Anticancer Drugs — MCQs

Anticancer Drugs Indian Medical PG Practice Questions and MCQs

Question 331: Which of the following is not an alkylating agent?

A. 5-fluorouracil (Correct Answer)
B. Melphalan
C. Cyclophosphamide
D. Chlorambucil

Explanation: **Explanation:** The correct answer is **5-fluorouracil (5-FU)** because it belongs to the **Antimetabolite** class of anticancer drugs, specifically the pyrimidine analogs. It works by inhibiting the enzyme *thymidylate synthase*, thereby interfering with DNA synthesis (S-phase specific), rather than by cross-linking DNA strands directly. **Analysis of Options:** * **5-fluorouracil (Option A):** As an antimetabolite, it mimics uracil and inhibits DNA synthesis. It is not an alkylating agent. * **Melphalan (Option B):** A nitrogen mustard derivative and a classic alkylating agent commonly used in the treatment of Multiple Myeloma. * **Cyclophosphamide (Option C):** A nitrogen mustard prodrug (activated by cytochrome P450) and one of the most widely used alkylating agents. * **Chlorambucil (Option D):** A nitrogen mustard alkylating agent primarily used in Chronic Lymphocytic Leukemia (CLL). **Mechanism of Alkylating Agents:** Alkylating agents work by attaching an alkyl group to the guanine base of DNA (at the N7 position). This leads to DNA cross-linking, strand breakage, and inhibition of DNA replication, which is cell-cycle non-specific. **High-Yield Clinical Pearls for NEET-PG:** * **Cyclophosphamide:** Watch for **Hemorrhagic Cystitis** caused by the metabolite **Acrolein**. This is prevented by aggressive hydration and **MESNA** (Mercaptoethane sulfonate). * **5-Fluorouracil:** Often administered with **Leucovorin** (folinic acid), which enhances its binding to thymidylate synthase, increasing its efficacy. * **Busulfan:** An alkylating agent notorious for causing **Pulmonary Fibrosis** and "Busulfan Tan" (skin hyperpigmentation). * **Nitrosoureas (Lomustine, Carmustine):** Alkylating agents that are highly lipid-soluble and cross the blood-brain barrier, making them first-line for brain tumors.

Question 332: What is the first-line drug of choice for Chronic Myeloid Leukemia (CML)?

A. Crizotinib
B. Ibrutinib
C. Imatinib (Correct Answer)
D. Gilterinib

Explanation: ### Explanation **Correct Answer: C. Imatinib** **Mechanism and Rationale:** 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 cellular proliferation. **Imatinib** is a 2-phenylaminopyrimidine derivative that acts as a specific **Tyrosine Kinase Inhibitor (TKI)**. It works by binding to the ATP-binding site of the BCR-ABL enzyme, effectively "turning off" the proliferative signal. It is the established first-line standard of care for CML in the chronic phase. **Analysis of Incorrect Options:** * **A. Crizotinib:** This is a TKI targeting **ALK (Anaplastic Lymphoma Kinase)** and ROS1. It is primarily used in Non-Small Cell Lung Cancer (NSCLC). * **B. Ibrutinib:** This is a **Bruton’s Tyrosine Kinase (BTK) inhibitor**. It is used for B-cell malignancies like Chronic Lymphocytic Leukemia (CLL) and Mantle Cell Lymphoma, not CML. * **D. Gilterinib:** This is a selective **FLT3 inhibitor** used in the treatment of relapsed or refractory Acute Myeloid Leukemia (AML) with FLT3 mutations. **High-Yield Clinical Pearls for NEET-PG:** * **Side Effects of Imatinib:** Most characteristic is **periorbital edema** (fluid retention). It can also cause GI upset and muscle cramps. * **Resistance:** Resistance to Imatinib often occurs due to the **T315I mutation**. In such cases, **Ponatinib** is the drug of choice. * **Second-generation TKIs:** Dasatinib and Nilotinib are used if Imatinib is not tolerated or if the disease is resistant. * **Monitoring:** Treatment response in CML is monitored via **cytogenetic analysis** and **RT-PCR** for BCR-ABL transcript levels.

