Anticancer Drugs — MCQs

Anticancer Drugs Indian Medical PG Practice Questions and MCQs

Question 381: Which of the following is NOT included in the management of febrile neutropenic patients receiving anti-cancer therapy?

A. Colony stimulating factors
B. Transfusion of granulocytes (Correct Answer)
C. Antibiotic prophylaxis
D. Repeated hand washing

Explanation: **Explanation:** Febrile neutropenia is a medical emergency defined as a single oral temperature of $\geq 38.3^\circ\text{C}$ (101$^\circ\text{F}$) or $\geq 38.0^\circ\text{C}$ (100.4$^\circ\text{F}$) sustained over one hour in a patient with an Absolute Neutrophil Count (ANC) $< 500$ cells/mm³. **Why Option B is Correct:** **Granulocyte transfusion** is **not** a standard or routine management for febrile neutropenia. While it seems logical, clinical trials have shown it does not significantly improve survival outcomes. Furthermore, it is associated with severe adverse effects, including transfusion-related acute lung injury (TRALI), alloimmunization, and transmission of CMV. It is only considered in very rare, life-threatening refractory infections where marrow recovery is expected. **Analysis of Incorrect Options:** * **A. Colony Stimulating Factors (G-CSF/Filgrastim):** These are used to shorten the duration and severity of neutropenia. They are indicated for primary prophylaxis in high-risk chemotherapy regimens or as adjunct therapy in patients with high-risk complications. * **C. Antibiotic Prophylaxis:** Empirical broad-spectrum antibiotics (e.g., Piperacillin-Tazobactam or Carbapenems) are the cornerstone of management and must be started immediately (within 1 hour) to cover Gram-negative organisms like *Pseudomonas*. * **D. Repeated Hand Washing:** This is the most effective and simplest method of infection control to prevent the transmission of exogenous pathogens to immunocompromised patients. **Clinical Pearls for NEET-PG:** * **MASCC Score:** Used to identify low-risk patients who can be managed with oral antibiotics (Ciprofloxacin + Amoxicillin-Clavulanate) as outpatients. * **Commonest Organisms:** While Gram-positive cocci are frequently isolated, **Gram-negative bacilli** (especially *Pseudomonas aeruginosa*) are associated with the highest mortality. * **Antifungals:** Added if the patient remains febrile after 4–7 days of broad-spectrum antibiotics.

Question 382: What is the mechanism by which Tamoxifen reduces breast cancer?

A. It competes with the estrogen receptor in breast tissue. (Correct Answer)
B. It decreases the blood supply to the tumor.
C. It is a directly acting anticancer drug.
D. It augments radiation therapy.

Explanation: ### Explanation **Mechanism of Action (Correct Answer: A)** Tamoxifen is a **Selective Estrogen Receptor Modulator (SERM)**. Its primary mechanism in breast tissue is **competitive antagonism** of the estrogen receptor (ER). By binding to the ER, it prevents endogenous estrogen from binding, thereby inhibiting the transcription of estrogen-responsive genes. This leads to a decrease in the proliferation of ER-positive breast cancer cells. **Analysis of Incorrect Options:** * **Option B:** While some anti-angiogenic drugs (like Bevacizumab) decrease blood supply, this is not the mechanism of Tamoxifen. * **Option C:** Tamoxifen is a hormonal therapy, not a cytotoxic (directly acting) chemotherapy drug. It is cytostatic (inhibits growth) rather than directly cytotoxic. * **Option D:** While Tamoxifen may be used alongside radiation, its primary mechanism is independent of augmenting radiation effects. **Clinical Pearls for NEET-PG:** * **Tissue-Specific Action:** Tamoxifen acts as an **antagonist in the breast** but as a **partial agonist in the endometrium and bone**. * **Side Effects:** Due to its agonist effect on the endometrium, it increases the risk of **endometrial carcinoma**. It also increases the risk of **thromboembolism** (DVT/PE). * **Benefits:** It helps prevent osteoporosis by maintaining bone mineral density (agonist effect on bone). * **Metabolism:** It is a prodrug converted to its active metabolite, **Endoxifen**, by the hepatic enzyme **CYP2D6**. * **Drug of Choice:** It is the gold standard for hormonal treatment in **pre-menopausal** women with ER-positive breast cancer.

Question 383: All of the following drugs are used in the treatment of Multiple myeloma, EXCEPT?

