Anticancer Drugs Practice Questions

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

Tamoxifen. **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.

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

Vincristine. 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.

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

Acute Lymphoblastic Leukemia (ALL). **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.

Q: Inotuzumab acts against which CD antigen?

CD22. **Inotuzumab ozogamicin** is an antibody-drug conjugate (ADC) consisting of a humanized monoclonal antibody targeting **CD22**, linked to a cytotoxic agent called calicheamicin . 1. **Why CD22 is correct:** CD22 is a cell surface antigen expressed on more than 90% of B-cell malignancies. When Inotuzumab binds to CD22, the complex is internalized, and calicheamicin is released, causing double-stranded DNA breaks and subsequent cell death. It is primarily used in the treatment of relapsed or refractory **B-cell precursor Acute Lymphoblastic Leukemia (ALL)**. 2. **Analysis of Incorrect Options:** * **CD11:** CD11c is a marker typically associated with Hairy Cell Leukemia and myeloid cells; no major monoclonal antibody used in ALL targets this. * **CD19:** This is the target for **Blinatumomab** (a BiTE - Bispecific T-cell Engager) and **Tisagenlecleucel** (CAR-T cell therapy). * **CD25:** This is the alpha chain of the IL-2 receptor, targeted by **Basiliximab** and **Daclizumab** (used in transplant medicine to prevent rejection). **High-Yield Clinical Pearls for NEET-PG:** * **Mnemonic:** Inotu-**ZZ**-umab targets CD-**22**. * **Black Box Warning:** Inotuzumab is associated with a high risk of **Hepatotoxicity**, specifically **Veno-Occlusive Disease (VOD)** or Sinusoidal Obstruction Syndrome, especially after hematopoietic stem cell transplant. * **Gemtuzumab ozogamicin:** A similar ADC that targets **CD33**, used in Acute Myeloid Leukemia (AML). Remember: **G**emtuzumab for **G**ranulocytes (Myeloid).

Q: Which of the following anticancer drugs causes nephrotoxicity as an adverse effect?

Cisplatin. ### Explanation **Correct Answer: D. Cisplatin** **Mechanism and Nephrotoxicity:** Cisplatin is a potent platinum-based alkylating-like agent that inhibits DNA synthesis by forming intra-strand cross-links. Its most significant dose-limiting toxicity is **nephrotoxicity**, specifically causing **Acute Tubular Necrosis (ATN)**. It accumulates in the proximal convoluted tubule cells, leading to oxidative stress and apoptosis. To mitigate this, clinicians use **aggressive hydration** with normal saline and may administer **Amifostine** (a cytoprotective free-radical scavenger). **Analysis of Incorrect Options:** * **A. Imatinib:** A selective Tyrosine Kinase Inhibitor (TKI) targeting the BCR-ABL protein. Its hallmark side effect is **fluid retention**, typically manifesting as periorbital edema. * **B. Irinotecan:** A Topoisomerase I inhibitor used in colorectal cancer. Its classic adverse effect is **severe diarrhea** ("I run to the can"), which can be acute (cholinergic) or delayed. * **C. Bleomycin:** An antitumor antibiotic that causes DNA strand breaks. Its dose-limiting toxicity is **Pulmonary Fibrosis**, not renal damage. It is unique because it lacks significant bone marrow suppression. **High-Yield Clinical Pearls for NEET-PG:** * **Cisplatin Triad of Toxicity:** Nephrotoxicity, Ototoxicity (high-frequency hearing loss), and severe Emetogenicity (requires Aprepitant/Ondansetron). * **Electrolyte Imbalance:** Cisplatin frequently causes **Hypomagnesemia** due to renal wasting. * **Carboplatin:** A related drug that is less nephrotoxic but more myelosuppressive (causes thrombocytopenia).

Q: Which of the following predominantly cause sensory neuropathy?

