Anticancer Drugs Practice Questions

Q: All of the following are monoclonal antibodies against CD-20 except?

Brentuximab. **Explanation:** The correct answer is **D. Brentuximab**. **1. Why Brentuximab is the correct answer:** Brentuximab vedotin is an antibody-drug conjugate (ADC) directed against **CD30**, not CD20. It consists of a chimeric IgG1 antibody linked to the microtubule-disrupting agent **Monomethyl Auristatin E (MMAE)**. It is primarily used in the treatment of Hodgkin Lymphoma and Systemic Anaplastic Large Cell Lymphoma (ALCL), where CD30 is highly expressed. **2. Analysis of Incorrect Options (CD20 Inhibitors):** CD20 is a surface antigen found on B-cells. Monoclonal antibodies against CD20 are used for B-cell malignancies and autoimmune disorders. * **Rituximab (Option A):** The prototype chimeric monoclonal antibody against CD20. It is the backbone of therapy for Non-Hodgkin Lymphoma (NHL) and Chronic Lymphocytic Leukemia (CLL). * **Ofatumumab (Option B):** A fully human monoclonal antibody that binds to a different epitope on CD20 than Rituximab. It is used in CLL and Multiple Sclerosis. * **Ocrelizumab (Option C):** A humanized anti-CD20 antibody specifically approved for both Relapsing and Primary Progressive Multiple Sclerosis. **3. High-Yield Clinical Pearls for NEET-PG:** * **Obinutuzumab:** Another important Type II anti-CD20 antibody used in CLL. * **CD20 vs. CD30:** Remember **"20 for B-cells"** (Rituximab) and **"30 for Reed-Sternberg cells"** (Brentuximab). * **Adverse Effect:** Infusion-related reactions are common with anti-CD20 drugs; premedication with antihistamines and acetaminophen is required. * **Brentuximab Side Effect:** Peripheral neuropathy is a significant dose-limiting toxicity due to the MMAE component.

Q: Which of the following conditions is NOT treated with ibrutinib?

Acute myeloid leukemia. **Explanation:** **Ibrutinib** is a first-in-class, potent, irreversible inhibitor of **Bruton’s Tyrosine Kinase (BTK)**. BTK is a critical signaling molecule in the B-cell receptor (BCR) pathway, which is essential for the survival, proliferation, and differentiation of **B-lymphocytes**. 1. **Why Acute Myeloid Leukemia (AML) is the correct answer:** AML is a malignancy of the **myeloid** lineage (granulocytes, monocytes, etc.), not the B-cell lineage. Since AML cells do not typically rely on the BTK signaling pathway for survival, Ibrutinib is ineffective and is not an approved treatment for this condition. 2. **Analysis of Incorrect Options:** * **Mantle Cell Lymphoma (MCL):** Ibrutinib is FDA-approved for patients with MCL who have received at least one prior therapy. * **Chronic Lymphocytic Leukemia (CLL):** It is a mainstay of treatment for CLL (and Small Lymphocytic Lymphoma), including cases with the high-risk 17p deletion. * **Waldenstrom’s Macroglobulinemia (WM):** This is a B-cell neoplasm characterized by excess IgM. Ibrutinib is highly effective here as these cells are dependent on BTK signaling. **High-Yield Clinical Pearls for NEET-PG:** * **Mechanism:** Covalent (irreversible) binding to a cysteine residue (Cys-481) in the BTK active site. * **Route:** Administered **orally**. * **Key Side Effects:** * **Atrial Fibrillation:** A classic board-favorite side effect. * **Increased Bleeding Risk:** Patients should be monitored for bruising or hemorrhage (avoid use with warfarin). * **Lymphocytosis:** A transient increase in lymphocyte count is common early in treatment as cells move from lymph nodes into the blood.

Q: Which drug can be used in a patient with CML and a T315i mutation?

Ponatinib. **Explanation:** The **T315I mutation** is known as the "gatekeeper mutation" in Chronic Myeloid Leukemia (CML). It involves a substitution of threonine (T) with isoleucine (I) at position 315 of the BCR-ABL tyrosine kinase enzyme. This specific structural change creates steric hindrance that prevents most Tyrosine Kinase Inhibitors (TKIs) from binding to the ATP-binding pocket. **Why Ponatinib is correct:** **Ponatinib** is a third-generation TKI specifically designed with a carbon-carbon triple bond (ethynyl group) that bypasses the steric bulk created by the isoleucine residue. It is currently the only approved TKI effective against the T315I mutation. **Why other options are incorrect:** * **Imatinib (1st Gen):** The prototype TKI; it is highly effective for wild-type BCR-ABL but is completely ineffective against the T315I mutation. * **Nilotinib & Dasatinib (2nd Gen):** While these are more potent than Imatinib and can overcome many other resistance mutations, they cannot bind to the BCR-ABL protein when the T315I mutation is present. **High-Yield Clinical Pearls for NEET-PG:** 1. **Adverse Effect of Ponatinib:** It is associated with a high risk of **arterial thrombosis** (myocardial infarction, stroke) and hepatotoxicity. 2. **Asciminib:** A newer drug (STAMP inhibitor) that binds to the myristoyl pocket; it is also used for T315I mutations in patients resistant to other therapies. 3. **Dasatinib Side Effect:** Classically associated with **pleural effusion**. 4. **Imatinib Side Effect:** Most common is **periorbital edema** and fluid retention.

