Anticancer Drugs Practice Questions

Q: Which of the following anti-cancer drugs does not possess anti-inflammatory or immunosuppressive properties?

L-Asparaginase. **Explanation:** The correct answer is **L-Asparaginase**. **1. Why L-Asparaginase is correct:** L-Asparaginase is a unique enzyme used primarily in **Acute Lymphoblastic Leukemia (ALL)**. Its mechanism involves degrading circulating **L-asparagine** into aspartic acid and ammonia. Since leukemic cells lack the enzyme *asparagine synthetase*, they cannot synthesize asparagine endogenously and die due to protein synthesis inhibition. Unlike most cytotoxic drugs, L-Asparaginase is **not a general bone marrow suppressant** and does not interfere with the proliferation of normal T or B lymphocytes in a way that provides anti-inflammatory or immunosuppressive benefits. Its side effect profile is distinct, focusing on hypersensitivity, pancreatitis, and clotting factor deficiencies. **2. Why the other options are incorrect:** * **Methotrexate (MTX):** A folate antagonist that inhibits dihydrofolate reductase. It is a potent immunosuppressant and is the "gold standard" Disease-Modifying Antirheumatic Drug (DMARD) for **Rheumatoid Arthritis**. * **Azathioprine:** A purine antimetabolite (prodrug of 6-Mercaptopurine) that inhibits lymphocyte proliferation. It is widely used for **organ transplant rejection** and autoimmune conditions like SLE. * **Cyclophosphamide:** An alkylating agent that suppresses both B-cell and T-cell functions. It is used in severe autoimmune diseases like **Wegener’s Granulomatosis** and Lupus Nephritis. **3. NEET-PG High-Yield Pearls:** * **L-Asparaginase Toxicity:** Look for "Acute Pancreatitis" or "Thrombosis/Bleeding" (due to decreased synthesis of clotting factors and Antithrombin III) in clinical vignettes. * **Unique Property:** It is one of the few anticancer drugs that is **bone marrow sparing**. * **Resistance:** Occurs due to increased expression of asparagine synthetase by tumor cells.

Q: SIADH is caused by all of the following drugs except:

Actinomycin D. **Explanation:** The Syndrome of Inappropriate Antidiuretic Hormone (SIADH) is a common paraneoplastic syndrome, but it is also a well-documented side effect of several chemotherapeutic agents. **Why Actinomycin D is the correct answer:** Actinomycin D (Dactinomycin) is an antitumor antibiotic used primarily in pediatric tumors like Wilms' tumor and Ewing sarcoma. Unlike the other options listed, it is **not** associated with the induction of SIADH. Its primary dose-limiting toxicities are bone marrow suppression and gastrointestinal mucosal damage. **Analysis of incorrect options:** * **Vincristine & Vinblastine (Vinca Alkaloids):** These are classic causes of drug-induced SIADH. They are thought to exert a direct toxic effect on the neurohypophysis or the hypothalamic-neurohypophyseal tract, leading to the unregulated release of ADH. * **Cyclophosphamide:** This alkylating agent is a high-yield cause of SIADH, particularly when administered in high doses. It enhances the effect of ADH on the renal tubules. **Clinical Note:** This is particularly dangerous because patients receiving cyclophosphamide are often aggressively hydrated to prevent hemorrhagic cystitis, increasing the risk of severe hyponatremia. **NEET-PG High-Yield Pearls:** 1. **Common Drugs causing SIADH (Mnemonic: "S-S-C-V"):** **S**SRIs (Fluoxetine), **S**ulfonylureas (Chlorpropamide), **C**arbamazepine/Cyclophosphamide, and **V**inca Alkaloids. 2. **Management:** The mainstay of treatment for drug-induced SIADH is the discontinuation of the offending agent and fluid restriction. In chronic cases, **Demeclocycline** (an ADH antagonist) or **Tolvaptan** (V2 receptor antagonist) may be used. 3. **Diagnosis:** Look for hyponatremia, low serum osmolality, and inappropriately high urine osmolality in a normovolemic patient.

Q: Crizotinib is used in the treatment of which of the following conditions?

