Anticancer Drugs — MCQs

Anticancer Drugs Indian Medical PG Practice Questions and MCQs

Question 251: What is the drug of choice in multiple myeloma?

A. Mechlorethamine
B. Vincristine
C. Vinblastine
D. Melphalan (Correct Answer)

Explanation: **Explanation:** **Melphalan** is an alkylating agent belonging to the nitrogen mustard group. It is considered the traditional drug of choice for Multiple Myeloma (MM) because it specifically targets plasma cells. Its mechanism involves cross-linking DNA strands, which inhibits DNA synthesis and leads to apoptosis in the rapidly dividing malignant plasma cells. While newer proteasome inhibitors (like Bortezomib) and immunomodulators (like Lenalidomide) are now used in induction therapy, Melphalan remains the gold standard for conditioning regimens prior to Autologous Stem Cell Transplantation (ASCT). **Analysis of Incorrect Options:** * **Mechlorethamine:** This was the first nitrogen mustard used clinically. It is primarily used in the MOPP regimen for Hodgkin’s Lymphoma, but it is highly toxic and rarely used for MM. * **Vincristine:** A vinca alkaloid that inhibits microtubule assembly. While it was part of the older VAD (Vincristine, Adriamycin, Dexamethasone) regimen for MM, it is no longer a first-line choice due to peripheral neuropathy and the superior efficacy of newer agents. * **Vinblastine:** Also a vinca alkaloid, but its primary clinical utility is in Hodgkin’s Lymphoma, bladder cancer, and testicular cancer, rather than plasma cell dyscrasias. **High-Yield Clinical Pearls for NEET-PG:** * **Melphalan Side Effect:** Significant bone marrow suppression (dose-limiting toxicity). * **MP Regimen:** The combination of Melphalan + Prednisolone was the historical standard for elderly patients with MM. * **Drug of Choice for MM (Modern):** For transplant-eligible patients, the current initial treatment of choice is **Bortezomib + Lenalidomide + Dexamethasone (VRd)**. * **Thalidomide:** Originally a teratogen (phocomelia), it is now a key drug in MM management due to its anti-angiogenic properties.

Question 252: Aromatase inhibitors are used in the treatment of which of the following cancers?

A. Lung cancer
B. Breast cancer (Correct Answer)
C. Liver cancer
D. Colon cancer

Explanation: **Explanation:** **Aromatase inhibitors (AIs)**, such as Letrozole, Anastrozole, and Exemestane, are the treatment of choice for hormone receptor-positive (ER/PR+) **breast cancer** in postmenopausal women. The underlying medical concept involves the synthesis of estrogen. In postmenopausal women, the ovaries stop producing estrogen; instead, the enzyme **aromatase** converts adrenal androgens (androstenedione and testosterone) into estrogens (estrone and estradiol) in peripheral tissues like fat and muscle. Since many breast tumors are estrogen-dependent, inhibiting this enzyme deprives the tumor cells of the growth signals they need, leading to tumor regression. **Analysis of Incorrect Options:** * **A. Lung Cancer:** Primarily treated with surgery, radiotherapy, and chemotherapy (e.g., Cisplatin) or targeted therapies (e.g., EGFR inhibitors like Erlotinib), but not hormonal manipulation via aromatase. * **C. Liver Cancer (HCC):** Management involves surgical resection, kinase inhibitors (e.g., Sorafenib), or transplant; it is not driven by estrogen pathways. * **D. Colon Cancer:** Standard treatment involves the FOLFOX regimen (5-Fluorouracil, Leucovorin, Oxaliplatin). It does not respond to aromatase inhibition. **High-Yield Clinical Pearls for NEET-PG:** * **Drug of Choice:** AIs are preferred over Tamoxifen in **postmenopausal** women because they are more effective and lack the risk of endometrial cancer. * **Tamoxifen vs. AIs:** Tamoxifen is a SERM used in **premenopausal** women. AIs are ineffective in premenopausal women because they cannot overcome the high estrogen production from functional ovaries. * **Side Effects:** The most characteristic side effect of AIs is **osteoporosis** and increased risk of fractures (due to total estrogen deprivation), whereas Tamoxifen increases the risk of **thromboembolism** and **endometrial carcinoma**.

Question 253: Which of the following is an inhibitor of dihydrofolate reductase?