Cisplatin. **Explanation:** The correct answer is **Cisplatin**. This platinum-based chemotherapeutic agent is notorious for causing a dose-dependent, **predominantly sensory peripheral neuropathy**. **1. Why Cisplatin is correct:** Cisplatin accumulates in the **dorsal root ganglia (DRG)**, which lack a robust blood-nerve barrier. It causes DNA damage and oxidative stress in the sensory neurons, leading to a "dying-back" axonal degeneration. Patients typically present with a "glove-and-stocking" distribution of sensory loss, paresthesia, and loss of vibratory sense. Unlike many other drugs, it rarely affects motor fibers. **2. Analysis of Incorrect Options:** * **Pyridoxine (Vitamin B6) excess:** While chronic high doses of Pyridoxine *can* cause a pure sensory neuropathy, it is less commonly tested in this context compared to Cisplatin. Furthermore, in the context of NEET-PG, Cisplatin is the classic pharmacological prototype for drug-induced sensory neuropathy. * **Diphtheria:** This causes a **mixed** neuropathy. The toxin typically leads to cranial nerve palsies (palatal paralysis) followed by a generalized sensorimotor polyneuropathy. * **Guillain-Barre Syndrome (GBS):** This is the classic example of an acute inflammatory demyelinating polyradiculoneuropathy (AIDP). It is characterized by **predominantly motor**, ascending paralysis. **Clinical Pearls for NEET-PG:** * **Other drugs causing Sensory Neuropathy:** Taxanes (Paclitaxel), Thalidomide, and Ethambutol. * **Drugs causing Motor Neuropathy:** Dapsone, Lead poisoning (wrist drop/foot drop), and Vincristine (though Vincristine is often mixed, motor involvement is prominent). * **Cisplatin Toxicity Triad:** Nephrotoxicity (prevented by Amifostine/hydration), Ototoxicity, and Peripheral Neuropathy.

Q: Which of the following drugs is used for Acute Myeloid Leukemia (AML)?

Ozogamicin. ### **Explanation** **Correct Option: C. Ozogamicin** **Gemtuzumab ozogamicin** is a monoclonal antibody conjugated with a cytotoxic agent (calicheamicin). It specifically targets **CD33**, a cell surface antigen expressed on the blasts of approximately 90% of patients with **Acute Myeloid Leukemia (AML)**. Once bound, the complex is internalized, releasing calicheamicin to cause DNA double-strand breaks and cell death. It is FDA-approved for both newly diagnosed and relapsed/refractory CD33-positive AML. **Incorrect Options:** * **A. Bevacizumab:** This is a humanized monoclonal antibody against **VEGF** (Vascular Endothelial Growth Factor). It acts as an angiogenesis inhibitor and is primarily used in solid tumors like colorectal cancer, renal cell carcinoma, and glioblastoma. * **B. Rituximab:** This targets the **CD20** antigen found on B-cells. It is the cornerstone treatment for B-cell Non-Hodgkin Lymphomas (NHL), Chronic Lymphocytic Leukemia (CLL), and various autoimmune conditions, but not AML (which is of myeloid origin). * **D. Trastuzumab:** This is a monoclonal antibody against the **HER2/neu** receptor. It is used specifically in HER2-positive breast cancer and gastric adenocarcinoma. **High-Yield Clinical Pearls for NEET-PG:** * **Gemtuzumab ozogamicin Side Effect:** A significant and specific adverse effect is **Sinusoidal Obstruction Syndrome (SOS)**, formerly known as Veno-Occlusive Disease (VOD). * **Other "Mabs" in Hemat-Oncology:** * **Brentuximab vedotin:** Targets **CD30** (used in Hodgkin Lymphoma). * **Alemtuzumab:** Targets **CD52** (used in CLL). * **Blinatumomab:** A BiTE (Bispecific T-cell Engager) targeting **CD19** and **CD3** (used in ALL).

Q: What is the most important adverse effect of Bleomycin?