Question 333: Cardiotoxicity induced by Doxorubicin can be reduced by:

A. Dexrazoxane (Correct Answer)
B. Amifostine
C. Leucovorin
D. Bisphosphonates

Explanation: ### Explanation **Correct Option: A. Dexrazoxane** Doxorubicin (an Anthracycline) causes dose-dependent cardiotoxicity primarily through the generation of **iron-mediated free radicals** (reactive oxygen species) [1]. These radicals damage the myocardium, which is particularly vulnerable due to low levels of catalase. **Dexrazoxane** is an iron-chelating agent that binds to intracellular iron, preventing the formation of the iron-anthracycline complex and subsequent oxidative stress [1]. It is FDA-approved specifically to reduce the incidence and severity of cardiomyopathy associated with doxorubicin administration. **Analysis of Incorrect Options:** * **B. Amifostine:** A cytoprotective agent (free radical scavenger) used primarily to reduce **nephrotoxicity** associated with Cisplatin and to prevent xerostomia during radiation therapy. * **C. Leucovorin (Folinic Acid):** Used as a "rescue" therapy to prevent bone marrow toxicity after high-dose **Methotrexate** or to enhance the efficacy of 5-Fluorouracil (5-FU) in colorectal cancer. * **D. Bisphosphonates:** Used in oncology to manage **hypercalcemia of malignancy** and to prevent skeletal-related events (fractures) in patients with bone metastases. **High-Yield Clinical Pearls for NEET-PG:** * **Doxorubicin Toxicity:** Look for "dilated cardiomyopathy" or "congestive heart failure" in clinical vignettes [1]. * **Cumulative Dose:** The risk of cardiotoxicity increases significantly when the cumulative dose of Doxorubicin exceeds **450–550 mg/m²** [1]. * **Monitoring:** Baseline and periodic evaluation of **LVEF (Left Ventricular Ejection Fraction)** via ECHO or MUGA scan is mandatory [1]. * **Other Protective Agents:** Mesna is used to prevent hemorrhagic cystitis caused by Cyclophosphamide/Ifosfamide.

Question 334: Which of the following is a radioactive anti-cancer monoclonal antibody?

A. Basiliximab
B. Bevacizumab
C. Ibritumomab (Correct Answer)
D. Rituximab

Explanation: **Explanation:** **Correct Answer: C. Ibritumomab** Ibritumomab tiuxetan is a murine monoclonal antibody directed against the **CD20 antigen** found on the surface of B-lymphocytes. It is unique because it acts as a carrier for a radioisotope (Radioimmunotherapy). In clinical practice, it is conjugated with **Yttrium-90** ($^{90}$Y). The antibody targets the B-cells, and the attached radioisotope delivers targeted radiation, causing DNA damage and cell death to both the target cell and neighboring tumor cells (the "bystander effect"). It is primarily used in the treatment of relapsed or refractory follicular B-cell non-Hodgkin lymphoma. **Analysis of Incorrect Options:** * **A. Basiliximab:** This is a chimeric monoclonal antibody that binds to the **IL-2 receptor (CD25)** on T-cells. It is used as an immunosuppressant to prevent acute organ rejection in renal transplants, not as a radioactive anticancer agent. * **B. Bevacizumab:** This is a humanized monoclonal antibody that targets **VEGF** (Vascular Endothelial Growth Factor). It acts as an angiogenesis inhibitor used in various cancers (colorectal, lung, renal), but it does not carry a radioisotope. * **D. Rituximab:** While Rituximab also targets the **CD20 antigen** (like Ibritumomab), it is a "naked" monoclonal antibody. It works via antibody-dependent cellular cytotoxicity (ADCC) and complement-mediated lysis rather than radiation. **High-Yield Clinical Pearls for NEET-PG:** * **Radioimmunotherapy (RIT) Examples:** Ibritumomab ($^{90}$Y) and Tositumomab ($^{131}$I). * **Suffix "–mab":** Monoclonal Antibody. * **Suffix "–ximab":** Chimeric (e.g., Rituximab). * **Suffix "–zumab":** Humanized (e.g., Bevacizumab). * **Suffix "–umab":** Fully Human (e.g., Panitumumab). * **Common Target:** CD20 is the most common target for B-cell lymphomas (Rituximab, Ibritumomab, Ofatumumab).