A. Phenytoin
B. Alcohol
C. Methotrexate (Correct Answer)
D. Yeast

Explanation: **Explanation:** **1. Mechanism of the Correct Answer (Methotrexate):** Methotrexate (MTX) is a folate antagonist and a cell cycle-specific antimetabolite (S-phase). It works by competitively inhibiting the enzyme **Dihydrofolate Reductase (DHFR)**. This enzyme is responsible for converting dihydrofolate into tetrahydrofolate (THF), the active form of folic acid. THF is a crucial one-carbon carrier required for the synthesis of thymidylate and purines. By blocking DHFR, MTX halts DNA synthesis, leading to "thymineless death" of rapidly dividing cancer cells. **2. Analysis of Incorrect Options:** * **Phenytoin:** This is an anti-epileptic drug. While it can cause folate deficiency (leading to megaloblastic anemia) by interfering with intestinal folate absorption or increasing folate catabolism, it does **not** inhibit the DHFR enzyme. * **Alcohol:** Chronic alcohol consumption can lead to folate deficiency by impairing folate absorption and increasing urinary excretion, but it has no direct inhibitory effect on DHFR. * **Yeast:** Yeast is actually a rich dietary **source** of folic acid. It does not inhibit folate metabolism; rather, it helps prevent deficiency. **3. NEET-PG High-Yield Clinical Pearls:** * **Leucovorin Rescue:** To minimize the systemic toxicity of high-dose MTX, **Folinic acid (Leucovorin)** is administered. It bypasses the blocked DHFR enzyme to provide a source of reduced folate to healthy cells. * **Resistance:** The most common mechanism of resistance to MTX is the synthesis of altered DHFR with reduced affinity for the drug or gene amplification leading to increased DHFR production. * **Other DHFR Inhibitors:** Remember the "MTP" mnemonic for DHFR inhibitors: **M**ethotrexate (Humans), **T**rimethoprim (Bacteria), and **P**yrimethamine (Protozoa). * **Adverse Effects:** Notable side effects include myelosuppression, mucositis, and hepatotoxicity (cirrhosis with long-term use).

Question 254: A 60-year-old female with breast carcinoma was prescribed herceptin (trastuzumab). Which of the following statements regarding this drug is TRUE?

A. It is an antibody produced entirely from mouse containing no human component.
B. It is a monoclonal antibody produced by injecting the HER2 antigen. (Correct Answer)
C. Injection of herceptin increases antibody response.
D. The protein HER2/Neu is expressed in increased amounts by breast cancer cells.

Explanation: ### Explanation **Trastuzumab (Herceptin)** is a recombinant DNA-derived monoclonal antibody used primarily in the treatment of HER2-positive breast cancer [1]. **1. Why Option B is Correct:** Monoclonal antibodies (mAbs) are produced using **hybridoma technology**. The process involves injecting a specific antigen (in this case, the **HER2/neu receptor protein**) into a laboratory animal (usually a mouse). The animal’s B-lymphocytes produce antibodies against this antigen, which are then fused with immortal myeloma cells to create a hybridoma cell line that secretes large quantities of the specific antibody. **2. Analysis of Incorrect Options:** * **Option A:** Trastuzumab is a **humanized** monoclonal antibody (indicated by the suffix *-zumab*). It is approximately 95% human and 5% murine. This reduces immunogenicity compared to pure mouse antibodies (*-omab*). * **Option C:** Trastuzumab does not work by increasing a general antibody response. It works by **selective binding** to the extracellular domain of the HER2 receptor [1], leading to the inhibition of cell proliferation and induction of antibody-dependent cellular cytotoxicity (ADCC). * **Option D:** While it is true that HER2 is overexpressed in about 20-30% of breast cancers, this statement describes the **pathology** of the disease rather than a characteristic of the **drug** itself. In the context of pharmacology questions regarding "statements regarding this drug," Option B more accurately describes the pharmacological nature/production of the agent. **3. NEET-PG High-Yield Pearls:** * **Mechanism:** Targets the HER2/neu (ErbB2) receptor [1], a member of the EGFR family with intrinsic tyrosine kinase activity. * **Adverse Effect:** The most significant side effect is **Cardiotoxicity** (decreased LVEF/Heart Failure) [1]. Unlike anthracyclines, trastuzumab-induced cardiotoxicity is usually **reversible** and not dose-dependent. * **Contraindication:** Avoid concurrent use with **Doxorubicin** due to synergistic cardiotoxicity [1]. * **Nomenclature:** * *-omab*: 100% Mouse * *-ximab*: Chimeric * *-zumab*: Humanized * *-umab*: 100% Human

Question 255: Which of the following anticancer agents has specific activity in a subset of female breast cancers?

