Anticancer Drugs — MCQs
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Which of the following is an antimitotic drug of plant origin?
What is lxabepilone?
Which of the following anticancer drugs is cell cycle specific?
Which of the following is an anti HER 2/neu antibody?
What is the most important dose-limiting toxicity of cancer chemotherapy?
All of the following can potentially be cured by chemotherapy, except?
Which drug is used for HER-2/neu positive breast cancer?
Which of the following drugs does not act on tubulin?
What is the drug of choice for palliative treatment of pancreatic carcinoma?
Which of the following drugs is used in the management of estrogen receptor-positive breast cancer?
Anticancer Drugs Indian Medical PG Practice Questions and MCQs
Question 71: Which of the following is an antimitotic drug of plant origin?
- A. Vincristine (Correct Answer)
- B. Isotretinoin
- C. Bleomycin
- D. Methotrexate
Explanation: **Explanation:** **Vincristine** is the correct answer because it is a natural alkaloid derived from the **Periwinkle plant (*Vinca rosea*)**. It functions as an **antimitotic agent** by binding to tubulin, preventing the polymerization of microtubules. This inhibits the formation of the mitotic spindle, leading to cell cycle arrest in the **M-phase**. **Analysis of Incorrect Options:** * **Isotretinoin:** A retinoid (Vitamin A derivative) primarily used in severe acne. While retinoids are used in some cancers (like APL), it is not an antimitotic drug of plant origin. * **Bleomycin:** An antitumor antibiotic derived from the bacterium *Streptomyces verticillus*. It acts by inducing DNA strand breaks through free radical formation (G2 phase specific), not by inhibiting mitosis. * **Methotrexate:** An antimetabolite that acts as a **dihydrofolate reductase (DHFR) inhibitor**. It is cell cycle-specific for the **S-phase** and is a synthetic compound, not plant-derived. **High-Yield Clinical Pearls for NEET-PG:** 1. **Vinca Alkaloids vs. Taxanes:** Both are plant-derived antimitotics. Vincas (Vincristine, Vinblastine) **inhibit polymerization**, while Taxanes (Paclitaxel, Docetaxel) **inhibit depolymerization** ("freeze" the spindle). 2. **Dose-Limiting Toxicity:** The major side effect of Vincristine is **peripheral neuropathy** (paresthesia, loss of reflexes), whereas Vinblastine is more associated with **bone marrow suppression** ("Blast" the marrow). 3. **Vincristine is "Bone Marrow Sparing":** It is a preferred component in regimens like MOPP or CHOP because it causes minimal myelosuppression.
Question 72: What is lxabepilone?
- A. lxabepilone
- B. Antineoplastic (Correct Answer)
- C. Antidiarrheal
- D. Antihelminth
Explanation: **Explanation:** **Ixabepilone** is a semi-synthetic analog of epothilone B, a class of cytotoxic agents derived from the myxobacterium *Sorangium cellulosum*. It is classified as an **antineoplastic (anticancer) agent**. **Mechanism of Action:** Ixabepilone works by binding directly to **β-tubulin subunits**, leading to the stabilization of microtubules and inhibition of microtubule dynamics. This action arrests the cell cycle at the **G2-M phase**, ultimately inducing apoptosis. While its mechanism is similar to taxanes (like Paclitaxel), Ixabepilone is unique because it remains active in cells that have developed resistance to taxanes, often due to its low affinity for the P-glycoprotein efflux pump. **Analysis of Options:** * **Option B (Correct):** As a microtubule stabilizer used primarily in the treatment of metastatic or locally advanced **breast cancer** (especially those resistant to anthracyclines and taxanes), it is a potent antineoplastic agent. * **Option C (Incorrect):** It has no role in treating diarrhea; in fact, gastrointestinal upset is a potential side effect. * **Option D (Incorrect):** While some microtubule inhibitors (like Benzimidazoles) are anthelmintics, Ixabepilone is specifically designed for human oncology. **High-Yield Clinical Pearls for NEET-PG:** * **Indication:** Approved for advanced breast cancer as monotherapy or in combination with **Capecitabine**. * **Resistance Profile:** Effective in taxane-resistant tumors because it is not a substrate for the **MDR-1 (P-glycoprotein)** efflux pump. * **Side Effects:** The dose-limiting toxicity is **peripheral sensory neuropathy** and neutropenia.
