Anticancer Drugs — MCQs

Anticancer Drugs Indian Medical PG Practice Questions and MCQs

Question 211: All of the following drugs are used in the management of ALL except?

A. Methotrexate
B. All-trans retinoic acid (Correct Answer)
C. Prednisolone
D. L-Asparaginase

Explanation: **Explanation:** The management of **Acute Lymphoblastic Leukemia (ALL)** involves a multi-drug regimen divided into induction, consolidation, and maintenance phases. **Why All-trans retinoic acid (ATRA) is the correct answer:** ATRA is a differentiating agent specifically used for **Acute Promyelocytic Leukemia (APL)**, which is the **M3 subtype of Acute Myeloid Leukemia (AML)**. It works by binding to the PML-RARα fusion protein (caused by the t(15;17) translocation), inducing the maturation of malignant promyelocytes into mature neutrophils. It has no therapeutic role in the management of lymphoid malignancies like ALL. **Analysis of incorrect options:** * **Methotrexate:** A folate antagonist that inhibits dihydrofolate reductase (DHFR). It is a cornerstone of ALL therapy, used both systemically and intrathecally for CNS prophylaxis. * **Prednisolone:** Glucocorticoids are lympholytic and are essential in the induction phase of ALL treatment to rapidly reduce the blast burden. * **L-Asparaginase:** This enzyme depletes asparagine in the serum. Since leukemic lymphoblasts lack asparagine synthetase, they cannot synthesize asparagine and undergo apoptosis. This drug is highly specific for ALL. **High-Yield Clinical Pearls for NEET-PG:** * **ATRA Side Effect:** Watch for **"Retinoic Acid Syndrome"** (fever, dyspnea, pleural effusion), treated with high-dose dexamethasone. * **L-Asparaginase Side Effects:** Acute pancreatitis, thrombosis (due to decreased Antithrombin III), and hypersensitivity reactions. * **Vincristine:** Another key drug for ALL induction; its dose-limiting toxicity is peripheral neuropathy. * **Maintenance Therapy for ALL:** Usually consists of 6-Mercaptopurine (daily) and Methotrexate (weekly).

Question 212: Rituximab is used for the treatment of which of the following conditions?

A. Rheumatoid arthritis
B. Crohn's disease
C. Non-Hodgkin's lymphoma (Correct Answer)
D. Colorectal carcinoma

Explanation: **Rituximab** is a chimeric monoclonal antibody directed against the **CD20 antigen**, which is primarily expressed on the surface of normal and malignant B-lymphocytes [1].1. **Why Option C is Correct:** Rituximab binds to CD20, triggering B-cell lysis through complement-dependent cytotoxicity (CDC) and antibody-dependent cell-mediated cytotoxicity (ADCC). Since **Non-Hodgkin’s Lymphoma (NHL)**, specifically the diffuse large B-cell subtype and follicular lymphoma, is characterized by malignant B-cell proliferation, Rituximab is a cornerstone of therapy (often as part of the R-CHOP regimen) [1].2. **Why Other Options are Incorrect:** * **A. Rheumatoid Arthritis:** While Rituximab *is* used off-label or for refractory cases of RA, it is primarily classified as an anticancer drug in this context. However, it is not the first-line choice compared to its definitive role in B-cell malignancies. * **B. Crohn’s Disease:** This is typically treated with TNF-α inhibitors (e.g., Infliximab, Adalimumab) or integrin inhibitors (Vedolizumab), not CD20 blockers. * **D. Colorectal Carcinoma:** This solid tumor is treated with drugs targeting VEGF (Bevacizumab) or EGFR (Cetuximab), not B-cell specific markers.**High-Yield Clinical Pearls for NEET-PG:** * **Mechanism:** Anti-CD20 monoclonal antibody.* **Other Indications:** Chronic Lymphocytic Leukemia (CLL) [1], Wegener’s Granulomatosis (GPA), and Pemphigus Vulgaris.* **Specific Side Effect:** **Infusion-related reactions** (hypotension, bronchospasm) are common; patients are often premedicated with antihistamines and acetaminophen [1].* **Black Box Warning:** Risk of **Progressive Multifocal Leukoencephalopathy (PML)** due to JC virus reactivation and Hepatitis B reactivation.