A. Anastrozole
B. Doxorubicin
C. Fluoxymesterone
D. Trastuzumab (Correct Answer)

Explanation: **Explanation:** **Trastuzumab** is the correct answer because it is a recombinant DNA-derived humanized monoclonal antibody specifically designed to target the **HER2/neu (ErbB2) receptor**. This receptor is overexpressed in approximately 15–25% of female breast cancers. Trastuzumab inhibits the proliferation of tumor cells that overexpress HER2, making its activity specific to this molecular subset. **Analysis of Incorrect Options:** * **Anastrozole:** While used in breast cancer, it is a non-steroidal **Aromatase Inhibitor**. It works by blocking the peripheral conversion of androgens to estrogens. It is used in postmenopausal women with estrogen receptor-positive (ER+) cancer, but it is not considered "subset-specific" in the same targeted molecular context as Trastuzumab. * **Doxorubicin:** An anthracycline antibiotic that acts via DNA intercalation and inhibition of Topoisomerase II. It is a **broad-spectrum** cytotoxic agent used in many cancers (including breast cancer) regardless of specific receptor subsets. * **Fluoxymesterone:** An oral androgen occasionally used as palliative therapy in breast cancer, but it lacks the targeted specificity for a modern molecular subset. **High-Yield Clinical Pearls for NEET-PG:** * **Mechanism of Trastuzumab:** Binds to the extracellular domain of HER2; induces cell cycle arrest and antibody-dependent cellular cytotoxicity (ADCC). * **Key Side Effect:** **Cardiotoxicity** (manifests as a decrease in LVEF/congestive heart failure). Unlike Doxorubicin, Trastuzumab-induced cardiotoxicity is usually **reversible** and not dose-dependent. * **Monitoring:** Baseline and periodic Echocardiography/MUGA scans are mandatory. * **Combination Warning:** Never combine Trastuzumab with Anthracyclines (like Doxorubicin) due to synergistic cardiotoxicity.

Question 256: All of the following anticancer drugs act on the G2 phase except?

A. Paclitaxel (Correct Answer)
B. Etoposide
C. Irinotecan
D. Bleomycin

Explanation: **Explanation:** The cell cycle consists of specific phases (G1, S, G2, M), and many anticancer drugs are **cell-cycle specific**. To answer this question, one must distinguish between drugs acting on the **G2 phase** (pre-mitotic interval) and the **M phase** (mitosis). **1. Why Paclitaxel is the correct answer:** **Paclitaxel** (a Taxane) acts specifically on the **M phase**. Its mechanism involves stabilizing microtubules and inhibiting their depolymerization. This prevents the formation of the mitotic spindle, leading to mitotic arrest. Since it acts on the M phase and not the G2 phase, it is the "except" in this list. **2. Analysis of incorrect options (Drugs acting on G2):** * **Bleomycin:** This is a classic G2-specific drug. It causes DNA fragmentation by generating free radicals, arresting cells in the **G2 phase**. * **Etoposide:** A Topoisomerase II inhibitor. While it has some activity in the S phase, its primary lethal effect occurs in the **late S and G2 phases**. * **Irinotecan:** A Topoisomerase I inhibitor. These drugs typically cause arrest in the **S and G2 phases** by preventing the religation of DNA strands. **High-Yield Clinical Pearls for NEET-PG:** * **M-Phase Specific:** Vinca alkaloids (Vincristine/Vinblastine) and Taxanes (Paclitaxel/Docetaxel). * **S-Phase Specific:** Antimetabolites (Methotrexate, 5-FU, Cytarabine). * **G2-Phase Specific:** Bleomycin and Etoposide. * **Cell-Cycle Non-Specific (CCNS):** Alkylating agents (Cyclophosphamide) and Platinum compounds (Cisplatin). * **Side Effect Tip:** Bleomycin is notorious for **Pulmonary Fibrosis**, while Paclitaxel is known for **Peripheral Neuropathy** and hypersensitivity reactions.