Pulmonary fibrosis. **Explanation:** **Bleomycin** is a unique cytotoxic antibiotic that acts by binding to DNA and causing single- and double-strand breaks through the generation of free radicals (ferrous iron oxidation). **Why Pulmonary Fibrosis is the correct answer:** The most serious and dose-limiting toxicity of Bleomycin is **Pulmonary Fibrosis**. This occurs because the enzyme responsible for inactivating Bleomycin (**Bleomycin hydrolase**) is significantly deficient in the lungs and skin. Consequently, the drug accumulates in pulmonary tissues, leading to oxidative stress, inflammation, and eventual fibrosis. It typically presents as dry cough and progressive dyspnea. **Analysis of Incorrect Options:** * **A. Myelosuppression:** Unlike most conventional anticancer drugs, Bleomycin is famously **"bone marrow sparing."** This makes it a vital component of combination regimens (like ABVD for Hodgkin’s Lymphoma) as it does not worsen leukopenia or thrombocytopenia. * **B. Hepatotoxicity:** While some chemotherapeutic agents (like Methotrexate or 6-Mercaptopurine) are hepatotoxic, it is not a characteristic or dose-limiting side effect of Bleomycin. * **D. Peripheral Neuropathy:** This is the classic dose-limiting toxicity of **Vinca alkaloids** (Vincristine) and **Taxanes** (Paclitaxel), not Bleomycin. **High-Yield Clinical Pearls for NEET-PG:** * **Monitoring:** Patients on Bleomycin should undergo periodic **Pulmonary Function Tests (PFTs)**; a decrease in DLCO (Diffusion Capacity of Carbon Monoxide) is an early sign of toxicity. * **Dermatological Toxicity:** Bleomycin can cause **Flagellate hyperpigmentation** (whip-like streaks on the skin). * **Cell Cycle:** It is a **G2-phase specific** drug. * **Cumulative Dose:** The risk of fibrosis increases significantly when the cumulative dose exceeds **400 units**.

Q: Which of the following drugs is used as an immunosuppressant but lacks anticancer activity?

Azathioprine. **Explanation** The correct answer is **Azathioprine**. **Why Azathioprine is correct:** Azathioprine is a prodrug of **6-Mercaptopurine (6-MP)**. While 6-MP is used in the treatment of acute leukemias (anticancer), Azathioprine is specifically designed to release 6-MP slowly. This slow release results in a sustained suppression of T-lymphocyte proliferation, making it an excellent **immunosuppressant** for organ transplantation and autoimmune diseases (like Rheumatoid Arthritis or SLE). However, because it does not achieve the rapid, high peak concentrations required to kill rapidly dividing malignant cells, it **lacks significant anticancer activity**. **Analysis of Incorrect Options:** * **Methotrexate:** A folate antagonist that inhibits dihydrofolate reductase (DHFR). It is used both as an anticancer agent (choriocarcinoma, osteosarcoma) and as an immunosuppressant (RA, Psoriasis). * **6-Mercaptopurine:** A purine analog that inhibits de novo purine synthesis. It is a potent anticancer drug used primarily in Acute Lymphoblastic Leukemia (ALL). * **5-Fluorouracil:** A pyrimidine analog that inhibits thymidylate synthase. It is a mainstay in the treatment of solid tumors, particularly colorectal and breast cancers, but is not used as a systemic immunosuppressant. **High-Yield Clinical Pearls for NEET-PG:** * **Drug Interaction:** Both Azathioprine and 6-MP are metabolized by **Xanthine Oxidase**. If a patient is also taking **Allopurinol** (a xanthine oxidase inhibitor), the dose of Azathioprine/6-MP must be reduced by **75%** to avoid life-threatening bone marrow toxicity. * **Pharmacogenomics:** Patients with a genetic deficiency of the enzyme **TPMT** (Thiopurine Methyltransferase) are at high risk of severe myelosuppression when taking these drugs. * **Leflunomide** is another example of a drug used as an immunosuppressant (DMARD) that lacks anticancer activity.