Question 213: What is the first-line drug therapy for chronic myeloid leukemia?

A. Hydroxycarbamide
B. Alpha-interferon
C. Busulphan
D. Imatinib (Correct Answer)

Explanation: ### Explanation **Correct Option: D. Imatinib** Chronic Myeloid Leukemia (CML) is characterized by 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** is a 2-phenylaminopyrimidine derivative that acts as a selective **Tyrosine Kinase Inhibitor (TKI)**. It binds to the ATP-binding site of the BCR-ABL enzyme, inhibiting its activity. Due to its high efficacy in achieving complete cytogenetic remission and its superior safety profile, it is the **first-line (gold standard) therapy** for CML in the chronic phase. **Why other options are incorrect:** * **A. Hydroxycarbamide (Hydroxyurea):** It is a ribonucleotide reductase inhibitor used primarily for rapid cytoreduction (lowering high WBC counts) before starting TKIs. It does not induce cytogenetic remission. * **B. Alpha-interferon:** Previously a mainstay of treatment, it is now rarely used due to significant systemic toxicity (flu-like symptoms, depression) and lower efficacy compared to TKIs. * **C. Busulphan:** An alkylating agent used historically for CML. It is now largely obsolete for this indication except as part of conditioning regimens for bone marrow transplantation due to risks like pulmonary fibrosis and prolonged myelosuppression. **High-Yield Clinical Pearls for NEET-PG:** * **Mechanism of Resistance:** The most common cause of Imatinib resistance is a **point mutation** in the BCR-ABL kinase domain (e.g., **T315I mutation**). * **Second-generation TKIs:** Nilotinib, Dasatinib, and Bosutinib (used if Imatinib fails). * **Third-generation TKI:** **Ponatinib** (effective against the T315I mutation). * **Side Effects of Imatinib:** Periorbital edema (most characteristic), fluid retention, and muscle cramps.

Question 214: What is the monoclonal antibody against VEGF?

A. Epratuzumab
B. Tocilizumab
C. Bevacizumab (Correct Answer)
D. Cetuximab

Explanation: **Explanation:** **Bevacizumab** is a recombinant humanized monoclonal antibody that targets **Vascular Endothelial Growth Factor (VEGF)**. By binding to VEGF, it prevents the growth factor from interacting with its receptors (VEGFR-1 and VEGFR-2) on the surface of endothelial cells. This inhibits **angiogenesis** (the formation of new blood vessels), thereby "starving" the tumor of the blood supply required for growth and metastasis. It is commonly used in treating colorectal cancer, non-small cell lung cancer (NSCLC), and renal cell carcinoma. **Analysis of Incorrect Options:** * **A. Epratuzumab:** A monoclonal antibody targeting **CD22**, primarily used in the treatment of Systemic Lupus Erythematosus (SLE) and certain lymphomas. * **B. Tocilizumab:** An **IL-6 receptor antagonist** used in Rheumatoid Arthritis and severe COVID-19 (cytokine release syndrome). * **D. Cetuximab:** A monoclonal antibody targeting the **Epidermal Growth Factor Receptor (EGFR)**, used in colorectal and head/neck cancers. **High-Yield Clinical Pearls for NEET-PG:** * **Adverse Effects:** The most characteristic side effects of Bevacizumab are **hypertension**, **proteinuria**, and **impaired wound healing**. It is also associated with an increased risk of **gastrointestinal perforation** and arterial thromboembolism. * **Nomenclature Tip:** Monoclonal antibodies ending in **"-umab"** are fully human, while **"-zumab"** indicates humanized (like Bevacizumab). * **Other VEGF Inhibitors:** **Ramucirumab** (targets VEGFR-2) and **Aflibercept** (a "VEGF trap" soluble receptor). * **Ophthalmic Use:** Bevacizumab (off-label) and Ranibizumab are used intravitreally for **Age-related Macular Degeneration (AMD)** to inhibit neovascularization.

Question 215: Which of the following is used to treat hormone-responsive breast cancer?