Question 257: All of the following statements about vincristine are true EXCEPT?

A. It acts by inhibiting mitosis
B. Its prominent adverse effect is peripheral neuropathy
C. It does not suppress bone marrow
D. It is a drug of choice for solid tumors (Correct Answer)

Explanation: **Explanation:** **1. Why Option D is the Correct Answer (The "Except" statement):** Vincristine is primarily used in the treatment of **hematological malignancies** (e.g., Acute Lymphoblastic Leukemia, Hodgkin’s and Non-Hodgkin’s Lymphoma) and specific pediatric tumors (e.g., Wilms' tumor). While it is part of combination regimens for some solid tumors, it is **not** considered a general "drug of choice" for the broad category of adult solid tumors (like breast, lung, or colon cancer), where drugs like taxanes, platinum compounds, or 5-FU are preferred. **2. Analysis of Other Options:** * **Option A (Inhibits Mitosis):** Vincristine is a **Vinca alkaloid** that binds to tubulin and prevents its polymerization into microtubules. This causes **mitotic arrest in the M-phase**, specifically preventing the formation of the mitotic spindle. * **Option B (Peripheral Neuropathy):** This is the **dose-limiting toxicity** of vincristine. It interferes with axonal microtubule transport, leading to symmetrical sensory-motor neuropathy, paresthesia, and loss of deep tendon reflexes. * **Option C (Does not suppress bone marrow):** Vincristine is unique among traditional cytotoxic drugs because it is **bone marrow sparing**. This makes it an ideal component for combination chemotherapy (e.g., the MOPP or CHOP regimens) as it does not add to the myelosuppression caused by other agents. **NEET-PG High-Yield Pearls:** * **Vincristine vs. Vinblastine:** Remember the mnemonic: **"B"** for Vin**b**lastine = **B**one marrow suppression; **"C"** for Vin**c**ristine = **C**onstipation (autonomic neuropathy) and **C**entral/Peripheral nerve damage. * **Fatal Route:** Vincristine is for **Intravenous (IV) use only**. Intrathecal administration is fatal due to progressive neurotoxicity. * **SIADH:** Vincristine is a well-known cause of the Syndrome of Inappropriate Antidiuretic Hormone secretion.

Question 258: Pulmonary fibrosis is the most common complication after treatment with?

A. 6-mercaptopurine
B. Vincristine
C. Bleomycin (Correct Answer)
D. Adriamycin

Explanation: **Explanation:** **Bleomycin** is the correct answer because pulmonary toxicity, specifically **interstitial pulmonary fibrosis**, is its most significant dose-limiting adverse effect. **Why Bleomycin causes Pulmonary Fibrosis:** Bleomycin works by generating free radicals that cause DNA strand breaks. Unlike other tissues, the lungs and skin lack the enzyme **Bleomycin hydrolase**, which inactivates the drug. Consequently, the drug accumulates in the lungs, leading to oxidative damage, inflammation, and eventual fibrosis. This risk is cumulative (typically occurring at doses >400 units) and is exacerbated by high concentrations of inspired oxygen (FiO2). **Analysis of Incorrect Options:** * **A. 6-Mercaptopurine:** An antimetabolite primarily associated with **bone marrow suppression** (myelosuppression) and hepatotoxicity. * **B. Vincristine:** A vinca alkaloid known for its **neurotoxicity** (peripheral neuropathy, foot drop, and paralytic ileus). It is notably "bone marrow sparing." * **C. Adriamycin (Doxorubicin):** An anthracycline antibiotic whose hallmark toxicity is **cardiotoxicity** (dilated cardiomyopathy), mediated by iron-dependent free radical formation. **High-Yield Clinical Pearls for NEET-PG:** * **Monitoring:** Patients on Bleomycin should undergo regular **Pulmonary Function Tests (PFTs)**; a decrease in DLCO (Diffusion Capacity of Carbon Monoxide) is an early sign of toxicity. * **Skin Toxicity:** Bleomycin also causes **flagellate hyperpigmentation** (whip-like streaks on the skin). * **Busulfan:** Another classic anticancer drug (alkylating agent) that causes "Busulfan Lung" (pulmonary fibrosis). * **Other drugs causing Pulmonary Fibrosis:** Remember the mnemonic **"B-B-A-M"**: **B**leomycin, **B**usulfan, **A**miodarone, and **M**ethotrexate.