Question 73: Which of the following anticancer drugs is cell cycle specific?
- A. Ifosfamide
- B. Melphalan
- C. Vinblastine (Correct Answer)
- D. Cyclophosphamide
Explanation: ### Explanation Anticancer drugs are broadly classified into two categories based on their relationship with the cell cycle: **Cell Cycle-Specific (CCS)** drugs, which act on cells during a particular phase (e.g., M or S phase), and **Cell Cycle-Nonspecific (CCNS)** drugs, which act on both cycling and resting cells. **Why Vinblastine is Correct:** Vinblastine is a **Vinca alkaloid** that acts specifically during the **M-phase (Mitosis)**. Its mechanism involves binding to tubulin and inhibiting its polymerization into microtubules. This prevents the formation of the mitotic spindle, leading to mitotic arrest in metaphase and subsequent cell death. Because it targets a specific event (mitosis), it is a classic CCS agent. **Why the Other Options are Incorrect:** * **A, B, and D (Ifosfamide, Melphalan, Cyclophosphamide):** These are all **Alkylating Agents** (Nitrogen mustards). Alkylating agents work by forming covalent bonds with DNA, leading to cross-linking and strand breaks. This damage occurs regardless of whether the cell is in a specific phase of the cycle; therefore, they are classified as **Cell Cycle-Nonspecific (CCNS)**. **High-Yield NEET-PG Pearls:** * **M-Phase Specific Drugs:** Vinca alkaloids (Vinblastine, Vincristine) and Taxanes (Paclitaxel, Docetaxel). * **S-Phase Specific Drugs:** Antimetabolites (Methotrexate, 5-FU, Cytarabine) and Topoisomerase inhibitors (Etoposide). * **G2-Phase Specific:** Bleomycin. * **Clinical Distinction:** Vinblastine is primarily associated with **bone marrow suppression** (Blast = Bone marrow), whereas Vincristine is more notorious for **peripheral neuropathy** (Cristine = CNS/Nerve).
Question 74: Which of the following is an anti HER 2/neu antibody?
- A. Bevacizumab
- B. Trastuzumab (Correct Answer)
- C. Rituximab
- D. Abciximab
Explanation: **Explanation:** **Trastuzumab** is a recombinant DNA-derived humanized monoclonal antibody that selectively binds to the extracellular domain of the **Human Epidermal Growth Factor Receptor 2 (HER2/neu)**. This receptor is a proto-oncogene with tyrosine kinase activity, overexpressed in approximately 20–30% of breast cancers. By binding to HER2, Trastuzumab inhibits ligand-independent signaling, prevents receptor shedding, and induces antibody-dependent cellular cytotoxicity (ADCC), thereby inhibiting tumor cell proliferation. **Analysis of Incorrect Options:** * **Bevacizumab:** A monoclonal antibody directed against **VEGF** (Vascular Endothelial Growth Factor). It acts as an angiogenesis inhibitor used in colorectal, lung, and renal cell carcinomas. * **Rituximab:** A chimeric monoclonal antibody against the **CD20** antigen found on the surface of B-lymphocytes. It is primarily used in Non-Hodgkin Lymphoma (NHL) and Chronic Lymphocytic Leukemia (CLL). * **Abciximab:** A glycoprotein **IIb/IIIa receptor antagonist**. It is an antiplatelet agent used to prevent ischemic complications during percutaneous coronary intervention (PCI). **High-Yield Clinical Pearls for NEET-PG:** * **Cardiotoxicity:** The most significant side effect of Trastuzumab is cardiomyopathy (manifesting as a decrease in Left Ventricular Ejection Fraction). Unlike anthracyclines, this cardiotoxicity is usually **reversible** and not dose-dependent. * **Combination Therapy:** It should **not** be administered concurrently with Doxorubicin due to synergistic cardiotoxicity. * **Other HER2 Inhibitors:** **Pertuzumab** (inhibits dimerization) and **Lapatinib** (a small molecule dual tyrosine kinase inhibitor of both EGFR and HER2).
Question 75: What is the most important dose-limiting toxicity of cancer chemotherapy?
