Anticancer Drugs Practice Questions

Q: "Radiation recall syndrome" is seen with all of the following except?

Bleomycin. **Explanation:** **Radiation Recall Syndrome (RRS)** is an inflammatory skin reaction that occurs in a previously irradiated area after the administration of certain cytotoxic drugs. It represents a "latent" radiation injury triggered by chemotherapy, even months or years after radiotherapy. **Why Bleomycin is the correct answer:** While **Bleomycin** is notorious for causing pulmonary fibrosis and skin hyperpigmentation (flagellate dermatitis), it is **not** typically associated with Radiation Recall Syndrome. In contrast, the other options are classic triggers for this phenomenon. **Analysis of other options:** * **Actinomycin D (Dactinomycin):** This is the most common and potent inducer of radiation recall. It is frequently tested in exams as the classic cause. * **Doxorubicin & Daunorubicin:** These Anthracyclines are well-documented triggers for RRS. They are potent radiosensitizers and can cause severe inflammatory reactions in previously treated skin or internal organs (like the esophagus or lungs). **Clinical Pearls for NEET-PG:** * **Common Triggers:** The "Big Three" for RRS are **Actinomycin D, Anthracyclines (Doxorubicin), and Taxanes (Paclitaxel).** Other triggers include Methotrexate and Gemcitabine. * **Clinical Presentation:** It mimics a severe sunburn (erythema, edema, blistering) localized strictly to the previous radiation field. * **Management:** Treatment involves stopping the offending drug and administering corticosteroids. * **High-Yield Distinction:** Do not confuse *Radiation Recall* (occurs after radiation) with *Radiosensitization* (occurs when drug and radiation are given concurrently). Bleomycin is a radiosensitizer but not a recall agent.

Q: Which of the following is used in the treatment of urinary bladder carcinoma?

Bacillus Calmette-Guérin (BCG). **Explanation:** The correct answer is **Bacillus Calmette-Guérin (BCG)**. **Why BCG is correct:** BCG is a live-attenuated strain of *Mycobacterium bovis*. In oncology, it is the gold standard for **intravesical immunotherapy** in patients with non-muscle invasive bladder cancer (NMIBC), particularly high-grade tumors and Carcinoma in situ (CIS). When instilled into the bladder, BCG triggers a local inflammatory response and a robust T-cell mediated immune reaction (Th1 response). This immune activation leads to the destruction of malignant cells by cytotoxic T lymphocytes and natural killer (NK) cells. **Why the other options are incorrect:** * **5-Fluorouracil (5FU):** An antimetabolite (pyrimidine analog) primarily used for colorectal, breast, and head/neck cancers. While used topically for actinic keratosis, it is not a standard treatment for bladder carcinoma. * **Cyclophosphamide:** An alkylating agent used for various malignancies (lymphomas, leukemia). Paradoxically, it is a **risk factor** for bladder cancer because its metabolite, **Acrolein**, causes hemorrhagic cystitis and chronic urothelial irritation. * **6-Mercaptopurine:** A purine analog used mainly in the maintenance therapy of Acute Lymphoblastic Leukemia (ALL). It has no role in bladder cancer management. **High-Yield Clinical Pearls for NEET-PG:** * **Acrolein Toxicity:** To prevent hemorrhagic cystitis caused by Cyclophosphamide, patients are given **MESNA** (2-Mercaptoethane sulfonate Na) and aggressive hydration. * **BCG Contraindications:** It should not be used in patients with gross hematuria, traumatic catheterization, or immunosuppression due to the risk of systemic BCG-osis (sepsis). * **Other Intravesical Agents:** If BCG fails or is unavailable, **Mitomycin C** or **Gemcitabine** are alternative intravesical chemotherapeutic agents used for bladder cancer.

Q: Which one of the following drugs is a Topoisomerase 1 inhibitor?

Irinotecan. **Explanation:** The correct answer is **Irinotecan**. **1. Mechanism of Action (Topoisomerase I Inhibitors):** Topoisomerase I is an enzyme responsible for creating single-strand breaks in DNA to relieve torsional strain during replication. Drugs like **Irinotecan** and **Topotecan** (derivatives of Camptothecin) bind to the DNA-topoisomerase I complex, preventing the religation of these single-strand breaks. This leads to lethal double-strand DNA damage and cell death. **2. Analysis of Incorrect Options:** * **Doxorubicin:** An anthracycline antibiotic that inhibits **Topoisomerase II**, intercalates DNA, and generates free radicals. * **Etoposide:** A podophyllotoxin derivative that specifically inhibits **Topoisomerase II**, leading to double-strand DNA breaks. * **Vincristine:** A Vinca alkaloid that inhibits **microtubule polymerization** by binding to tubulin, causing mitotic arrest in the M-phase. **3. High-Yield Clinical Pearls for NEET-PG:** * **Irinotecan Side Effects:** Known for causing severe **diarrhea**. * *Early-onset:* Occurs within 24 hours (cholinergic crisis); treated with **Atropine**. * *Late-onset:* Occurs after 24 hours; treated with **Loperamide**. * **Pharmacogenomics:** Patients with **UGT1A1*28 polymorphism** (Gilbert syndrome) are at a higher risk of severe toxicity from Irinotecan due to impaired glucuronidation of its active metabolite, SN-38. * **Mnemonic:** Remember **"I"** for **I**rinotecan and Topoisomerase **I**. Remember **"E"**toposide and **"D"**oxorubicin for Topoisomerase **II** (Two).

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.

Question 1

"Radiation recall syndrome" is seen with all of the following except?

Accepted Answer

Bleomycin

Answer

Actinomycin

Answer

Doxorubicin

Answer

Daunorubicin

Question 2

Which of the following is used in the treatment of urinary bladder carcinoma?

Accepted Answer

Bacillus Calmette-Guérin (BCG)

Answer

5-Fluorouracil (5FU)

Answer

Cyclophosphamide

Answer

6-Mercaptopurine

Question 3

Which one of the following drugs is a Topoisomerase 1 inhibitor?

Accepted Answer

Irinotecan

Answer

Doxorubicin

Answer

Etoposide

Answer

Vincristine

Question 4

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 5

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

Accepted Answer

Goserelin

Answer

Nilutamide

Answer

Cyproterone acetate

Answer

Finasteride

Question 6

Which of the following is NOT an alkylating agent?

Accepted Answer

Etoposide

Answer

Busulfan

Answer

Carmustine

Answer

Dacarbazine

Question 7

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 8

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

Accepted Answer

Venetoclax

Answer

Fludarabine

Answer

Cladribine

Answer

Pentostatin

Question 9

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 10

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

Anticancer Drugs — MCQs

Anticancer Drugs — MCQs

On this page

Practice by Chapter

Want unlimited practice?