Anticancer Drugs Practice Questions

Q: Which pair of drugs acts as protectors during cancer chemotherapy?

Dexrazoxane and Filgrastim. **Explanation:** Chemotherapy "protectors" or **cytoprotective agents** are drugs administered alongside antineoplastic therapy to mitigate specific toxicities without interfering with the antitumor efficacy. **Why Option A is Correct:** * **Dexrazoxane:** An iron chelator that prevents the formation of free radicals. It is used specifically to protect against **Anthracycline-induced cardiotoxicity** (e.g., Doxorubicin). * **Filgrastim:** A recombinant **Granulocyte Colony-Stimulating Factor (G-CSF)**. It stimulates neutrophil production to prevent or treat **chemotherapy-induced neutropenia**, thereby protecting the patient from life-threatening infections. **Analysis of Incorrect Options:** * **Option B:** While **Folinic acid (Leucovorin)** is a protector (used as "Leucovorin rescue" for Methotrexate toxicity), **Folic acid** is not typically used as a protective agent in this context; in fact, it can interfere with the action of certain antifolates. * **Option C:** **Amifostine** is a protector (scavenges free radicals to prevent Cisplatin-induced nephrotoxicity), but **Acrolein** is the toxic metabolite of Cyclophosphamide that causes hemorrhagic cystitis—it is the *cause* of toxicity, not a protector. (The protector for Acrolein is **MESNA**). * **Option D:** **Sargramostim (GM-CSF)** is a protector, but **Magnesium** is a supplement used to replace losses caused by Cisplatin; it is not classified as a primary cytoprotective drug in the same category as the others. **High-Yield Clinical Pearls for NEET-PG:** * **MESNA:** Protects against Hemorrhagic Cystitis (Cyclophosphamide/Ifosfamide). * **Amifostine:** Protects against Cisplatin-induced Nephrotoxicity and Xerostomia. * **Dexrazoxane:** Also used to treat extravasation of Anthracyclines. * **Palifermin:** Keratinocyte growth factor used to prevent severe oral mucositis.

Q: Which GnRH analogue is used in the hormonal treatment of carcinoma prostate?

Goserelin. **Explanation:** **Goserelin** is a synthetic **GnRH (Gonadotropin-Releasing Hormone) agonist**. In the treatment of prostate cancer, it works via the principle of "medical castration." While acute administration causes an initial surge in LH and FSH, **chronic administration** leads to the downregulation and desensitization of GnRH receptors in the pituitary. This results in a profound decrease in LH secretion, subsequently reducing testosterone production to castrate levels, which starves the androgen-dependent prostate cancer cells. **Analysis of Incorrect Options:** * **Nilutamide:** This is a **pure androgen receptor antagonist** (anti-androgen). While used in prostate cancer, it is not a GnRH analogue. It is often co-administered with GnRH agonists to prevent the "testosterone flare" phenomenon. * **Cyproterone Acetate:** This is a **steroidal anti-androgen** with progestational activity. It inhibits androgen receptors and suppresses LH secretion, but it is not a GnRH analogue. * **Finasteride:** This is a **5-alpha reductase inhibitor** that prevents the conversion of testosterone to the more potent dihydrotestosterone (DHT). It is primarily used for Benign Prostatic Hyperplasia (BPH) and male pattern baldness, not as a primary treatment for prostate carcinoma. **High-Yield Clinical Pearls for NEET-PG:** * **The "Flare" Phenomenon:** Initial GnRH agonist use causes a transient rise in testosterone, which can worsen symptoms (e.g., bone pain, spinal cord compression). This is prevented by starting an anti-androgen (like Flutamide or Nilutamide) beforehand. * **Other GnRH Analogues:** Leuprolide, Nafarelin, and Buserelin. * **GnRH Antagonists:** Drugs like **Degarelix** and **Abarelix** block receptors immediately, achieving rapid testosterone suppression without the initial flare.

Q: Which of the following is NOT an alkylating agent?