Q: Sterile hemorrhagic cystitis is caused by:

Cyclophosphamide. **Explanation:** **Cyclophosphamide** (and its analog Ifosfamide) is a nitrogen mustard alkylating agent. Its metabolism in the liver produces a toxic metabolite called **Acrolein**. Acrolein is excreted in the urine, where it causes direct irritation and sloughing of the bladder mucosa, leading to **sterile hemorrhagic cystitis** (characterized by hematuria without evidence of infection). **Why the other options are incorrect:** * **Busulfan:** An alkylating agent primarily used in CML. Its classic side effects include pulmonary fibrosis ("Busulfan lung"), skin hyperpigmentation, and adrenal insufficiency-like syndrome. * **Ketoprofen:** An NSAID. While it can cause renal impairment (interstitial nephritis or papillary necrosis), it is not associated with hemorrhagic cystitis. * **Methicillin:** A penicillinase-resistant penicillin. Its classic renal side effect is **Acute Interstitial Nephritis (AIN)**, often presenting with fever, rash, and eosinophiluria. **High-Yield Clinical Pearls for NEET-PG:** * **Prevention:** Hemorrhagic cystitis can be prevented by aggressive hydration and the administration of **MESNA** (2-Mercaptoethane Sulfonate Na). * **Mechanism of MESNA:** It contains a sulfhydryl group that binds to and neutralizes acrolein in the bladder to form a non-toxic compound. * **Other Side Effects of Cyclophosphamide:** Bone marrow suppression, alopecia, and increased risk of transitional cell carcinoma of the bladder. * **Specific Toxicity:** While Cyclophosphamide causes cystitis, **Busulfan** is notorious for causing **Veno-occlusive disease (VOD)** of the liver.

Question 1

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

Accepted Answer

Tamoxifen

Answer

Aminoglutethimide

Answer

Diethylstilbestrol

Answer

Flutamide

Question 2

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

Accepted Answer

Vincristine

Answer

Vinblastine

Answer

Bleomycin

Answer

Adriamycin

Question 3

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

Accepted Answer

Acute Lymphoblastic Leukemia (ALL)

Answer

Acute Myeloid Leukemia (AML)

Answer

Chronic Myeloid Leukemia (CML)

Answer

Chronic Lymphocytic Leukemia (CLL)

Question 4

Inotuzumab acts against which CD antigen?

Accepted Answer

CD22

Answer

CD11

Answer

CD19

Answer

CD25

Question 5

Which of the following anticancer drugs causes nephrotoxicity as an adverse effect?

Accepted Answer

Cisplatin

Answer

Imatinib

Answer

Irinotecan

Answer

Bleomycin

Question 6

Which of the following predominantly cause sensory neuropathy?

Accepted Answer

Cisplatin

Answer

Pyridoxine excess

Answer

Diphtheria

Answer

Guillain-Barre syndrome

Question 7

Which of the following drugs is used for Acute Myeloid Leukemia (AML)?

Accepted Answer

Ozogamicin

Answer

Bevacizumab

Answer

Rituximab

Answer

Trastuzumab

Question 8

What is the most important adverse effect of Bleomycin?

Accepted Answer

Pulmonary fibrosis

Answer

Myelosuppression

Answer

Hepatotoxicity

Answer

Peripheral neuropathy

Question 9

Which of the following drugs is used as an immunosuppressant but lacks anticancer activity?

Accepted Answer

Azathioprine

Answer

Methotrexate

Answer

6-Mercaptopurine

Answer

5-Fluorouracil

Question 10

Sterile hemorrhagic cystitis is caused by:

Accepted Answer

Cyclophosphamide

Answer

Busulfan

Answer

Ketoprofen

Answer

Methicillin

Anticancer Drugs — MCQs

Anticancer Drugs — MCQs

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