- A. Gastrointestinal toxicity
- B. Neurotoxicity
- C. Bone marrow suppression (Correct Answer)
- D. Nephrotoxicity
Explanation: **Explanation:** **Bone marrow suppression (Myelosuppression)** is the most common and significant dose-limiting toxicity for the majority of cytotoxic anticancer drugs. Most chemotherapeutic agents act by inhibiting rapidly dividing cells. Since hematopoietic stem cells in the bone marrow have a high turnover rate, they are highly susceptible to DNA damage. This leads to leukopenia (increasing infection risk), thrombocytopenia (increasing bleeding risk), and anemia. If the blood counts fall below a critical threshold, the next dose of chemotherapy must be delayed or reduced, directly limiting the intensity of treatment. **Analysis of Incorrect Options:** * **Gastrointestinal toxicity:** While very common (nausea, vomiting, mucositis), it is usually manageable with antiemetics (like Ondansetron) and rarely necessitates stopping treatment compared to life-threatening neutropenia. * **Neurotoxicity:** This is a specific dose-limiting toxicity for certain drugs (e.g., Vincristine, Cisplatin, Paclitaxel) but is not the "most common" across the entire class of chemotherapy. * **Nephrotoxicity:** This is primarily associated with specific agents like Cisplatin or Methotrexate. It is prevented with aggressive hydration and is not the universal dose-limiting factor for most regimens. **High-Yield Clinical Pearls for NEET-PG:** * **Exceptions:** Drugs that are **NOT** typically bone marrow suppressants include **Vincristine, Bleomycin, Cisplatin, and L-Asparaginase.** * **Nadir:** The point of lowest blood cell count, usually occurring 7–14 days after chemotherapy. * **Rescue Agents:** Filgrastim (G-CSF) is used to manage chemotherapy-induced neutropenia, allowing for maintained dosing schedules.
Question 76: All of the following can potentially be cured by chemotherapy, except?
- A. Hodgkin's lymphoma
- B. Acute lymphoblastic leukemia (ALL)
- C. Wilms' tumor
- D. Chondrosarcoma (Correct Answer)
Explanation: **Explanation:** The core concept behind the curability of cancers with chemotherapy lies in the **Growth Fraction**. Chemotherapeutic agents primarily target rapidly dividing cells. Cancers with a high growth fraction (fast-growing) are generally highly chemosensitive, whereas slow-growing tumors with a low growth fraction are often chemoresistant. **Why Chondrosarcoma is the Correct Answer:** Chondrosarcoma is a malignant tumor of cartilage. It is characterized by a **low growth fraction**, slow progression, and poor vascularity. These tumors are notoriously **resistant to both chemotherapy and radiotherapy**. The primary and often only curative treatment modality for chondrosarcoma is wide surgical excision. **Analysis of Incorrect Options:** * **Hodgkin’s Lymphoma:** One of the biggest success stories in oncology. With regimens like ABVD (Adriamycin, Bleomycin, Vinblastine, Dacarbazine), it has a very high cure rate (up to 80-90%). * **Acute Lymphoblastic Leukemia (ALL):** This is a highly aggressive, fast-growing malignancy. Because the cells divide rapidly, they are exquisitely sensitive to chemotherapy. It is potentially curable, especially in the pediatric population. * **Wilms’ Tumor (Nephroblastoma):** A common pediatric renal tumor that is highly responsive to a combination of surgery and chemotherapy (e.g., Actinomycin D and Vincristine), boasting high survival and cure rates. **NEET-PG High-Yield Pearls:** 1. **Highly Chemocurable Tumors:** Choriocarcinoma (most sensitive), Hodgkin’s Lymphoma, ALL, Wilms’ Tumor, Germ cell tumors (Testicular cancer), and Burkitt’s Lymphoma. 2. **Chemoresistant Tumors:** Chondrosarcoma, Pancreatic Cancer, Malignant Melanoma, and Renal Cell Carcinoma (RCC). 3. **Gompertzian Growth:** As tumors grow larger, their growth fraction decreases, making them less sensitive to chemotherapy; hence, early intervention is key.
Question 77: Which drug is used for HER-2/neu positive breast cancer?