Etoposide. **Explanation:** The correct answer is **D. Etoposide**. **1. Why Etoposide is the correct answer:** Etoposide belongs to the class of **Topoisomerase II inhibitors** (specifically, it is a semi-synthetic derivative of podophyllotoxin). Its mechanism of action involves binding to the Topoisomerase II-DNA complex, preventing the religation of DNA strands, which leads to double-strand breaks and cell death. It is not an alkylating agent. **2. Analysis of Incorrect Options (Alkylating Agents):** Alkylating agents work by attaching an alkyl group to DNA (usually at the N7 position of guanine), leading to cross-linking and strand breakage. * **Busulfan:** An **Alkyl sulfonate** used primarily in chronic myeloid leukemia (CML) and bone marrow ablation. * **Carmustine:** A **Nitrosourea**. These are highly lipid-soluble and can cross the blood-brain barrier, making them first-line for brain tumors (e.g., glioblastoma). * **Dacarbazine:** A **Triazene** derivative. It acts as a prodrug that is activated in the liver to a methylating agent, commonly used in Hodgkin’s lymphoma and melanoma. **3. High-Yield Clinical Pearls for NEET-PG:** * **Etoposide Side Effect:** Can cause secondary malignancies, specifically **Acute Myeloid Leukemia (AML)** with a short latency period. * **Busulfan Side Effect:** Classically associated with **"Busulfan Lung"** (interstitial pulmonary fibrosis) and adrenal insufficiency-like syndrome (hyperpigmentation). * **Cell Cycle Specificity:** Alkylating agents are **Cell Cycle Non-Specific (CCNS)**, whereas Etoposide is **Cell Cycle Specific (CCS)**, acting primarily in the **S and G2 phases**. * **Mnemonic for Topoisomerase Inhibitors:** **"ET"** (Etoposide/Teniposide) inhibits Topo **II**; **"Irinotecan/Topotecan"** inhibits Topo **I**.

Q: Sorafenib is most useful in which type of cancer?

Renal Cell Carcinoma (RCC). **Explanation:** **Sorafenib** is a multi-kinase inhibitor that targets several tyrosine kinases, most notably **VEGFR-2, VEGFR-3, PDGFR-beta, and Raf kinases** (specifically C-Raf and B-Raf). 1. **Why Renal Cell Carcinoma (RCC) is correct:** RCC is a highly vascular tumor often driven by the loss of the VHL (von Hippel-Lindau) gene, leading to the overproduction of VEGF. By inhibiting the VEGF receptor and the Raf/MEK/ERK signaling pathway, Sorafenib effectively inhibits angiogenesis and tumor cell proliferation. It was the first oral multi-kinase inhibitor approved for **advanced/metastatic RCC**. 2. **Analysis of Incorrect Options:** * **Hepatocellular Carcinoma (HCC):** While Sorafenib is a standard first-line treatment for advanced HCC, in the context of NEET-PG and historical pharmacology classification, it is classically associated first with **RCC**. (Note: If both are options, RCC is often the traditional textbook answer, though clinically it is vital for both). * **Glioblastoma:** The primary treatment involves surgery, radiotherapy, and **Temozolomide** (an alkylating agent). * **Multiple Myeloma:** Treatment typically involves proteasome inhibitors (**Bortezomib**), immunomodulators (**Lenalidomide**), and steroids. **High-Yield Clinical Pearls for NEET-PG:** * **Mechanism:** Dual action (Anti-angiogenic via VEGFR/PDGFR and Anti-proliferative via Raf kinase). * **Adverse Effects:** The most characteristic side effect is **Hand-Foot Skin Reaction (HFSR)**, presenting as redness, pain, and hyperkeratosis on palms and soles. It also commonly causes hypertension and fatigue. * **Other "Nibs" in RCC:** Sunitinib, Pazopanib, and Axitinib are also used. Sunitinib is often preferred as a first-line agent over Sorafenib in modern protocols.

Q: Which BCL-2 inhibitor is used in Chronic Lymphocytic Leukemia (CLL)?