A. Adriamycin
B. Clomiphene citrate
C. Diethylstibestrol
D. Tamoxifen (Correct Answer)

Explanation: **Explanation:** **Correct Answer: D. Tamoxifen** Tamoxifen is the gold standard for treating **hormone-responsive (ER/PR positive) breast cancer**. It is a **Selective Estrogen Receptor Modulator (SERM)**. Its mechanism of action is tissue-specific: it acts as a **competitive antagonist** at estrogen receptors in breast tissue, thereby inhibiting the growth of estrogen-dependent cancer cells. **Analysis of Incorrect Options:** * **A. Adriamycin (Doxorubicin):** This is a cytotoxic anthracycline antibiotic. While it is a cornerstone of breast cancer chemotherapy (AC regimen), it is **not hormone-specific**. It works by intercalating DNA and inhibiting Topoisomerase II. * **B. Clomiphene citrate:** Also a SERM, but it is primarily used as an **ovulation inducer** in infertility. It acts as an antagonist at the hypothalamus, blocking the negative feedback of estrogen, which leads to increased FSH/LH secretion. * **C. Diethylstilbestrol (DES):** A potent synthetic estrogen. Historically used for prostate cancer, it is now largely obsolete due to its association with **clear cell adenocarcinoma of the vagina** in the daughters of women who took it during pregnancy. **High-Yield Clinical Pearls for NEET-PG:** * **Dual Nature of Tamoxifen:** While it is an antagonist in the breast, it acts as an **agonist in the endometrium** (increasing risk of endometrial carcinoma) and **bone** (preventing osteoporosis). * **Drug of Choice:** Tamoxifen is used in both pre- and post-menopausal women, whereas **Aromatase Inhibitors** (e.g., Letrozole, Anastrozole) are preferred specifically for post-menopausal ER+ breast cancer. * **Side Effects:** Hot flashes (most common) and increased risk of venous thromboembolism (VTE).

Question 216: Sorafenib is used in which of the following conditions?

A. Multiple myeloma
B. Chronic lymphocytic leukemia (CLL)
C. Acute myeloid leukemia (AML) (Correct Answer)
D. Acute lymphoblastic leukemia (ALL)

Explanation: **Explanation:** **Sorafenib** is a multi-kinase inhibitor that targets several serine/threonine and receptor tyrosine kinases. Its primary mechanism involves inhibiting **RAF kinase** (part of the MAPK/ERK pathway), **VEGFR-2/3**, and **PDGFR-β**. Crucially for this question, it also inhibits **FLT3 (Fms-like tyrosine kinase 3)**. 1. **Why AML is correct:** Approximately 30% of patients with **Acute Myeloid Leukemia (AML)** possess a **FLT3 mutation** (specifically FLT3-ITD), which is associated with a poor prognosis. Sorafenib acts as a first-generation FLT3 inhibitor. While newer agents like Midostaurin and Gilteritinib are now more specific, Sorafenib remains a clinically recognized treatment option for FLT3-positive AML. 2. **Why other options are incorrect:** * **Multiple Myeloma:** Primarily treated with proteasome inhibitors (Bortezomib), IMiDs (Thalidomide/Lenalidomide), and monoclonal antibodies (Daratumumab). * **CLL:** Managed with BTK inhibitors (Ibrutinib), BCL-2 inhibitors (Venetoclax), or CD20 antibodies (Rituximab). * **ALL:** Treatment involves intensive chemotherapy (Vincristine, Asparaginase) and TKI like Imatinib only if Philadelphia chromosome-positive ($Ph+$). **High-Yield Clinical Pearls for NEET-PG:** * **FDA-Approved Indications:** Sorafenib is a first-line agent for **Advanced Hepatocellular Carcinoma (HCC)** and **Advanced Renal Cell Carcinoma (RCC)**. It is also used in differentiated Thyroid Carcinoma. * **Key Side Effect:** **Hand-foot skin reaction** (palmar-plantar erythrodysesthesia) is a classic board-exam association for Sorafenib. * **Mechanism Shortcut:** Remember Sorafenib as a "Multi-kinase inhibitor" (RAF + VEGF + FLT3).