- A. Imatinib
- B. Trastuzumab (Correct Answer)
- C. Erlotinib
- D. Cetuximab
Explanation: ### Explanation **Correct Answer: B. Trastuzumab** **Mechanism and Rationale:** Trastuzumab is a recombinant humanized monoclonal antibody specifically designed to target the **HER-2/neu (ErbB2)** receptor, a member of the Epidermal Growth Factor Receptor (EGFR) family. Approximately 20–30% of breast cancers overexpress this receptor, leading to aggressive tumor growth and poor prognosis. Trastuzumab binds to the extracellular domain of HER-2, inducing cell cycle arrest and mediating antibody-dependent cellular cytotoxicity (ADCC). **Analysis of Incorrect Options:** * **A. Imatinib:** A tyrosine kinase inhibitor (TKI) primarily targeting **BCR-ABL** (Philadelphia chromosome), c-KIT, and PDGFR. It is the first-line treatment for Chronic Myeloid Leukemia (CML) and Gastrointestinal Stromal Tumors (GIST). * **C. Erlotinib:** A small molecule TKI that targets **EGFR (ErbB1/HER1)**. It is primarily used in non-small cell lung cancer (NSCLC) with specific EGFR mutations and pancreatic cancer. * **D. Cetuximab:** A monoclonal antibody targeting **EGFR (ErbB1)**. It is used in the treatment of KRAS wild-type metastatic colorectal cancer and head and neck squamous cell carcinomas. **High-Yield Clinical Pearls for NEET-PG:** * **Cardiotoxicity:** The most significant side effect of Trastuzumab is **cardiac dysfunction** (decreased LVEF/heart failure). Unlike anthracyclines (Doxorubicin), Trastuzumab-induced cardiotoxicity is usually **reversible** and not dose-dependent. * **Combination Warning:** Avoid concurrent administration of Trastuzumab and Anthracyclines due to a synergistic increase in cardiotoxicity. * **Other HER-2 Drugs:** **Pertuzumab** (inhibits dimerization) and **Lapatinib** (a dual TKI targeting both EGFR and HER-2) are also used in HER-2 positive breast cancer.
Question 78: Which of the following drugs does not act on tubulin?
- A. Bleomycin (Correct Answer)
- B. Colchicine
- C. Paclitaxel
- D. Vincristine
Explanation: **Explanation:** The correct answer is **Bleomycin**. The question tests your knowledge of drugs that target the microtubule system versus those that damage DNA directly. **1. Why Bleomycin is the correct answer:** Bleomycin is a **cytotoxic antibiotic** that acts by a completely different mechanism. It binds to DNA and chelates metal ions (like ferrous iron), leading to the formation of free radicals (superoxide and hydroxyl radicals). These radicals cause **single and double-strand DNA breaks**, leading to cell cycle arrest in the **G2 phase**. It does not interact with tubulin or microtubules. **2. Why the other options are incorrect:** * **Colchicine:** This is an anti-inflammatory drug used in gout. It inhibits **tubulin polymerization** (prevents the assembly of microtubules), leading to the inhibition of leukocyte migration. * **Vincristine:** A Vinca alkaloid that also inhibits **tubulin polymerization**. By binding to tubulin, it prevents the formation of the mitotic spindle, causing cell cycle arrest in the **M phase**. * **Paclitaxel:** A Taxane that acts by **enhancing tubulin polymerization**. It stabilizes microtubules and prevents their disassembly (depolymerization), resulting in "frozen" spindles that inhibit mitosis. **Clinical Pearls for NEET-PG:** * **Bleomycin Toxicity:** The most significant side effect is **Pulmonary Fibrosis** (due to a lack of the enzyme bleomycin hydrolase in the lungs). It is notably **bone marrow sparing**. * **Vincristine Toxicity:** Characterized by **peripheral neuropathy** (areflexia, paresthesia) and paralytic ileus. * **Paclitaxel Toxicity:** Common side effects include **neutropenia** and hypersensitivity reactions (often premedicated with steroids/antihistamines). * **Cell Cycle Specificity:** Vincas and Taxanes are **M-phase specific**, while Bleomycin is **G2-phase specific**.
Question 79: What is the drug of choice for palliative treatment of pancreatic carcinoma?