Question 259: What is the drug of choice for the T790M mutation of EGFR in Non-Small Cell Lung Cancer?

A. Lapatinib
B. Crizotinib
C. Alemtuzumab
D. Osimertinib (Correct Answer)

Explanation: **Explanation:** **Osimertinib** is the correct answer because it is a **third-generation irreversible EGFR Tyrosine Kinase Inhibitor (TKI)** specifically designed to target the **T790M resistance mutation**. In Non-Small Cell Lung Cancer (NSCLC), patients treated with first-generation TKIs (like Gefitinib or Erlotinib) often develop resistance via the T790M mutation, which increases the ATP affinity of the EGFR kinase domain. Osimertinib selectively inhibits both sensitizing mutations and the T790M resistance mutation while sparing wild-type EGFR, reducing skin and GI toxicity. **Analysis of Incorrect Options:** * **Lapatinib:** A dual TKI targeting both **EGFR (ErbB1) and HER2 (ErbB2)**. It is primarily used in HER2-positive breast cancer, not for T790M-mutated lung cancer. * **Crizotinib:** An inhibitor of **ALK (Anaplastic Lymphoma Kinase)**, ROS1, and MET. It is the drug of choice for ALK-positive NSCLC, but ineffective against EGFR mutations. * **Alemtuzumab:** A monoclonal antibody against **CD52**, used in Chronic Lymphocytic Leukemia (CLL) and Multiple Sclerosis, with no role in EGFR-mutated lung cancer. **High-Yield Clinical Pearls for NEET-PG:** * **Generations of EGFR TKIs:** * 1st Gen (Reversible): Gefitinib, Erlotinib. * 2nd Gen (Irreversible): Afatinib, Dacomitinib. * 3rd Gen (T790M specific): **Osimertinib**. * **Adverse Effect:** While Osimertinib has fewer skin rashes than 1st gen drugs, it can cause **QT interval prolongation** and cardiomyopathy. * **Blood-Brain Barrier:** Osimertinib has excellent CNS penetration, making it preferred for patients with brain metastases.

Question 260: Arsenic compounds are used for the treatment of which of the following cancers?

A. Acute Promyelocytic Leukemia (APML) (Correct Answer)
B. Chronic Lymphocytic Leukemia (CLL)
C. Acute Lymphoblastic Leukemia (ALL)
D. Chronic Myeloid Leukemia (CML)

Explanation: **Explanation:** **Arsenic Trioxide ($As_2O_3$)** is a highly effective treatment for **Acute Promyelocytic Leukemia (APML)**, specifically for patients who are refractory to or have relapsed after treatment with All-Trans Retinoic Acid (ATRA). **Why the correct answer is right:** APML (FAB M3 subtype) is characterized by the $t(15;17)$ translocation, which creates the **PML-RARα fusion protein**. This protein arrests myeloid differentiation at the promyelocyte stage. Arsenic Trioxide works through a dual mechanism: 1. **Degradation of the PML-RARα protein:** It binds directly to the PML moiety, inducing its degradation and allowing the cells to differentiate. 2. **Induction of Apoptosis:** It triggers the mitochondrial pathway of programmed cell death in leukemic cells. **Why incorrect options are wrong:** * **CLL (B):** Primarily treated with BTK inhibitors (Ibrutinib), BCL-2 inhibitors (Venetoclax), or anti-CD20 monoclonal antibodies (Rituximab). * **ALL (C):** Managed with a combination of Vincristine, L-Asparaginase, Corticosteroids, and Anthracyclines. * **CML (D):** The mainstay of treatment is Tyrosine Kinase Inhibitors (TKIs) like **Imatinib**, which target the BCR-ABL fusion protein. **High-Yield Clinical Pearls for NEET-PG:** * **Side Effects:** The most critical side effect of Arsenic Trioxide is **QT interval prolongation**, which can lead to Torsades de Pointes. Regular ECG monitoring is mandatory. * **Differentiation Syndrome:** Similar to ATRA, Arsenic can cause "Differentiation Syndrome" (fever, dyspnea, weight gain, pulmonary infiltrates), treated with high-dose **Dexamethasone**. * **Historical Context:** Arsenic was historically used as "Fowler’s Solution," but its modern use is strictly limited to APML.

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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