A. Bortezomib
B. Melphalan
C. Hydroxyurea (Correct Answer)
D. Cyclophosphamide

Explanation: **Explanation:** The correct answer is **Hydroxyurea**. **1. Why Hydroxyurea is the correct answer:** Hydroxyurea is a ribonucleotide reductase inhibitor that primarily acts on the S-phase of the cell cycle. Its clinical utility is focused on **Myeloproliferative Neoplasms (MPNs)** such as Chronic Myeloid Leukemia (CML), Polycythemia Vera, and Essential Thrombocythemia. It is also used in Sickle Cell Anemia to increase fetal hemoglobin (HbF). It is **not** a standard treatment for Multiple Myeloma (MM), which is a plasma cell dyscrasia. **2. Analysis of incorrect options:** * **Bortezomib:** A first-line **Proteasome Inhibitor**. It inhibits the 26S proteasome, leading to the accumulation of pro-apoptotic proteins. It is a cornerstone of modern MM therapy. * **Melphalan:** An **Alkylating agent** (Nitrogen mustard). Historically, Melphalan + Prednisolone was the gold standard. Today, high-dose Melphalan is the standard conditioning regimen used before Autologous Stem Cell Transplantation (ASCT) in MM patients. * **Cyclophosphamide:** Another **Alkylating agent** frequently used in MM, especially in combination regimens (e.g., CyBorD: Cyclophosphamide + Bortezomib + Dexamethasone) or for patients with renal impairment. **3. Clinical Pearls for NEET-PG:** * **Mnemonic for MM Drugs:** "**ABCD-M**" — **A**lkylators (Melphalan/Cyclophosphamide), **B**ortezomib (Proteasome inhibitors), **C**orticosteroids (Dexamethasone), **D**aratumumab (Anti-CD38), **I**mmunomodulators (Thalidomide/Lenalidomide). * **Bortezomib Side Effect:** Peripheral neuropathy and Herpes Zoster reactivation (prophylactic Acyclovir is required). * **Thalidomide/Lenalidomide:** Act by binding to **Cereblon** (E3 ubiquitin ligase). * **Drug of Choice for MM:** Triple therapy (Bortezomib + Lenalidomide + Dexamethasone) is currently preferred.

Question 384: Which of the following statements regarding the management of iron toxicity in a 3-year-old child presenting with severe GI distress, hematemesis, a shock-like state with marked dehydration, and progressive hemorrhagic gastritis is accurate?

A. Gastric lavage should not be attempted due to the risk of aspiration.
B. The patient is likely to have a reduced anion gap.
C. Urinary alkalization increases the elimination of iron.
D. Deferoxamine should be administered as soon as possible. (Correct Answer)

Explanation: **Explanation:** Acute iron poisoning is a medical emergency, especially in children. The clinical presentation described—severe GI distress, hematemesis, and shock—indicates the **Gastrointestinal Phase** (Stage 1) of toxicity, where iron acts as a direct corrosive to the gastric mucosa. **1. Why Option D is Correct:** **Deferoxamine** is the specific parenteral chelating agent for iron. It binds ferric iron ($Fe^{3+}$) to form **ferrioxamine**, which is water-soluble and excreted by the kidneys. In cases of severe toxicity (shock, metabolic acidosis, or serum iron >500 µg/dL), it must be administered intravenously as soon as possible to prevent systemic cellular damage and multi-organ failure. **2. Why Other Options are Incorrect:** * **Option A:** Gastric lavage is actually **indicated** within the first hour of ingestion to remove unabsorbed iron tablets. However, it must be done with caution (using large-bore tubes) because iron tablets are radiopaque and often clump together. * **Option B:** Iron toxicity causes a **High Anion Gap Metabolic Acidosis (HAGMA)**, not a reduced anion gap. This occurs due to the release of protons during iron hydration and the accumulation of lactic acid from shock and mitochondrial dysfunction. * **Option C:** Urinary alkalization is used for weak acids (like salicylates or phenobarbital). It has **no role** in iron elimination. Iron is eliminated via chelation (Deferoxamine). **Clinical Pearls for NEET-PG:** * **Classic Sign:** "Vin-rose" (pinkish-orange) urine after starting Deferoxamine due to the excretion of the ferrioxamine complex. * **Imaging:** Iron tablets are **radiopaque**; an abdominal X-ray is a high-yield initial step to visualize the "pill burden." * **Late Complication:** Gastric outlet obstruction (pyloric stenosis) due to scarring from hemorrhagic gastritis (occurs 2–6 weeks post-ingestion). * **Oral Chelator:** Deferasirox is used for *chronic* iron overload (e.g., Thalassemia), not acute poisoning.

