Anticancer Drugs — MCQs

Anticancer Drugs Indian Medical PG Practice Questions and MCQs

Question 171: What is the primary treatment for neutropenia that occurs after chemotherapy?

A. Leucovorin
B. Filgrastim (Correct Answer)
C. Ondansetron
D. Darbepoetin

Explanation: **Explanation:** **Correct Answer: B. Filgrastim** Chemotherapy-induced neutropenia is a common dose-limiting toxicity. **Filgrastim** is a recombinant **Granulocyte Colony-Stimulating Factor (G-CSF)**. It works by binding to specific receptors on hematopoietic cells, stimulating the proliferation, differentiation, and activation of neutrophils. It is used both as prophylaxis (to prevent febrile neutropenia) and as treatment to accelerate bone marrow recovery after cytotoxic therapy. **Analysis of Incorrect Options:** * **A. Leucovorin (Folinic Acid):** This is a reduced form of folic acid. It is primarily used as a "rescue" agent after high-dose **Methotrexate** therapy to provide a source of folate for healthy cells, or to enhance the efficacy of **5-Fluorouracil** in colorectal cancer. * **C. Ondansetron:** This is a **5-HT3 receptor antagonist** used as an antiemetic to prevent chemotherapy-induced nausea and vomiting (CINV). It has no effect on blood cell counts. * **D. Darbepoetin:** This is a long-acting **erythropoiesis-stimulating agent (ESA)**. It is used to treat chemotherapy-induced **anemia**, not neutropenia, by stimulating red blood cell production. **NEET-PG High-Yield Pearls:** * **Sargramostim** is a recombinant **GM-CSF** (Granulocyte-Macrophage CSF) which stimulates both neutrophils and macrophages. * **Pegfilgrastim** is the pegylated (long-acting) version of Filgrastim, requiring less frequent dosing. * **Common Side Effect:** The most frequent side effect of G-CSF therapy is **bone pain** (due to marrow expansion). * **Timing:** G-CSF should generally not be administered within 24 hours before or after chemotherapy to avoid sensitizing rapidly dividing myeloid cells to the cytotoxic drugs.

Question 172: Which pair of drugs acts as protectors during cancer chemotherapy?

A. Dexrazoxane and Filgrastim (Correct Answer)
B. Folinic acid and Folic acid
C. Amifostine and Acrolein
D. Magnesium and Sargramostim

Explanation: **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.

Question 173: Which GnRH analogue is used in the hormonal treatment of carcinoma prostate?

A. Goserelin (Correct Answer)
B. Nilutamide
C. Cyproterone acetate
D. Finasteride

Explanation: **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.

Question 174: Medical adrenalectomy can be done by:

A. Vincristine
B. Vinblastine
C. Mitotane (Correct Answer)
D. Methotrexate

Explanation: ### Explanation **Correct Answer: C. Mitotane** **Mechanism and Rationale:** Mitotane is a cytotoxic drug chemically related to the insecticide DDT. It is specifically used for **medical adrenalectomy** because it exerts a selective **adrenolytic** effect on the adrenal cortex. It causes atrophy and destruction of the *zona fasciculata* and *zona reticularis*, leading to a rapid reduction in adrenocortical hormone synthesis. **Clinical Use:** It is primarily indicated for the treatment of inoperable or metastatic **adrenocortical carcinoma** and occasionally for refractory Cushing’s syndrome. --- ### Why the other options are incorrect: * **Vincristine & Vinblastine (Options A & B):** These are **Vinca alkaloids** that act as spindle poisons by binding to tubulin and inhibiting microtubule polymerization. Vincristine is known for peripheral neuropathy, while Vinblastine is known for bone marrow suppression. Neither has a specific affinity for adrenal tissue. * **Methotrexate (Option D):** This is an **antimetabolite** (folate antagonist) that inhibits dihydrofolate reductase (DHFR). It is used for various malignancies (leukemias, choriocarcinoma) and autoimmune conditions (RA, psoriasis), but it does not cause adrenal destruction. --- ### NEET-PG High-Yield Pearls: * **Medical Adrenalectomy Agents:** Apart from Mitotane (which is cytotoxic/adrenolytic), other drugs used to suppress adrenal function include **Ketoconazole** (inhibits 17α-hydroxylase and 11β-hydroxylase), **Metyrapone** (selective 11β-hydroxylase inhibitor), and **Aminoglutethimide**. * **Mitotane Side Effect:** It is highly lipid-soluble and can cause significant GI distress and neurological symptoms (lethargy, dizziness). * **Replacement Therapy:** Patients undergoing medical adrenalectomy with Mitotane usually require lifelong glucocorticoid and mineralocorticoid replacement.

Question 175: Which of the following acts on both Her-1 and Her-2 receptors?

A. Imatinib
B. Erlotinib
C. Lapatinib (Correct Answer)
D. Gefitinib

Explanation: **Explanation:** **Lapatinib** is the correct answer because it is a **dual tyrosine kinase inhibitor (TKI)**. It reversibly inhibits both **HER-1** (also known as Epidermal Growth Factor Receptor - EGFR) and **HER-2** (ErbB2). By binding to the intracellular ATP-binding domain of these receptors, it prevents autophosphorylation and subsequent downstream signaling pathways that drive tumor cell proliferation. It is primarily used in the management of HER-2 positive advanced or metastatic breast cancer. **Analysis of Incorrect Options:** * **Imatinib (A):** This is the first-line TKI for Chronic Myeloid Leukemia (CML). It targets **BCR-ABL**, c-KIT, and PDGFR, but has no significant activity against HER-1 or HER-2. * **Erlotinib (B) and Gefitinib (D):** These are **selective HER-1 (EGFR) inhibitors**. They are used primarily in Non-Small Cell Lung Cancer (NSCLC) with EGFR mutations. They do not inhibit HER-2. **High-Yield Clinical Pearls for NEET-PG:** * **Lapatinib** is unique because it can cross the **blood-brain barrier**, making it useful for treating brain metastases in HER-2 positive breast cancer. * **Trastuzumab** also targets HER-2 but is a monoclonal antibody (extracellular) rather than a TKI (intracellular). Unlike Lapatinib, Trastuzumab is associated with significant cardiotoxicity. * **Afatinib** is another dual inhibitor (irreversible) often tested alongside Lapatinib. * **Side Effect Profile:** Lapatinib commonly causes diarrhea and skin rash (acneiform), which is a class effect of EGFR inhibitors.