Question 335: Which of the following is not an antineoplastic antibiotic?

A. Actinomycin D
B. Doxorubicin
C. Bleomycin
D. Spiramycin (Correct Answer)

Explanation: **Explanation:** The correct answer is **Spiramycin** because it is a **Macrolide antibiotic**, not an antineoplastic (anticancer) agent. It is primarily used to treat toxoplasmosis and various bacterial infections by inhibiting protein synthesis (binding to the 50S ribosomal subunit). **Why the other options are incorrect:** * **Actinomycin D (Dactinomycin):** An antineoplastic antibiotic derived from *Streptomyces*. It acts by intercalating between DNA base pairs and inhibiting RNA polymerase, primarily used in pediatric tumors like Wilms' tumor and Ewing’s sarcoma. * **Doxorubicin:** An **Anthracycline** antibiotic. It works via DNA intercalation, inhibition of Topoisomerase II, and the generation of free radicals. It is a broad-spectrum anticancer drug but is notorious for cardiotoxicity. * **Bleomycin:** A glycopeptide antibiotic that causes DNA strand scission by generating free radicals. It is unique because it is "cell cycle specific" (G2 phase) and lacks significant bone marrow toxicity. **High-Yield Clinical Pearls for NEET-PG:** * **Bleomycin:** Most significant side effect is **Pulmonary Fibrosis**. It is "bone marrow sparing." * **Doxorubicin:** Dose-limiting toxicity is **Dilated Cardiomyopathy**. **Dexrazoxane** is used to prevent this cardiotoxicity. * **Actinomycin D:** Highly effective against gestational choriocarcinoma and Wilms' tumor. * **Spiramycin:** The drug of choice for **Toxoplasmosis in pregnancy** to prevent vertical transmission to the fetus.

Question 336: Thalidomide is used in the treatment of:

A. Multiple myeloma (Correct Answer)
B. Melanoma
C. Lung carcinoma
D. None of the above

Explanation: **Explanation:** **Thalidomide** is a potent immunomodulatory drug (IMiD) that has undergone a significant clinical evolution—from a sedative associated with severe teratogenicity to a cornerstone in hemato-oncology. **Why Multiple Myeloma is correct:** Thalidomide is highly effective in **Multiple Myeloma (MM)** due to its multi-modal mechanism of action: 1. **Anti-angiogenic:** It inhibits Vascular Endothelial Growth Factor (VEGF) and Basic Fibroblast Growth Factor (bFGF), starving the tumor of its blood supply. 2. **Immunomodulation:** It enhances T-cell and Natural Killer (NK) cell-mediated cytotoxicity against myeloma cells. 3. **Direct Apoptosis:** It induces cell cycle arrest and inhibits the binding of myeloma cells to bone marrow stromal cells. It is currently used (often with dexamethasone) for both newly diagnosed and refractory cases of MM. **Why other options are incorrect:** * **Melanoma & Lung Carcinoma:** While anti-angiogenic properties are useful in solid tumors, Thalidomide is not a standard-of-care or first-line treatment for these malignancies. These cancers are typically managed with targeted therapies (like BRAF inhibitors for melanoma), immunotherapy (Checkpoint inhibitors), or platinum-based chemotherapy. **High-Yield Clinical Pearls for NEET-PG:** * **Mechanism:** It acts by binding to **Cereblon (CRBN)**, a component of the E3 ubiquitin ligase complex. * **Teratogenicity:** It is a notorious human teratogen causing **Phocomelia** (seal-like limbs). It must be avoided in pregnancy (Category X). * **Other Uses:** Erythema Nodosum Leprosum (ENL), Aphthous ulcers in HIV, and Graft-versus-host disease (GVHD). * **Side Effects:** Peripheral neuropathy, sedation, and increased risk of venous thromboembolism (VTE). * **Derivatives:** Lenalidomide and Pomalidomide (more potent with fewer side effects).