Venetoclax. ### Explanation **Correct Answer: D. Venetoclax** **Mechanism and Rationale:** Venetoclax is a first-in-class, orally bioavailable, selective small-molecule inhibitor of **BCL-2 (B-cell lymphoma 2)**. BCL-2 is an anti-apoptotic protein that is frequently overexpressed in Chronic Lymphocytic Leukemia (CLL) cells. By binding to BCL-2, Venetoclax displaces pro-apoptotic proteins (like BIM), leading to mitochondrial outer membrane permeabilization, activation of caspases, and subsequent **programmed cell death (apoptosis)** of the leukemia cells. It is specifically indicated for CLL and Small Lymphocytic Lymphoma (SLL). **Analysis of Incorrect Options:** * **A. Fludarabine:** A purine analog that inhibits DNA polymerase and ribonucleotide reductase. It was historically a first-line treatment for CLL but acts as a cytotoxic antimetabolite, not a BCL-2 inhibitor. * **B. Cladribine:** Another purine analog resistant to adenosine deaminase. It is the **drug of choice for Hairy Cell Leukemia**, not primarily used for standard CLL. * **C. Pentostatin:** An adenosine deaminase inhibitor also used primarily in Hairy Cell Leukemia. **High-Yield Clinical Pearls for NEET-PG:** * **Tumor Lysis Syndrome (TLS):** Venetoclax is so potent that it can cause rapid cell death leading to severe TLS. A "ramp-up" dosing schedule and aggressive hydration/prophylaxis are mandatory. * **Resistance Mechanism:** Mutations in the BCL-2 protein (e.g., G101V) can lead to acquired resistance. * **Other "Clax" drugs:** Navitoclax is another BCL-2 inhibitor but causes dose-limiting thrombocytopenia (as it also inhibits BCL-XL, which is vital for platelet survival). Venetoclax is BCL-2 selective and spares platelets.

Q: What is the drug of choice for the treatment of gastrointestinal stromal tumors?

Imatinib mesylate. **Explanation:** **Imatinib mesylate** is the drug of choice for **Gastrointestinal Stromal Tumors (GIST)**. The underlying pathophysiology of GIST involves a gain-of-function mutation in the **c-KIT proto-oncogene** (a receptor tyrosine kinase). Imatinib acts as a potent selective inhibitor of the tyrosine kinase domain of c-KIT, as well as BCR-ABL (used in CML) and PDGFR. By blocking these receptors, it inhibits tumor cell proliferation and induces apoptosis. **Analysis of Incorrect Options:** * **Rituximab:** A monoclonal antibody against **CD20** found on B-cells. It is primarily used in Non-Hodgkin Lymphoma (NHL), Chronic Lymphocytic Leukemia (CLL), and certain autoimmune conditions. * **Anagrelide:** An orally active agent used to reduce platelet counts in patients with **Essential Thrombocythemia**. It works by inhibiting megakaryocyte maturation. * **Denileukin diftitox:** A fusion protein combining Interleukin-2 (IL-2) and diphtheria toxin. It targets the IL-2 receptor and is used for **Cutaneous T-cell lymphoma (Mycosis Fungoides)**. **High-Yield Clinical Pearls for NEET-PG:** * **Imatinib** is also the first-line treatment for **Chronic Myeloid Leukemia (CML)**, targeting the Philadelphia chromosome ($t[9;22]$ / BCR-ABL). * **Resistance:** Resistance to Imatinib in GIST often occurs due to secondary mutations in the c-KIT gene. In such cases, **Sunitinib** or **Regorafenib** are used as second-line agents. * **Adverse Effect:** A characteristic side effect of Imatinib is **periorbital edema** (fluid retention).

Q: A patient on treatment for leukemia develops chest pain, pulmonary infiltrates, and pleural effusion. What is the likely cause?

Tretinoin. ### Explanation The patient is experiencing **Differentiation Syndrome** (formerly known as Retinoic Acid Syndrome), a life-threatening complication specifically associated with **Tretinoin (All-trans Retinoic Acid - ATRA)** and Arsenic Trioxide. **1. Why Tretinoin is correct:** Tretinoin is the first-line treatment for **Acute Promyelocytic Leukemia (APL - M3)**. It works by forcing the malignant promyelocytes to differentiate into mature neutrophils. During this process, these cells release a massive amount of inflammatory cytokines and gain increased adhesion molecules, leading to pulmonary capillary leak. * **Clinical Triad:** Fever, respiratory distress (pulmonary infiltrates/pleural effusion), and weight gain (edema). * **Management:** High-dose intravenous **Dexamethasone** is the immediate treatment of choice. **2. Why other options are incorrect:** * **Daunorubicin:** An anthracycline primarily known for **cardiotoxicity** (dilated cardiomyopathy/congestive heart failure) rather than acute pulmonary infiltrates. * **Hydroxyurea:** Commonly causes myelosuppression and painful leg ulcers; it does not typically cause acute pleural effusions or pulmonary infiltrates. * **Cytarabine:** Its classic high-yield side effects include **cerebellar ataxia** and conjunctivitis. While it can cause "Ara-C lung," it is less common than Differentiation Syndrome in the context of leukemia induction. **3. High-Yield Clinical Pearls for NEET-PG:** * **APL Cytogenetics:** t(15;17) involving the PML-RARα gene. * **Differentiation Syndrome Timing:** Usually occurs within the first 2–21 days of starting ATRA. * **Prophylaxis:** If the initial WBC count is high (>5,000–10,000/µL), steroids are often started prophylactically. * **Other ATRA Side Effects:** Pseudotumor cerebri (idiopathic intracranial hypertension) and dry skin/mucosa.