Question 385: What is the mechanism of action of bevacizumab?

A. Inhibitor of HER-2/Neu
B. Inhibitor of VEGF (Correct Answer)
C. Inhibitor of c-kit
D. None of the above

Explanation: **Explanation:** **Bevacizumab** is a recombinant humanized monoclonal antibody that acts as a potent **angiogenesis inhibitor**. Its primary mechanism of action is binding to and neutralizing **Vascular Endothelial Growth Factor (VEGF-A)**. By preventing VEGF from binding to its receptors (VEGFR-1 and VEGFR-2) on endothelial cells, bevacizumab inhibits the formation of new blood vessels (angiogenesis), thereby "starving" the tumor of the blood supply and nutrients required for growth and metastasis. **Analysis of Options:** * **Option A (Inhibitor of HER-2/neu):** This describes **Trastuzumab**. It is used primarily in HER-2 positive breast cancer and gastric cancer. * **Option B (Inhibitor of VEGF):** **Correct.** Bevacizumab specifically targets the VEGF ligand. * **Option C (Inhibitor of c-kit):** This describes **Imatinib**, a tyrosine kinase inhibitor used in Chronic Myeloid Leukemia (CML) and Gastrointestinal Stromal Tumors (GIST). **High-Yield NEET-PG Clinical Pearls:** 1. **Clinical Uses:** Bevacizumab is used in metastatic colorectal cancer, non-small cell lung cancer (NSCLC), renal cell carcinoma, and glioblastoma multiforme. 2. **Ocular Use:** It is frequently used "off-label" via intravitreal injection for **Age-related Macular Degeneration (ARMD)** and diabetic retinopathy to reduce neovascularization. 3. **Adverse Effects:** The most characteristic side effects include **hypertension**, proteinuria, impaired wound healing, and an increased risk of arterial thromboembolism or gastrointestinal perforation. 4. **Contraindication:** It should be avoided for at least 28 days before or after major surgery due to its impact on wound healing.

Question 386: Multiple myeloma is treated by all of the following EXCEPT:

A. Lenalidomide
B. Bortezomib
C. Thalidomide
D. All of the above (Correct Answer)

Explanation: **Explanation:** Multiple Myeloma (MM) is a plasma cell dyscrasia that has seen a paradigm shift in treatment with the introduction of Immunomodulatory drugs (IMiDs) and Proteasome inhibitors. **1. Why "All of the above" is correct:** The management of Multiple Myeloma typically involves a combination of different classes of drugs to achieve remission. All three listed drugs—Lenalidomide, Bortezomib, and Thalidomide—are cornerstone FDA-approved therapies for MM. **2. Analysis of Options:** * **Thalidomide (Option C):** Historically used as a sedative, it is now a first-line agent for MM. It acts by inhibiting TNF-α and has potent anti-angiogenic properties. * **Lenalidomide (Option A):** A more potent derivative of thalidomide with fewer side effects (less peripheral neuropathy). It is currently a standard of care for both induction and maintenance therapy in MM. * **Bortezomib (Option B):** A reversible inhibitor of the **26S proteasome**. By inhibiting the degradation of pro-apoptotic proteins and blocking the NF-κB pathway, it leads to the death of malignant plasma cells. **3. High-Yield Clinical Pearls for NEET-PG:** * **Mechanism of IMiDs:** Thalidomide and Lenalidomide bind to a protein called **Cereblon**, leading to the degradation of transcription factors (Ikaros/Aiolos) essential for myeloma cell survival. * **Side Effects:** * **Thalidomide:** Highly teratogenic (**Phocomelia**) and causes significant peripheral neuropathy. * **Lenalidomide:** Main dose-limiting toxicity is **myelosuppression** (neutropenia/thrombocytopenia). * **Bortezomib:** Associated with **Herpes Zoster reactivation** (prophylactic acyclovir is often given) and peripheral neuropathy. * **Other MM Drugs:** Daratumumab (Anti-CD38 monoclonal antibody) and Dexamethasone are also frequently used in combination regimens (e.g., VRd: Velcade/Bortezomib, Revlimid/Lenalidomide, dexamethasone).

Question 387: All are true statements about anticancer drugs except?