Question 337: What medication should be administered prophylactically to individuals at high risk for developing breast cancer?

A. Tamoxifen (Correct Answer)
B. Aminoglutethimide
C. Diethylstilbestrol
D. Flutamide

Explanation: **Explanation:** **Tamoxifen** is the drug of choice for the chemoprevention of breast cancer in high-risk individuals (e.g., those with a strong family history or biopsy-confirmed atypical hyperplasia) [1]. It is a **Selective Estrogen Receptor Modulator (SERM)** that acts as a competitive antagonist at estrogen receptors in breast tissue, thereby inhibiting the proliferation of estrogen-dependent cancer cells [1]. Large clinical trials (like NSABP P-1) demonstrated that Tamoxifen reduces the incidence of invasive breast cancer by approximately 50% in high-risk pre- and post-menopausal women. **Analysis of Incorrect Options:** * **Aminoglutethimide:** This is a first-generation aromatase inhibitor and adrenal steroid synthesis inhibitor. While it was used in advanced breast cancer, it is not used for prophylaxis due to its significant side-effect profile (adrenal suppression). * **Diethylstilbestrol (DES):** A synthetic non-steroidal estrogen. It is actually associated with an *increased* risk of clear cell adenocarcinoma of the vagina in daughters of women who took it during pregnancy; it is never used for cancer prophylaxis. * **Flutamide:** A non-steroidal anti-androgen used primarily in the management of prostate cancer. It has no role in breast cancer prevention. **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:** Increased risk of **endometrial carcinoma** and **thromboembolism** (DVT/PE) [1]. It also causes "hot flashes." * **Alternative:** **Raloxifene** is also used for prophylaxis in post-menopausal women and carries a lower risk of endometrial cancer compared to Tamoxifen [1]. * **Drug Interaction:** Tamoxifen is a prodrug activated by **CYP2D6**. Potent inhibitors like Fluoxetine or Paroxetine can decrease its efficacy.

Question 338: Apalutamide was approved by FDA for which type of cancer?

A. Prostate cancer (Correct Answer)
B. Breast cancer
C. Hypertension
D. HIV

Explanation: **Explanation:** **Apalutamide** is a potent, second-generation **androgen receptor (AR) antagonist**. It works by binding directly to the ligand-binding domain of the AR, inhibiting receptor translocation to the nucleus and preventing DNA binding. This effectively blocks the growth-promoting effects of testosterone on prostate cancer cells. It is specifically FDA-approved for **Non-Metastatic Castration-Resistant Prostate Cancer (nmCRPC)** and Metastatic Castration-Sensitive Prostate Cancer (mCSPC). **Analysis of Incorrect Options:** * **B. Breast Cancer:** While hormonal therapy (like Tamoxifen or Aromatase inhibitors) is central to breast cancer treatment, Apalutamide is specific to the androgen pathway, not the estrogen pathway. * **C. Hypertension:** This is a cardiovascular condition. Drugs used here include ACE inhibitors or Beta-blockers. Apalutamide has no role in blood pressure management; in fact, hypertension can be a side effect of some AR inhibitors. * **D. HIV:** This is a viral infection treated with Highly Active Antiretroviral Therapy (HAART), such as Protease inhibitors or Reverse Transcriptase inhibitors. **High-Yield Clinical Pearls for NEET-PG:** * **Class:** Apalutamide belongs to the same class as **Enzalutamide** and **Darolutamide**. * **Advantage:** Unlike first-generation anti-androgens (e.g., Bicalutamide), second-generation drugs have a much higher affinity for the AR and do not exhibit agonist activity. * **Side Effect Profile:** A unique side effect to remember for Apalutamide is an increased risk of **seizures** and **skin rash**. * **Mechanism:** It inhibits three steps: AR binding, nuclear translocation, and DNA transcription.

Question 339: Which of the following is NOT used in the treatment protocol of Hodgkin's lymphoma?