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

All-trans retinoic acid. **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).

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

Non-Hodgkin's lymphoma. **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.

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

Imatinib. ### 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.

Q: Sorafenib is used in which of the following conditions?

Acute myeloid leukemia (AML). **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).

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

Bleomycin. ### 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).

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

None of the above. ### 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.

Q: A 35-year-old patient with carcinoma of the lung and a past history of lung disease is to be treated. Which of the following anticancer drugs should be avoided?

Bleomycin. **Explanation:** The correct answer is **Bleomycin**. **1. Why Bleomycin is the correct answer:** Bleomycin is a glycopeptide antibiotic used as a chemotherapeutic agent that acts by causing DNA strand scission. Its most notorious and dose-limiting toxicity is **Pulmonary Fibrosis**. The drug concentrates in the lungs because the enzyme that inactivates it (bleomycin hydrolase) is found in very low concentrations in pulmonary tissue. In a patient with a pre-existing history of lung disease, the risk of developing fatal interstitial pneumonitis and subsequent fibrosis is significantly increased. Therefore, it is strictly avoided or used with extreme caution in such patients. **2. Why the other options are incorrect:** * **Vinblastine:** A Vinca alkaloid that inhibits microtubule assembly. Its primary dose-limiting toxicity is **bone marrow suppression** (myelosuppression), not pulmonary toxicity. * **Mithramycin (Plicamycin):** Primarily used for refractory hypercalcemia and Paget’s disease. Its major toxicities are **thrombocytopenia** and hepatotoxicity. * **Adriamycin (Doxorubicin):** An anthracycline antibiotic. Its classic dose-limiting toxicity is **Cardiotoxicity** (dilated cardiomyopathy), not lung disease. **3. NEET-PG High-Yield Pearls:** * **Bleomycin:** "Lung-sparing" for the bone marrow (causes minimal myelosuppression) but "Marrow-sparing" for the lungs (causes maximal lung damage). * **Monitoring:** Patients on Bleomycin require serial **Pulmonary Function Tests (PFTs)**, specifically looking for a decrease in DLCO (Diffusion Capacity of the Lung for Carbon Monoxide). * **Other drugs causing Pulmonary Fibrosis:** Busulfan, Methotrexate, and Amiodarone. * **Dose Limit:** The risk of fibrosis increases significantly when the cumulative dose of Bleomycin exceeds **400-450 units**.

Question 1

All of the following are monoclonal antibodies against CD-20 except?

Accepted Answer

Brentuximab

Answer

Rituximab

Answer

Ofatumumab

Answer

Ocrelizumab

Question 2

Which of the following conditions is NOT treated with ibrutinib?

Accepted Answer

Acute myeloid leukemia

Answer

Mantle cell lymphoma

Answer

Chronic lymphocytic leukemia

Answer

Waldenstrom's macroglobulinemia

Question 3

Which drug can be used in a patient with CML and a T315i mutation?

Accepted Answer

Ponatinib

Answer

Imatinib

Answer

Nilotinib

Answer

Dasatinib

Question 4

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

Accepted Answer

All-trans retinoic acid

Answer

Methotrexate

Answer

Prednisolone

Answer

L-Asparaginase

Question 5

Rituximab is used for the treatment of which of the following conditions?

Accepted Answer

Non-Hodgkin's lymphoma

Answer

Rheumatoid arthritis

Answer

Crohn's disease

Answer

Colorectal carcinoma

Question 6

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

Accepted Answer

Imatinib

Answer

Hydroxycarbamide

Answer

Alpha-interferon

Answer

Busulphan

Question 7

Sorafenib is used in which of the following conditions?

Accepted Answer

Acute myeloid leukemia (AML)

Answer

Multiple myeloma

Answer

Chronic lymphocytic leukemia (CLL)

Answer

Acute lymphoblastic leukemia (ALL)

Question 8

Which of the following anticancer drugs is cell cycle specific?

Accepted Answer

Bleomycin

Answer

Dactinomycin

Answer

Mitomycin C

Answer

Daunorubicin

Question 9

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

Accepted Answer

None of the above

Answer

Vincristine

Answer

Methotrexate

Answer

Bleomycin

Question 10

A 35-year-old patient with carcinoma of the lung and a past history of lung disease is to be treated. Which of the following anticancer drugs should be avoided?

Accepted Answer

Bleomycin

Answer

Vinblastine

Answer

Mithramycin

Answer

Adriamycin

Anticancer Drugs — MCQs

Anticancer Drugs — MCQs

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