A. Vincristine is a marrow sparing anticancer drug
B. Irinotecan is a topoisomerase II inhibitor (Correct Answer)
C. L-asparaginase can cause acute pancreatitis
D. Anthracyclines cause cardiotoxicity

Explanation: **Explanation:** The correct answer is **B**, as Irinotecan is a **Topoisomerase I inhibitor**, not a Topoisomerase II inhibitor. 1. **Why Option B is the correct answer (False statement):** Topoisomerase inhibitors are classified based on the enzyme they target. **Irinotecan** and **Topotecan** (Camptothecin derivatives) inhibit Topoisomerase I, which is responsible for single-strand DNA breaks. In contrast, Topoisomerase II inhibitors include **Etoposide**, **Teniposide**, and **Anthracyclines** (like Doxorubicin), which facilitate double-strand DNA breaks. 2. **Analysis of other options (True statements):** * **Option A:** **Vincristine** is famously known as a "marrow-sparing" drug. Unlike most cytotoxic agents, its dose-limiting toxicity is peripheral neuropathy rather than myelosuppression. * **Option C:** **L-asparaginase** is unique because it interferes with protein synthesis. Its classic side effects include **acute pancreatitis**, hyperglycemia (due to insulin deficiency), and clotting factor deficiencies. * **Option D:** **Anthracyclines** (Doxorubicin, Daunorubicin) are notorious for causing **cardiotoxicity** (dilated cardiomyopathy) mediated by free radical generation. This can be mitigated by the iron-chelating agent **Dexrazoxane**. **High-Yield Clinical Pearls for NEET-PG:** * **Mnemonic for Topoisomerase II inhibitors:** "**ET**" (**E**toposide, **T**eniposide). * **Mnemonic for Topoisomerase I inhibitors:** "**I** can **Top**" (**I**rinotecan, **Top**otecan). * **Vincristine vs. Vinblastine:** Vincristine spares the marrow (**C**risps the nerves), while Vin**b**lastine **b**lasts the marrow (causes myelosuppression). * **Bleomycin** and **Busulfan** are known for causing pulmonary fibrosis. * **Cyclophosphamide** is associated with hemorrhagic cystitis (prevented by **MESNA**).

Question 388: What class of drug is Tamoxifen?

A. SSRI (Selective Serotonin Reuptake Inhibitor)
B. SERM (Selective Estrogen Receptor Modulator) (Correct Answer)
C. SNRI (Serotonin-Norepinephrine Reuptake Inhibitor)
D. DNRI (Dopamine-Norepinephrine Reuptake Inhibitor)

Explanation: **Explanation:** **Tamoxifen** is the prototypical **Selective Estrogen Receptor Modulator (SERM)** [1]. The core pharmacological concept of SERMs is their **tissue-specific action**: they act as competitive antagonists of estrogen in some tissues while acting as agonists in others [3]. * **Mechanism in Breast:** Tamoxifen acts as an **antagonist** on estrogen receptors in breast tissue, inhibiting the growth of estrogen-receptor-positive (ER+) breast cancer cells [1]. * **Mechanism in Other Tissues:** It acts as a partial **agonist** in the bone (preventing osteoporosis) and the endometrium [4]. **Analysis of Incorrect Options:** * **SSRI (A), SNRI (C), and DNRI (D):** These are classes of **antidepressants** that modulate neurotransmitters (Serotonin, Norepinephrine, and Dopamine) in the synaptic cleft. They have no structural or functional relationship to estrogen receptor modulation. Note: Some SSRIs (like Paroxetine) can actually inhibit the metabolism of Tamoxifen via CYP2D6, potentially reducing its efficacy. **High-Yield Clinical Pearls for NEET-PG:** 1. **Drug of Choice:** Tamoxifen is the gold standard for pre-menopausal women with ER-positive breast cancer [1]. 2. **Metabolism:** It is a prodrug converted to its active metabolite, **Endoxifen**, by the hepatic enzyme **CYP2D6**. 3. **Adverse Effects:** Due to its agonist effect on the endometrium, it increases the risk of **Endometrial Carcinoma** [2]. It also increases the risk of **Thromboembolism** (DVT/PE) and causes "hot flashes" [2]. 4. **Raloxifene:** Another SERM used for osteoporosis; unlike Tamoxifen, it is an *antagonist* in the uterus and does not increase endometrial cancer risk [3], [4].

Question 389: All of the following are mTOR inhibitors except?