A. Vincristine (Correct Answer)
B. Vinblastine
C. Bleomycin
D. Adriamycin

Explanation: To answer this question correctly, one must distinguish between the two primary chemotherapy regimens used for Hodgkin’s Lymphoma (HL): the historical **MOPP** regimen and the current gold standard **ABVD** regimen. ### 1. Why Vincristine is the Correct Answer While **Vincristine** is a mainstay in the treatment of Non-Hodgkin Lymphoma (as part of the CHOP regimen) and Pediatric Hodgkin’s (in the OEPA/COPP protocols), it is **not** part of the standard **ABVD** regimen, which is the first-line treatment for adult Hodgkin’s Lymphoma. Historically, Vincristine was used in the MOPP regimen (Mustine, Oncovin/Vincristine, Procarbazine, Prednisolone), but this has been largely phased out due to high toxicity and secondary malignancy risks. ### 2. Analysis of Incorrect Options (Components of ABVD) * **B. Vinblastine:** This is the "V" in ABVD. Unlike Vincristine, which causes significant neurotoxicity, Vinblastine is more associated with bone marrow suppression. * **C. Bleomycin:** The "B" in ABVD. It is an antitumor antibiotic known for causing pulmonary fibrosis but is unique because it lacks significant myelosuppression. * **D. Adriamycin (Doxorubicin):** The "A" in ABVD. It is an anthracycline that works via topoisomerase II inhibition and DNA intercalation. Its dose-limiting toxicity is cardiotoxicity. ### 3. High-Yield Clinical Pearls for NEET-PG * **ABVD Regimen:** **A**driamycin, **B**leomycin, **V**inblastine, **D**acarbazine. * **Vincristine vs. Vinblastine:** Remember the mnemonic: **"Vincristine blasts the nerves (Neurotoxicity), Vinblastine blasts the marrow (Bone marrow suppression)."** * **Dacarbazine:** An alkylating agent that is the "D" in ABVD. * **Drug of Choice:** ABVD is preferred over MOPP because it does not cause sterility and has a lower risk of inducing secondary leukemias.

Question 340: L–asparaginase is particularly used in which type of leukemia?

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

Explanation: **Explanation:** **Mechanism of Action & Rationale for ALL:** L-asparaginase is an enzyme that catalyzes the hydrolysis of circulating **L-asparagine** into aspartic acid and ammonia. Normal cells can synthesize their own asparagine using the enzyme *asparagine synthetase*. However, **Acute Lymphoblastic Leukemia (ALL)** cells lack this enzyme and are entirely dependent on exogenous (blood-derived) asparagine for protein synthesis. By depleting the systemic supply of asparagine, L-asparaginase selectively induces metabolic stress and apoptosis in lymphoblasts while sparing most normal tissues. **Analysis of Options:** * **Acute Lymphoblastic Leukemia (ALL):** This is the primary indication. It is a cornerstone of induction therapy, especially in pediatric populations. * **AML, CML, and CLL:** These myeloid and chronic lymphoid malignancies typically possess sufficient levels of asparagine synthetase. Therefore, they are not "asparagine-dependent" and do not respond significantly to L-asparaginase therapy. **High-Yield Clinical Pearls for NEET-PG:** * **Unique Toxicity Profile:** Unlike most cytotoxic drugs, L-asparaginase is **not bone marrow suppressive** (it is "bone marrow sparing"). * **Key Side Effects:** 1. **Hypersensitivity Reactions:** Being a foreign bacterial protein (derived from *E. coli*), it frequently causes anaphylaxis. 2. **Acute Pancreatitis:** A classic, high-yield association. 3. **Clotting Abnormalities:** It decreases the synthesis of clotting factors and Antithrombin III, leading to both thrombosis and hemorrhage. 4. **Hyperammonemia:** Due to the byproduct of asparagine breakdown.

Practice by Chapter

Principles of Cancer Chemotherapy

Practice Questions

Alkylating Agents

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Antimetabolites

Practice Questions

Antitumor Antibiotics

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Plant Alkaloids

Practice Questions

Topoisomerase Inhibitors

Practice Questions

Hormonal Agents

Practice Questions

Targeted Therapy

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Immunotherapy

Practice Questions

Management of Chemotherapy Side Effects

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