ALK positive Non-small cell carcinoma of lung. **Explanation:** **Crizotinib** is a first-generation tyrosine kinase inhibitor (TKI) that primarily targets the **ALK (Anaplastic Lymphoma Kinase)** protein. In approximately 3–5% of Non-Small Cell Lung Cancer (NSCLC) cases, a chromosomal rearrangement occurs (typically the EML4-ALK fusion gene), leading to constitutive activation of ALK signaling, which drives tumor growth. Crizotinib effectively inhibits this signaling pathway, making it the standard initial therapy for **ALK-positive NSCLC**. **Analysis of Incorrect Options:** * **Option A & C (FLT-3 positive):** FLT-3 mutations are hallmark drivers in **Acute Myeloid Leukemia (AML)**. The drugs used for FLT-3 positive AML include **Midostaurin** and **Gilteritinib**, not Crizotinib. * **Option D (BRCA-2 positive):** BRCA mutations involve DNA repair pathways. The treatment of choice for BRCA-positive metastatic breast or ovarian carcinoma involves **PARP inhibitors** such as **Olaparib** or **Niraparib**. **Clinical Pearls for NEET-PG:** * **Mechanism:** Crizotinib inhibits ALK, **ROS1**, and **c-MET** tyrosine kinases. * **Resistance:** Most patients eventually develop resistance to Crizotinib (often via the L1196M "gatekeeper" mutation). Second-generation ALK inhibitors like **Ceritinib**, **Alectinib**, and **Brigatinib** are used to overcome this. * **Side Effects:** Notable side effects include **visual disturbances** (flashes of light), hepatotoxicity, and QT interval prolongation. * **High-Yield Association:** Always associate **ALK rearrangement** with **younger age** and **non-smokers** in the context of lung adenocarcinoma.

Q: Amifostine protects all of the following organs, EXCEPT:

CNS. **Explanation:** **Amifostine** is a cytoprotective agent (a prodrug) that is converted by alkaline phosphatase into its active thiol metabolite, **WR-1065**. This metabolite acts as a potent scavenger of free radicals generated by cisplatin and radiation therapy, thereby protecting normal tissues from toxicity. **Why CNS is the correct answer:** Amifostine **does not cross the blood-brain barrier (BBB)**. Consequently, it cannot provide any protective effect to the Central Nervous System (CNS). This is a critical pharmacological limitation that makes it ineffective against neurotoxicity. **Analysis of incorrect options:** * **Kidneys:** Amifostine is FDA-approved to reduce cumulative **nephrotoxicity** associated with cisplatin in patients with advanced ovarian cancer. * **Salivary glands:** It is used to reduce the incidence of **xerostomia** (dry mouth) in patients undergoing post-operative radiation therapy for head and neck cancer. * **GIT:** It provides protection to the gastrointestinal mucosa against radiation-induced damage (proctitis/mucositis) and reduces bone marrow suppression (neutropenia). **High-Yield Clinical Pearls for NEET-PG:** * **Differential Uptake:** Amifostine protects normal cells more than tumor cells because normal cells have higher alkaline phosphatase activity and better vascularity, leading to higher concentrations of the active metabolite. * **Common Side Effect:** The most significant dose-limiting side effect of Amifostine is **hypotension** (seen in ~60% of patients), followed by nausea and vomiting. * **Drug Class:** It is specifically known as a **"Radioprotector."** * **Other Cytoprotectants to remember:** * **Mesna:** Prevents hemorrhagic cystitis (Cyclophosphamide/Ifosfamide). * **Dexrazoxane:** Prevents cardiotoxicity (Anthracyclines). * **Leucovorin:** Rescues bone marrow (Methotrexate).

Q: Which of the following statements about Cytarabine is false?

