3 N's):** **N**ephrotoxicity, **N**eurotoxicity (peripheral neuropathy), and **N**ausea/Vomiting (highly emetogenic). It is also **Ototoxic** (high-frequency hearing loss). * **Amifostine:** Specifically used to reduce cisplatin-induced nephrotoxicity. * **Testicular Cancer Regimen:** The combination used in the question is the **BEP regimen** (Bleomycin, Etoposide, Platinum/Cisplatin). * **Carboplatin:** A cisplatin analogue that is less nephrotoxic but more myelosuppressive (causes thrombocytopenia).

Q: Which enzyme is used as an anticancer drug?

L-asparaginase. **Explanation:** **1. Why L-asparaginase is the correct answer:** L-asparaginase is a unique chemotherapy agent because it is an **enzyme** derived from *E. coli* or *Erwinia chrysanthemi*. Its mechanism of action relies on a metabolic vulnerability in neoplastic cells (specifically in **Acute Lymphoblastic Leukemia/ALL**). Normal cells can synthesize the amino acid **L-asparagine** from aspartic acid using the enzyme *asparagine synthetase*. However, certain leukemic cells lack this enzyme and depend on exogenous (blood-borne) asparagine for protein synthesis. L-asparaginase catalyzes the conversion of circulating L-asparagine into aspartic acid and ammonia, effectively "starving" the cancer cells and leading to cell death. **2. Why the other options are incorrect:** * **B. Cytosine arabinoside (Ara-C):** This is an **antimetabolite** (pyrimidine analog) that inhibits DNA polymerase. * **C. Methotrexate:** This is an **antimetabolite** (folate antagonist) that inhibits the enzyme dihydrofolate reductase (DHFR). * **D. Vincristine:** This is a **vinca alkaloid** (mitotic inhibitor) that binds to tubulin and prevents microtubule polymerization. **3. NEET-PG High-Yield Pearls:** * **Clinical Use:** Primarily used in induction therapy for **Acute Lymphoblastic Leukemia (ALL)**. * **Major Side Effects:** Unlike most anticancer drugs, it is **not bone marrow suppressive**. Instead, it causes: * **Hypersensitivity reactions** (anaphylaxis) because it is a foreign bacterial protein. * **Acute Pancreatitis** (High-yield: look for abdominal pain in clinical vignettes). * **Hypofibrinogenemia** and clotting factor deficiencies leading to thrombosis or hemorrhage. * **Route:** Administered IM or IV.

Question 1

Skin pigmentation is caused by:

Accepted Answer

Busulphan

Answer

Methotrexate

Answer

Dactinomycin

Answer

Cyclophosphamide

Question 2

Which of the following anticancer drugs causes hemolytic uremic syndrome?

Accepted Answer

Mitomycin

Answer

Vincristine

Answer

Vinblastine

Answer

Cisplatin

Question 3

All of the following is true about hydroxyurea except:

Accepted Answer

Oral bioavailability is very low.

Answer

Causes myelosuppression.

Answer

Used in CML.

Answer

Acts as a radiosensitizer.

Question 4

Practically all antineoplastic drugs can produce the following toxic effects except?

Accepted Answer

Cardiomyopathy

Answer

Depression of leucocyte count

Answer

Mucositis

Answer

Oligozoospermia

Question 5

Which of the following agents acts as a proteasome inhibitor?

Accepted Answer

Bortezomib

Answer

Fludarabine

Answer

Thioguanine

Answer

Rivaroxaban

Question 6

Vismodegib is a new anticancer drug approved for the treatment of Basal Cell Carcinoma. It acts as an inhibitor of which pathway?

Accepted Answer

Hedgehog pathway

Answer

Poly ADP Ribose Polymerase

Answer

Cyclin Dependent Kinase-4

Answer

Her-2/neu

Question 7

A patient receiving cisplatin, vinblastine, and bleomycin for a testicular neoplasm develops renal impairment. This is the effect of which drug(s)?

Accepted Answer

Cisplatin only

Answer

Bleomycin only

Answer

Vinblastine only

Answer

Both cisplatin and vinblastine

Question 8

Which teratogen causes deafness?

Accepted Answer

Imatinib is used in the treatment of Chronic myelomonocytic leukemia

Answer

Imatinib is used in the treatment of MDS

Answer

Imatinib is used in the treatment of ALL

Answer

Imatinib is used in the treatment of GIST

Question 9

What is the mechanism of action of vincristine in the treatment of acute lymphoblastic leukemia (ALL)?

Accepted Answer

Inhibition of polymerization of tubulin to form microtubules

Answer

Inhibition of topoisomerase II to cause breaks in DNA strands

Answer

Alkylation and cross linking DNA strands

Answer

Inhibition of DNA mediated RNA synthesis

Question 10

Which enzyme is used as an anticancer drug?

Accepted Answer

L-asparaginase

Answer

Cytosine arabinoside

Answer

Methotrexate

Answer

Vincristine

Anticancer Drugs — MCQs

Anticancer Drugs — MCQs

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