Question 217: All of the following are true regarding ifosfamide EXCEPT:

A. Metabolized by cytochrome P450 enzymes
B. Less neurotoxic than cyclophosphamide (Correct Answer)
C. Chloroacetaldehyde is a metabolite of ifosfamide
D. It is a nitrogen mustard

Explanation: Ifosfamide is a nitrogen mustard alkylating agent and an analog of cyclophosphamide [1, 2]. While they share similar mechanisms, their toxicity profiles differ significantly. **Why Option B is the correct answer (The Exception):** Contrary to the statement, **ifosfamide is significantly MORE neurotoxic than cyclophosphamide.** [1] This is because ifosfamide is metabolized at a higher rate into **chloroacetaldehyde**, a potent neurotoxin. Clinical manifestations of ifosfamide-induced encephalopathy include confusion, hallucinations, and seizures. In contrast, cyclophosphamide rarely causes neurotoxicity. **Analysis of Incorrect Options:** * **Option A:** Both ifosfamide and cyclophosphamide are prodrugs that require activation by the hepatic **Cytochrome P450 system** (specifically CYP3A4 and CYP2B6) to form their active cytotoxic metabolites (phosphoramide mustard) [1, 2]. * **Option C:** Chloroacetaldehyde is a major byproduct of ifosfamide metabolism. It is responsible for both the increased neurotoxicity and a higher incidence of nephrotoxicity compared to cyclophosphamide. * **Option D:** Ifosfamide belongs to the **Nitrogen Mustard** class of alkylating agents, which work by cross-linking DNA strands, thereby inhibiting DNA replication [1, 2]. **High-Yield Clinical Pearls for NEET-PG:** * **Urotoxicity:** Both drugs produce **acrolein**, which causes hemorrhagic cystitis. However, ifosfamide is more urotoxic; therefore, **MESNA** (2-mercaptoethane sulfonate) and aggressive hydration are mandatory [2]. * **Mnemonic:** **I**fosfamide causes **I**ncreased neurotoxicity (due to chloroacetaldehyde). * **Treatment of Neurotoxicity:** Methylene blue is sometimes used to treat or prevent ifosfamide-induced encephalopathy by inhibiting the oxidative deamination pathway that produces chloroacetaldehyde.

Question 218: Which of the following anticancer drugs is cell cycle specific?

A. Dactinomycin
B. Mitomycin C
C. Daunorubicin
D. Bleomycin (Correct Answer)

Explanation: ### Explanation Anticancer drugs are broadly classified into **Cell Cycle-Specific (CCS)** agents, which act on cells during a particular phase (e.g., S or M phase), and **Cell Cycle-Non-Specific (CCNS)** agents, which act on cells regardless of their phase in the cycle. **Why Bleomycin is Correct:** Bleomycin is a unique glycopeptide antibiotic that is **Cell Cycle-Specific**, acting primarily in the **G2 phase**. It works by binding to DNA and producing free radicals (superoxide and hydroxyl radicals) that cause single- and double-strand breaks. Because it targets a specific phase of the cell cycle, its efficacy is schedule-dependent. **Why the Other Options are Incorrect:** * **Dactinomycin (Actinomycin D):** This is an antitumor antibiotic that intercalates into DNA. It is considered **CCNS**, although it shows some increased activity in the G1 phase. * **Mitomycin C:** This is a potent alkylating agent that causes DNA cross-linking. Like most alkylating agents, it is **CCNS**. * **Daunorubicin:** Along with Doxorubicin, this belongs to the Anthracycline class. While they have maximum toxicity during the S phase, they are traditionally classified as **CCNS** because they intercalate DNA and inhibit Topoisomerase II throughout the cycle. **High-Yield NEET-PG Pearls:** * **Bleomycin Toxicity:** The most characteristic side effect is **Pulmonary Fibrosis**. Unlike most cytotoxic drugs, it is **not bone marrow suppressant** (it is "myelosuppressive-sparing"). * **G2 Phase Specificity:** Bleomycin is the classic example of a G2-specific drug. * **M-Phase Specific:** Vinca alkaloids (Vincristine/Vinblastine) and Taxanes (Paclitaxel). * **S-Phase Specific:** Antimetabolites (Methotrexate, 5-FU, Cytarabine).

Question 219: Which of the following is a cell cycle non-specific antineoplastic drug?