It is a purine analogue.. ### **Explanation** **1. Why Option D is the Correct Answer (The False Statement):** Cytarabine (Ara-C) is a **Pyrimidine analogue**, not a purine analogue. It is a deoxycytidine analogue that acts as an antimetabolite. Its mechanism involves being phosphorylated into its active form (Ara-CTP), which then competes with deoxycytidine triphosphate for incorporation into DNA. This inhibits **DNA polymerase**, leading to the termination of DNA chain elongation during the **S-phase** of the cell cycle. **2. Analysis of Other Options:** * **Option A (Short acting):** Cytarabine has a very short half-life (approximately 10–20 minutes) because it is rapidly deaminated by the enzyme **cytidine deaminase** into the inactive metabolite uracil arabinoside (Ara-U). * **Option B (Continuous IV infusion):** Due to its rapid metabolism and S-phase specificity, it must be administered via continuous intravenous infusion to ensure that cells entering the S-phase are consistently exposed to the drug. * **Option C (Cerebellar toxicity):** High-dose Cytarabine (HiDAC) can cross the blood-brain barrier. A classic and specific side effect is **cerebellar ataxia** (dysarthria, nystagmus, and dysmetria). **3. Clinical Pearls for NEET-PG:** * **Drug of Choice:** It is the backbone of the "7+3" induction regimen for **Acute Myeloid Leukemia (AML)**. * **Specific Side Effects:** Apart from cerebellar toxicity, it causes **conjunctivitis** (prophylactic steroid eye drops are used) and severe myelosuppression. * **Resistance:** Resistance often develops due to a decrease in the activating enzyme **deoxycytidine kinase**. * **Mnemonics:** Remember **"Cy-tarabine = Cy-tosine"** (Pyrimidine) and **"C for Cerebellum."**

Q: Which of the following is NOT a radiosensitizing drug?

Cyclophosphamide. **Radiosensitizers** are drugs that enhance the lethal effects of ionizing radiation on tumor cells. The correct answer is **Cyclophosphamide** because it is a cell-cycle non-specific alkylating agent that does not significantly sensitize cells to radiation; rather, it is typically used as a primary chemotherapeutic agent [1, 2, 3].**Why the other options are Radiosensitizers:** * **5-Fluorouracil (5-Fu):** An antimetabolite that inhibits thymidylate synthase. It sensitizes cells by depleting nucleotide pools and interfering with DNA repair mechanisms following radiation damage [1]. * **5-Bromo-2'-deoxyuridine (BUDR):** A halogenated pyrimidine analog that incorporates into DNA in place of thymidine. This makes the DNA strand more susceptible to breakage when exposed to radiation. * **Hydroxyurea:** This drug inhibits ribonucleotide reductase, arresting cells in the **G1-S phase**. Since cells are most sensitive to radiation in the late G1 and early S phases, it acts as a potent radiosensitizer.**High-Yield NEET-PG Pearls:**1. **Mechanism:** Radiosensitizers often work by increasing the production of free radicals or by inhibiting the repair of sublethal radiation damage.2. **Hypoxic Cell Sensitizers:** **Misonidazole** and **Nimorazole** are specific agents designed to mimic oxygen (the best natural radiosensitizer) in hypoxic tumor centers.3. **Gemcitabine** and **Cisplatin** are also clinically significant radiosensitizers used in concurrent chemoradiotherapy (e.g., in cervical or head and neck cancers).4. **Cell Cycle:** Remember that cells are most **radiosensitive** in the **M and G2 phases** and most **radioresistant** in the **S phase**.

Q: A patient undergoing treatment with R-CHOP chemotherapy for non-Hodgkin's lymphoma develops symmetric 'stocking and glove' type distal neuropathy, presenting as tingling in the hands and feet. If these symptoms are a side effect of the chemotherapy, which drug in the regimen is most likely responsible, and at which stage of the cell cycle does it cause arrest?