A. Sirolimus
B. Everolimus
C. Tacrolimus (Correct Answer)
D. Temsirolimus

Explanation: ### Explanation The Mammalian Target of Rapamycin (mTOR) is a protein kinase that regulates cell growth, proliferation, and survival. mTOR inhibitors are a class of drugs used primarily as immunosuppressants and in the treatment of certain malignancies (like renal cell carcinoma). **Why Tacrolimus is the correct answer:** While **Tacrolimus** (FK506) and Sirolimus both bind to the same intracellular protein—the **FK-binding protein (FKBP-12)**—their downstream mechanisms differ significantly. The Tacrolimus-FKBP complex inhibits **Calcineurin**, a phosphatase required for the activation of NFAT (Nuclear Factor of Activated T-cells), thereby preventing IL-2 transcription. It does **not** inhibit the mTOR pathway. **Analysis of incorrect options (mTOR Inhibitors):** * **Sirolimus (Rapamycin):** The prototype mTOR inhibitor. The Sirolimus-FKBP complex binds to and inhibits mTOR, blocking the cell cycle transition from G1 to S phase. * **Everolimus:** A derivative of sirolimus with better oral bioavailability. It is used in drug-eluting stents and for treating advanced renal cell carcinoma and breast cancer. * **Temsirolimus:** An intravenous prodrug of sirolimus specifically indicated for advanced renal cell carcinoma. **High-Yield Clinical Pearls for NEET-PG:** * **Side Effects:** Unlike Calcineurin inhibitors (Tacrolimus/Cyclosporine), mTOR inhibitors are **not nephrotoxic**. However, they commonly cause **hyperlipidemia**, thrombocytopenia, and impaired wound healing. * **Mnemonic:** Remember the **"Limus"** family. While all end in "-limus," **Tacrolimus** is the "odd one out" as a Calcineurin inhibitor, while **S**irolimus, **E**verolimus, and **T**emsirolimus (**SET**) are mTOR inhibitors. * **Drug-Eluting Stents:** Sirolimus and Everolimus are frequently used to prevent neointimal hyperplasia (restenosis).

Question 390: What is the drug of choice for Chronic Myeloid Leukemia (CML)?

A. Imatinib mesylate (Correct Answer)
B. Fludarabine
C. All-trans retinoic acid (for AML M3)
D. Methotrexate

Explanation: **Explanation:** **Correct Answer: A. Imatinib mesylate** Imatinib is the first-line treatment (Drug of Choice) for Chronic Myeloid Leukemia (CML). The underlying pathophysiology of CML involves the **Philadelphia chromosome t(9;22)**, which creates the **BCR-ABL fusion gene**. This gene encodes a constitutively active **tyrosine kinase** protein that drives uncontrolled myeloid proliferation. Imatinib acts as a selective **Tyrosine Kinase Inhibitor (TKI)** by binding to the ATP-binding site of the BCR-ABL enzyme, effectively "turning off" the signal for cell division. **Analysis of Incorrect Options:** * **B. Fludarabine:** A purine analog primarily used as the drug of choice for **Chronic Lymphocytic Leukemia (CLL)**. * **C. All-trans retinoic acid (ATRA):** The specific targeted therapy for **Acute Promyelocytic Leukemia (AML-M3)**. It works by inducing the differentiation of leukemic promyelocytes. * **D. Methotrexate:** A folate antagonist used in various regimens for Acute Lymphoblastic Leukemia (ALL), ectopic pregnancy, and rheumatoid arthritis, but it does not target the specific molecular defect in CML. **High-Yield Clinical Pearls for NEET-PG:** * **Mechanism:** Imatinib is a competitive inhibitor of the ATP-binding site on the BCR-ABL tyrosine kinase. * **Resistance:** Resistance to Imatinib often occurs due to a point mutation in the BCR-ABL gene (most notably the **T315I mutation**). * **Second-generation TKIs:** Dasatinib and Nilotinib are used if Imatinib fails or is not tolerated. **Ponatinib** is used specifically for the T315I mutation. * **Side Effects:** A characteristic side effect of Imatinib is **periorbital edema** (fluid retention).

Practice by Chapter

Principles of Cancer Chemotherapy

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Alkylating Agents

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Antimetabolites

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Antitumor Antibiotics

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Plant Alkaloids

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Topoisomerase Inhibitors

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Hormonal Agents

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Targeted Therapy

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Immunotherapy

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Management of Chemotherapy Side Effects

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