- A. Paclitaxel
- B. Gemcitabine (Correct Answer)
- C. Methotrexate
- D. FOLFOX regimen
Explanation: **Explanation:** **Gemcitabine** is considered the cornerstone of palliative chemotherapy for advanced or metastatic pancreatic carcinoma. 1. **Why Gemcitabine is Correct:** Gemcitabine is a pyrimidine antimetabolite (nucleoside analog) that inhibits DNA synthesis by substituting for cytidine during DNA replication. In pancreatic cancer, it is preferred not just for its modest survival benefit, but primarily for its **"Clinical Benefit Response."** This includes significant improvement in pain control (reduced opioid requirement), performance status, and weight gain, which are the primary goals of palliative care in this aggressive malignancy. 2. **Analysis of Incorrect Options:** * **Paclitaxel:** While nab-paclitaxel (albumin-bound) is used *in combination* with Gemcitabine to improve outcomes, Paclitaxel monotherapy is not the standard of choice for pancreatic cancer. It is more commonly used in breast, ovarian, and lung cancers. * **Methotrexate:** This folate antagonist has minimal activity against pancreatic adenocarcinoma and is not part of standard treatment protocols for this condition. * **FOLFOX Regimen:** While platinum-based regimens (like FOLFIRINOX) are superior in patients with excellent performance status, they are highly toxic. For general palliative treatment, especially in patients who cannot tolerate intensive therapy, Gemcitabine remains the traditional benchmark. **High-Yield Clinical Pearls for NEET-PG:** * **Mechanism of Action:** Gemcitabine is a prodrug phosphorylated by *deoxycytidine kinase* into its active triphosphate form. * **Major Side Effect:** Myelosuppression (specifically **thrombocytopenia**) is the dose-limiting toxicity. * **Other Uses:** It is also a first-line agent for Non-Small Cell Lung Cancer (NSCLC) and bladder cancer. * **Current Standard:** For fit patients, **FOLFIRINOX** (5-FU, Leucovorin, Irinotecan, Oxaliplatin) is now preferred over Gemcitabine for better survival, though Gemcitabine remains the "classic" answer for palliative monotherapy.
Question 80: Which of the following drugs is used in the management of estrogen receptor-positive breast cancer?
- A. Bevacizumab
- B. Tamoxifen (Correct Answer)
- C. Cyclophosphamide
- D. Adalimumab
Explanation: **Explanation:** **Tamoxifen** is the correct answer because it is a **Selective Estrogen Receptor Modulator (SERM)**. In breast tissue, it acts as a competitive antagonist at the estrogen receptor (ER). Since approximately 70% of breast cancers are ER-positive, blocking estrogen-mediated signaling inhibits the growth of these hormone-dependent tumor cells. It is considered the gold standard for hormonal therapy in premenopausal women with ER-positive breast cancer. **Analysis of Incorrect Options:** * **Bevacizumab:** This is a monoclonal antibody against **VEGF** (Vascular Endothelial Growth Factor). It is an angiogenesis inhibitor used in colorectal, lung, and renal cancers, but it does not target estrogen receptors. * **Cyclophosphamide:** An **alkylating agent** (nitrogen mustard) that causes DNA cross-linking. While used in breast cancer chemotherapy regimens (e.g., CMF or AC protocols), it is not specific to ER-positive status and acts via cytotoxic rather than hormonal mechanisms. * **Adalimumab:** A monoclonal antibody targeting **TNF-alpha**. It is an immunosuppressant used for autoimmune conditions like Rheumatoid Arthritis and Crohn’s disease, not for malignancy. **High-Yield Clinical Pearls for NEET-PG:** * **Dual Action:** Tamoxifen is an **antagonist in the breast** but an **agonist in the endometrium and bone**. * **Side Effects:** Due to its partial agonist effect on the uterus, it increases the risk of **endometrial carcinoma**. It also increases the risk of thromboembolism (DVT/PE). * **Bone Benefit:** It helps prevent osteoporosis in postmenopausal women due to its estrogenic effect on bone. * **Drug of Choice:** For postmenopausal ER+ breast cancer, **Aromatase Inhibitors** (e.g., Letrozole, Anastrozole) are generally preferred over Tamoxifen.
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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