M phase. The patient is presenting with **peripheral neuropathy** (stocking-and-glove distribution), a classic dose-limiting toxicity of **Vincristine** [2, 3], which is the 'O' (Oncovin) in the **R-CHOP** regimen (Rituximab, Cyclophosphamide, Hydroxydaunorubicin/Doxorubicin, Oncovin, Prednisolone) [2]. Vincristine belongs to the **Vinca Alkaloids** class [1, 2]. These drugs work by binding to tubulin and **inhibiting microtubule polymerization** (preventing the formation of the mitotic spindle). Since the mitotic spindle is essential for chromosome separation, the cell cannot progress through mitosis, leading to **M phase arrest** [1, 2]. The neuropathy occurs because microtubules are also vital for axonal transport in neurons. ### 2. Why Incorrect Options are Wrong * **A & B (G1-S transition / S phase):** Drugs like **Antimetabolites** (e.g., Methotrexate, 5-Fluorouracil) act specifically during the S phase by inhibiting DNA synthesis. While Cyclophosphamide (in R-CHOP) is cell-cycle non-specific, its primary impact is on DNA cross-linking, not spindle formation. * **C (G2-M transition):** This is the site of action for **Bleomycin** (which causes G2 arrest) and sometimes Etoposide. These do not typically cause the symmetric peripheral neuropathy described. ### 3. NEET-PG High-Yield Pearls * **Vincristine vs. Vinblastine:** Remember the mnemonic: **"Vincristine blasts the Nerves (Neurotoxicity); Vinblastine blasts the Marrow (Bone marrow suppression)."** [3] * **Taxanes (Paclitaxel):** Also act on the **M phase** but via the opposite mechanism—they **hyper-stabilize** microtubules (inhibiting *depolymerization*) [3]. * **R-CHOP Side Effects:** * **D**oxorubicin: Cardiotoxicity (Dilated Cardiomyopathy). * **C**yclophosphamide: Hemorrhagic cystitis (prevented by **MESNA**). * **V**incristine: Peripheral neuropathy and paralytic ileus [2, 3].

Q: Pulmonary fibrosis is a complication of which of the following drugs?

Busulfan. **Explanation:** **1. Why Busulfan is Correct:** Busulfan is an alkylating agent primarily used in chronic myeloid leukemia (CML) and as a conditioning agent before bone marrow transplantation [2]. Its most notorious long-term side effect is **"Busulfan Lung,"** characterized by chronic interstitial pulmonary fibrosis. The mechanism involves oxidative stress and direct damage to alveolar epithelial cells, leading to fibroblast proliferation. Clinically, this presents as progressive dyspnea and a dry cough, often occurring months to years after starting therapy. **2. Analysis of Incorrect Options:** * **A. Methotrexate:** While Methotrexate can cause lung injury, it typically presents as an **acute hypersensitivity pneumonitis** (reversible) rather than chronic progressive fibrosis. * **B. Doxorubicin:** The dose-limiting toxicity of this anthracycline is **Cardiotoxicity** (dilated cardiomyopathy/congestive heart failure) due to free radical generation in the myocardium [1]. * **C. Cisplatin:** The primary dose-limiting toxicities for Cisplatin are **Nephrotoxicity** (acute tubular necrosis) and **Ototoxicity** (high-frequency hearing loss). It is not typically associated with pulmonary fibrosis. **3. NEET-PG High-Yield Pearls:** * **Mnemonic for Pulmonary Fibrosis (BBAM):** **B**leomycin (most common) [1], **B**usulfan, **A**miodarone, **M**ethotrexate/Nitrofurantoin. * **Bleomycin:** Causes fibrosis by inducing oxidative damage; it is the most frequently tested drug for this side effect [1]. * **Monitoring:** Patients on Busulfan or Bleomycin should undergo periodic **Pulmonary Function Tests (PFTs)**; a decrease in DLCO (Diffusing capacity of the lungs for carbon monoxide) is an early indicator of toxicity. * **Busulfan other side effects:** Skin hyperpigmentation (Addisonian-like pigmentation) and profound myelosuppression [2].

Q: Which of the following drugs used in the treatment of lung cancer is also used in the treatment of ovarian carcinoma?