Q: Hand and foot syndrome can be caused by which of the following agents?

Capecitabine. **Explanation:** **Hand-Foot Syndrome (HFS)**, also known as **Palmar-Plantar Erythrodysesthesia**, is a distinct dermatological toxicity characterized by redness, swelling, and pain on the palms and soles. 1. **Why Capecitabine is correct:** Capecitabine is an oral prodrug of **5-Fluorouracil (5-FU)**. It is the most common agent associated with HFS. The underlying mechanism involves the high levels of the enzyme **thymidine phosphorylase** in the skin of palms and soles, which converts the prodrug into active 5-FU, leading to localized cytotoxic damage. Other drugs frequently causing HFS include **5-FU (infusion)** and **Liposomal Doxorubicin**. 2. **Why other options are incorrect:** * **Cisplatin:** Primarily known for **nephrotoxicity** (prevented by amifostine/hydration) and **ototoxicity**. * **Vincristine:** Characterized by **peripheral neuropathy** (stocking-glove pattern) and autonomic dysfunction (constipation/paralytic ileus). It is notably bone marrow sparing. * **Mitomycin-C:** Associated with **Delayed Myelosuppression** and **Hemolytic Uremic Syndrome (HUS)**. **High-Yield Clinical Pearls for NEET-PG:** * **Management of HFS:** Dose reduction/interruption and topical emollients (Urea cream) or Pyridoxine (Vitamin B6). * **Hand-Foot Skin Reaction (HFSR):** Distinct from HFS; it presents with hyperkeratosis/calluses and is caused by **Tyrosine Kinase Inhibitors (TKIs)** like **Sorafenib** and **Sunitinib**. * **5-FU Toxicity:** Deficiency of the enzyme **DPD (Dihydropyrimidine dehydrogenase)** increases the risk of severe toxicity.

Q: Pemetrexed, a drug useful in breast cancer, belongs to which of the following categories?

Antimetabolite. **Explanation:** **Pemetrexed** is a multi-targeted **antimetabolite** (Option D). Antimetabolites are cell-cycle specific drugs that act primarily during the **S-phase** by interfering with DNA and RNA synthesis. Pemetrexed works by inhibiting three key enzymes involved in folate metabolism: 1. **Thymidylate synthase (TS)** 2. **Dihydrofolate reductase (DHFR)** 3. **Glycinamide ribonucleotide formyltransferase (GARFT)** By inhibiting these enzymes, it prevents the formation of precursor purine and pyrimidine nucleotides, thereby halting DNA synthesis and inducing apoptosis in cancer cells. **Why other options are incorrect:** * **A. Antitumor agents (Antibiotics):** These are derived from microorganisms (e.g., Doxorubicin, Bleomycin) and typically act by intercalating DNA or causing strand breaks, not by mimicking metabolites. * **B. Alkylating agents:** These drugs (e.g., Cyclophosphamide, Cisplatin) work by forming covalent bonds with DNA, leading to cross-linking and strand breakage. They are cell-cycle non-specific. * **C. Hormonal agents:** These include Tamoxifen or Anastrozole, which modulate hormone receptors or synthesis in hormone-dependent cancers. **High-Yield Clinical Pearls for NEET-PG:** * **Indications:** Primarily used in **Malignant Pleural Mesothelioma** (in combination with Cisplatin) and **Non-Small Cell Lung Cancer (NSCLC)**. * **Toxicity Management:** To reduce hematologic and GI toxicity, patients must be pre-treated with **Vitamin B12 and Folic Acid** supplementation. * **Skin Reactions:** Dexamethasone is often co-administered to prevent pemetrexed-induced cutaneous rashes.