Question 176: Which of the following is NOT an alkylating agent?

A. Busulfan
B. Carmustine
C. Dacarbazine
D. Etoposide (Correct Answer)

Explanation: **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**.

Question 177: What is true about Biclutamide?

A. Binds to androgen receptor
B. Causes gynecomastia
C. It can be given as monotherapy in prostatic carcinoma
D. All are true (Correct Answer)

Explanation: **Explanation:** **Bicalutamide** is a potent, non-steroidal **competitive androgen receptor antagonist**. It is a second-generation anti-androgen widely used in the management of prostate cancer. * **Option A (Binds to androgen receptor):** Bicalutamide works by competitively inhibiting the binding of dihydrotestosterone (DHT) and testosterone to the nuclear androgen receptors in the prostate gland. This prevents the transcription of genes required for the growth and survival of prostatic cancer cells. * **Option B (Causes gynecomastia):** Unlike GnRH agonists, pure anti-androgens like Bicalutamide do not decrease LH levels; in fact, they may cause a reactive increase in LH and testosterone. This excess testosterone is peripherally aromatized into estrogen, leading to **gynecomastia** and breast pain in approximately 40-70% of patients. * **Option C (Monotherapy in prostatic carcinoma):** While often used as part of **Combined Androgen Blockade (CAB)** alongside GnRH analogs (to prevent the initial "testosterone flare"), Bicalutamide is also FDA-approved as monotherapy for localized or locally advanced prostate cancer as an alternative to surgical or medical castration. **High-Yield Clinical Pearls for NEET-PG:** * **Superiority:** Bicalutamide is preferred over **Flutamide** because it has a longer half-life (allowing once-daily dosing) and significantly **lower hepatotoxicity**. * **Enzalutamide:** A newer, more potent "second-generation" agent that also inhibits androgen receptor translocation to the nucleus. * **Side Effects:** Apart from gynecomastia, it can cause hot flashes and mild elevation in liver enzymes. Unlike Flutamide, it rarely causes diarrhea.

Question 178: Sorafenib is most useful in which type of cancer?

A. Renal Cell Carcinoma (RCC) (Correct Answer)
B. Hepatocellular Carcinoma (Hepatoma)
C. Glioblastoma
D. Multiple Myeloma

Explanation: **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.

Question 179: Which of the following tyrosine kinase inhibitors is used in carcinoma of the lung?

A. Afatinib
B. Ceritinib
C. Erlotinib
D. All of the above (Correct Answer)

Explanation: The correct answer is **D. All of the above**. Tyrosine Kinase Inhibitors (TKIs) are a mainstay in the management of Non-Small Cell Lung Cancer (NSCLC), specifically targeting driver mutations like EGFR and ALK [1]. 1. **Erlotinib (Option C):** This is a **1st generation EGFR TKI**. It reversibly inhibits the Epidermal Growth Factor Receptor (EGFR). It is used as a first-line treatment for NSCLC patients harboring EGFR exon 19 deletions or exon 21 (L858R) substitution mutations [2, 3]. 2. **Afatinib (Option A):** This is a **2nd generation EGFR TKI**. Unlike Erlotinib, it is an **irreversible** inhibitor of the ErbB family (EGFR/HER1, HER2, and HER4). It is indicated for first-line treatment of metastatic NSCLC with non-resistant EGFR mutations. 3. **Ceritinib (Option B):** This is a **2nd generation ALK (Anaplastic Lymphoma Kinase) inhibitor**. It is used in patients with ALK-positive metastatic NSCLC, particularly those who have progressed on or are intolerant to Crizotinib. **High-Yield Clinical Pearls for NEET-PG:** * **EGFR Inhibitors Side Effects:** The most common side effect is an **acneiform skin rash** and diarrhea [3]. Interestingly, the appearance of the rash often correlates with a better therapeutic response. * **Osimertinib:** A 3rd generation TKI used specifically for the **T790M resistance mutation**. * **ALK Inhibitors:** Crizotinib (1st gen), Ceritinib/Alectinib/Brigatinib (2nd gen), and Lorlatinib (3rd gen). * **Gefitinib:** Another 1st generation EGFR TKI frequently used in lung cancer [1].

Question 180: Which BCL-2 inhibitor is used in Chronic Lymphocytic Leukemia (CLL)?

A. Fludarabine
B. Cladribine
C. Pentostatin
D. Venetoclax (Correct Answer)

Explanation: ### 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.

Practice by Chapter

Principles of Cancer Chemotherapy

Practice Questions

Alkylating Agents

Practice Questions

Antimetabolites

Practice Questions

Antitumor Antibiotics

Practice Questions

Plant Alkaloids

Practice Questions

Topoisomerase Inhibitors

Practice Questions

Hormonal Agents

Practice Questions

Targeted Therapy

Practice Questions

Immunotherapy

Practice Questions

Management of Chemotherapy Side Effects

Practice Questions

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