Cisplatin. **Explanation:** **Cisplatin** is the correct answer because it is a cornerstone platinum-based alkylating agent used in the treatment of various solid tumors [1], [2]. Its mechanism involves forming intra-strand cross-links in DNA, which inhibits replication and triggers apoptosis [1], [3]. * **Why Cisplatin is correct:** It is a first-line agent for **Non-Small Cell Lung Cancer (NSCLC)** and **Small Cell Lung Cancer (SCLC)**, typically used in combination with etoposide or gemcitabine. Simultaneously, it (or its analog Carboplatin) is the standard of care for **Epithelial Ovarian Carcinoma**, often paired with Paclitaxel [1], [3]. **Analysis of Incorrect Options:** * **Methotrexate:** A folate antagonist primarily used in leukemias, lymphomas, osteosarcoma, and choriocarcinoma. While used in some lung protocols historically, it is not a standard treatment for ovarian cancer. * **Cyclophosphamide:** An alkylating agent (nitrogen mustard) used for breast cancer, lymphomas, and nephrotic syndrome. While it has activity in ovarian cancer, it is not a primary choice for lung cancer compared to platinum compounds [3]. * **Dacarbazine:** Primarily used for **Malignant Melanoma** and **Hodgkin’s Lymphoma** (as part of the ABVD regimen). It has negligible roles in lung or ovarian carcinoma. **High-Yield Clinical Pearls for NEET-PG:** * **Toxicity Profile:** Cisplatin is notorious for **nephrotoxicity** (prevented by aggressive hydration and Amifostine) and is the **most emetogenic** anticancer drug [3]. * **Ototoxicity:** It can cause high-frequency hearing loss [3]. * **Carboplatin vs. Cisplatin:** Carboplatin is often preferred in ovarian cancer due to a better side-effect profile (less vomiting/nephrotoxicity) but causes more **myelosuppression** (thrombocytopenia) [3].

Question 1

Which of the following anti-cancer drugs does not possess anti-inflammatory or immunosuppressive properties?

Accepted Answer

L-Asparaginase

Answer

Methotrexate

Answer

Azathioprine

Answer

Cyclophosphamide

Question 2

SIADH is caused by all of the following drugs except:

Accepted Answer

Actinomycin D

Answer

Vincristine

Answer

Vinblastine

Answer

Cyclophosphamide

Question 3

Crizotinib is used in the treatment of which of the following conditions?

Accepted Answer

ALK positive Non-small cell carcinoma of lung

Answer

FLT-3 positive Non-small cell carcinoma of lung

Answer

FLT-3 positive Acute myeloid leukemia

Answer

BRCA-2 positive metastatic breast carcinoma

Question 4

Amifostine protects all of the following organs, EXCEPT:

Accepted Answer

CNS

Answer

GIT

Answer

Kidneys

Answer

Salivary glands

Question 5

Which of the following statements about Cytarabine is false?

Accepted Answer

It is a purine analogue.

Answer

It is very short acting.

Answer

It is given as continuous IV infusion.

Answer

It can lead to cerebellar toxicity.

Question 6

Which of the following is NOT a radiosensitizing drug?

Accepted Answer

Cyclophosphamide

Answer

5-Fluorouracil (5-Fu)

Answer

5-Bromo-2'-deoxyuridine (BUDR)

Answer

Hydroxyurea

Question 7

A patient undergoing treatment with R-CHOP chemotherapy for non-Hodgkin's lymphoma develops symmetric 'stocking and glove' type distal neuropathy, presenting as tingling in the hands and feet. If these symptoms are a side effect of the chemotherapy, which drug in the regimen is most likely responsible, and at which stage of the cell cycle does it cause arrest?

Accepted Answer

M phase

Answer

G1-S transition

Answer

S phase

Answer

G2-M transition

Question 8

Pulmonary fibrosis is a complication of which of the following drugs?

Accepted Answer

Busulfan

Answer

Methotrexate

Answer

Doxorubicin

Answer

Cisplatin

Question 9

Chemotherapy can be successful during the treatment of which of the following conditions?

Accepted Answer

Leukemia

Answer

Anneloblastoma

Answer

Fibrosarcoma

Answer

Basal cell carcinoma

Question 10

Which of the following drugs used in the treatment of lung cancer is also used in the treatment of ovarian carcinoma?

Accepted Answer

Cisplatin

Answer

Methotrexate

Answer

Cyclophosphamide

Answer

Dacarbazine

Anticancer Drugs — MCQs

Anticancer Drugs — MCQs

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