A. Vincristine
B. Methotrexate
C. Bleomycin
D. None of the above (Correct Answer)

Explanation: ### Explanation The correct answer is **None of the above** because all three drugs listed (Vincristine, Methotrexate, and Bleomycin) are **Cell Cycle Specific (CCS)** agents. #### 1. Understanding the Concept Antineoplastic drugs are classified into two categories based on their kinetics: * **Cell Cycle Specific (CCS):** These drugs act only on specific phases of the cell cycle (e.g., S-phase or M-phase). They are most effective against rapidly dividing tumors. * **Cell Cycle Non-Specific (CCNS):** These drugs act on cells regardless of the phase they are in (including the resting G0 phase). Examples include **Alkylating agents** (Cyclophosphamide, Busulfan) and **Anthracyclines** (Doxorubicin). #### 2. Analysis of Options * **Vincristine (Option A):** This is a Vinca alkaloid that inhibits tubulin polymerization. It is highly specific for the **M-phase** (Mitosis), causing metaphase arrest. * **Methotrexate (Option B):** An Antimetabolite (folate antagonist) that inhibits Dihydrofolate Reductase (DHFR). It acts specifically during the **S-phase** (DNA synthesis). * **Bleomycin (Option C):** Unlike most antitumor antibiotics which are CCNS, Bleomycin is unique as it is CCS, acting primarily in the **G2 phase** (and late S-phase) by causing oxidative DNA strand scission. #### 3. NEET-PG High-Yield Pearls * **Mnemonic for CCS drugs:** "**V**ery **B**usy **M**etabolizing **S**pecialists" (**V**inca alkaloids - M phase; **B**leomycin - G2 phase; **M**ethotrexate/Antimetabolites - S phase; **S**teroids - G1 phase). * **CCNS Drugs:** Remember **"ABCD"**—**A**lkylating agents, **B**enzene derivatives (Nitrosoureas), **C**isplatin, and **D**actinomycin/Doxorubicin. * **Clinical Note:** CCNS drugs generally follow linear dose-response curves (the more drug given, the more cells killed), whereas CCS drugs are "schedule-dependent" and reach a plateau in cell killing.

Question 220: Mesna is used in the management of which condition?

A. Hemorrhagic cystitis (Correct Answer)
B. Acute promyelocytic leukemia
C. Serous otitis media
D. Polycythemia vera

Explanation: **Explanation:** **Mesna (2-Mercaptoethane Sulfonate Na)** is a cytoprotective agent specifically used to prevent **hemorrhagic cystitis**, a dose-limiting toxicity associated with Oxazaphosphorine drugs like **Cyclophosphamide** and **Ifosfamide**. ### Why Option A is Correct: When Cyclophosphamide or Ifosfamide are metabolized, they produce a toxic metabolite called **Acrolein**. Acrolein accumulates in the urinary bladder, causing irritation and sloughing of the bladder mucosa, leading to gross hematuria (hemorrhagic cystitis). Mesna works by: 1. Concentrating in the bladder. 2. Providing a free sulfhydryl (-SH) group that binds to and neutralizes Acrolein. 3. Forming a non-toxic, stable thioether that is safely excreted. ### Why Other Options are Incorrect: * **B. Acute Promyelocytic Leukemia (APL):** The drug of choice is **All-trans Retinoic Acid (ATRA)** or Arsenic Trioxide. Mesna has no antineoplastic activity. * **C. Serous Otitis Media:** This is managed with decongestants, antibiotics, or myringotomy; Mesna has no role in ENT pathologies. * **D. Polycythemia Vera:** This is typically managed with phlebotomy or myelosuppressive agents like **Hydroxyurea** and Ruxolitinib. ### High-Yield Clinical Pearls for NEET-PG: * **Administration:** Mesna must be administered concurrently with Ifosfamide/Cyclophosphamide because it has a shorter half-life than the parent drugs. * **Hydration:** Vigorous intravenous hydration is also essential alongside Mesna to reduce the risk of cystitis. * **Other Protective Agents:** * **Amifostine:** Prevents cisplatin-induced nephrotoxicity. * **Dexrazoxane:** Prevents doxorubicin-induced cardiotoxicity. * **Leucovorin (Folinic Acid):** "Rescue" therapy for Methotrexate toxicity.

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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