Q: Which of the following anticancer drugs is excreted by the lungs?

5-Fluorouracil. **Explanation:** **Correct Answer: A. 5-Fluorouracil (5-FU)** 5-Fluorouracil is a pyrimidine analog that undergoes extensive hepatic metabolism. The rate-limiting enzyme, **dihydropyrimidine dehydrogenase (DPD)**, converts 5-FU into dihydrofluorouracil [1]. Ultimately, it is broken down into **carbon dioxide (CO₂)**, urea, and α-fluoro-β-alanine. The CO₂ produced during this metabolic degradation is primarily **excreted through the lungs**. This unique pharmacokinetic property is the basis for the "13C-FU breath test" used to assess DPD activity in patients. **Analysis of Incorrect Options:** * **B. Cyclophosphamide:** This alkylating agent is a prodrug activated by hepatic CYP450 enzymes. Its metabolites, including the toxic byproduct **acrolein** (which causes hemorrhagic cystitis), are primarily excreted via the **kidneys**. * **C. Doxorubicin:** This anthracycline antibiotic is metabolized by the liver and is predominantly excreted via the **biliary system** (feces). Dose adjustment is required in patients with hepatic dysfunction. * **D. Cisplatin:** This platinum compound is cleared almost exclusively by the **kidneys** through glomerular filtration and tubular secretion [2]. It is notorious for causing nephrotoxicity. **High-Yield Clinical Pearls for NEET-PG:** * **DPD Deficiency:** Patients with a genetic deficiency of dihydropyrimidine dehydrogenase (DPD) are at high risk for severe, life-threatening toxicity (mucositis, myelosuppression) when given 5-FU. * **Hand-Foot Syndrome:** A common dermatological side effect associated with 5-FU and its oral prodrug, Capecitabine. * **Rescue Agent:** **Uridine triacetate** is the specific antidote for 5-FU overdose or toxicity.

Question 1

Which pair of drugs acts as protectors during cancer chemotherapy?

Accepted Answer

Dexrazoxane and Filgrastim

Answer

Folinic acid and Folic acid

Answer

Amifostine and Acrolein

Answer

Magnesium and Sargramostim

Question 2

Which GnRH analogue is used in the hormonal treatment of carcinoma prostate?

Accepted Answer

Goserelin

Answer

Nilutamide

Answer

Cyproterone acetate

Answer

Finasteride

Question 3

Which of the following is NOT an alkylating agent?

Accepted Answer

Etoposide

Answer

Busulfan

Answer

Carmustine

Answer

Dacarbazine

Question 4

Sorafenib is most useful in which type of cancer?

Accepted Answer

Renal Cell Carcinoma (RCC)

Answer

Hepatocellular Carcinoma (Hepatoma)

Answer

Glioblastoma

Answer

Multiple Myeloma

Question 5

Which BCL-2 inhibitor is used in Chronic Lymphocytic Leukemia (CLL)?

Accepted Answer

Venetoclax

Answer

Fludarabine

Answer

Cladribine

Answer

Pentostatin

Question 6

What is the drug of choice for the treatment of gastrointestinal stromal tumors?

Accepted Answer

Imatinib mesylate

Answer

Rituximab

Answer

Anagrelide

Answer

Denileukin diftitox

Question 7

A patient on treatment for leukemia develops chest pain, pulmonary infiltrates, and pleural effusion. What is the likely cause?

Accepted Answer

Tretinoin

Answer

Daunorubicin

Answer

Hydroxyurea

Answer

Cytarabine

Question 8

Hand and foot syndrome can be caused by which of the following agents?

Accepted Answer

Capecitabine

Answer

Cisplatin

Answer

Vincristine

Answer

Mitomycin-C

Question 9

Pemetrexed, a drug useful in breast cancer, belongs to which of the following categories?

Accepted Answer

Antimetabolite

Answer

Antitumor agent

Answer

Alkylating agent

Answer

Hormonal agent

Question 10

Which of the following anticancer drugs is excreted by the lungs?

Accepted Answer

5-Fluorouracil

Answer

Cyclophosphamide

Answer

Doxorubicin

Answer

Cisplatin

Anticancer Drugs — MCQs

Anticancer Drugs — MCQs

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