Anticancer Drugs Practice Questions

Q: All of the following drugs are components of the MOPP cancer chemotherapy regimen EXCEPT:

Methotrexate. **Explanation:** The **MOPP regimen** was the first highly effective combination chemotherapy used for the treatment of **Hodgkin Lymphoma**. The acronym stands for: * **M: Mechlorethamine** (Nitrogen mustard; an alkylating agent) * **O: Oncovin** (Brand name for **Vincristine**; a microtubule inhibitor) * **P: Procarbazine** (A methylhydrazine derivative/alkylating agent) [1] * **P: Prednisolone** (A glucocorticoid) **Why Methotrexate is the correct answer:** Methotrexate is a folate antagonist (antimetabolite) [2] used in various regimens like CMF (Breast cancer) or for maintenance in ALL, but it is **not** a component of the MOPP regimen. **Analysis of Incorrect Options:** * **Mechlorethamine:** It is the "M" in MOPP. It is a bifunctional alkylating agent that causes DNA cross-linking. * **Vincristine (Oncovin):** It is the "O" in MOPP. It acts by binding to tubulin and inhibiting microtubule assembly, leading to M-phase arrest. * **Procarbazine:** It is the first "P" in MOPP [1]. It is unique because it also acts as a weak MAO inhibitor. **High-Yield Clinical Pearls for NEET-PG:** 1. **ABVD Regimen:** Due to the high risk of secondary malignancies (like AML) and infertility associated with MOPP, it has largely been replaced by the **ABVD regimen** (Adriamycin, Bleomycin, Vinblastine, Dacarbazine) as the gold standard for Hodgkin Lymphoma. 2. **Procarbazine Side Effect:** It can cause a **Disulfiram-like reaction** with alcohol and hypertensive crises with tyramine-rich foods (due to MAO inhibition). 3. **Vincristine Side Effect:** The dose-limiting toxicity is **peripheral neuropathy** (areflexia, foot drop), unlike Vinblastine, which is more bone marrow suppressive ("Blastine blasts the marrow").

Q: What is the mechanism by which Tamoxifen reduces breast cancer?

It competes with the estrogen receptor in breast tissue.. ### Explanation **Mechanism of Action (Correct Answer: A)** Tamoxifen is a **Selective Estrogen Receptor Modulator (SERM)**. Its primary mechanism in breast tissue is **competitive antagonism** of the estrogen receptor (ER). By binding to the ER, it prevents endogenous estrogen from binding, thereby inhibiting the transcription of estrogen-responsive genes. This leads to a decrease in the proliferation of ER-positive breast cancer cells. **Analysis of Incorrect Options:** * **Option B:** While some anti-angiogenic drugs (like Bevacizumab) decrease blood supply, this is not the mechanism of Tamoxifen. * **Option C:** Tamoxifen is a hormonal therapy, not a cytotoxic (directly acting) chemotherapy drug. It is cytostatic (inhibits growth) rather than directly cytotoxic. * **Option D:** While Tamoxifen may be used alongside radiation, its primary mechanism is independent of augmenting radiation effects. **Clinical Pearls for NEET-PG:** * **Tissue-Specific Action:** Tamoxifen acts as an **antagonist in the breast** but as a **partial agonist in the endometrium and bone**. * **Side Effects:** Due to its agonist effect on the endometrium, it increases the risk of **endometrial carcinoma**. It also increases the risk of **thromboembolism** (DVT/PE). * **Benefits:** It helps prevent osteoporosis by maintaining bone mineral density (agonist effect on bone). * **Metabolism:** It is a prodrug converted to its active metabolite, **Endoxifen**, by the hepatic enzyme **CYP2D6**. * **Drug of Choice:** It is the gold standard for hormonal treatment in **pre-menopausal** women with ER-positive breast cancer.

Q: All of the following drugs are used in the treatment of Multiple myeloma, EXCEPT?

Hydroxyurea. **Explanation:** The correct answer is **Hydroxyurea**. **1. Why Hydroxyurea is the correct answer:** Hydroxyurea is a ribonucleotide reductase inhibitor that primarily acts on the S-phase of the cell cycle. Its clinical utility is focused on **Myeloproliferative Neoplasms (MPNs)** such as Chronic Myeloid Leukemia (CML), Polycythemia Vera, and Essential Thrombocythemia. It is also used in Sickle Cell Anemia to increase fetal hemoglobin (HbF). It is **not** a standard treatment for Multiple Myeloma (MM), which is a plasma cell dyscrasia. **2. Analysis of incorrect options:** * **Bortezomib:** A first-line **Proteasome Inhibitor**. It inhibits the 26S proteasome, leading to the accumulation of pro-apoptotic proteins. It is a cornerstone of modern MM therapy. * **Melphalan:** An **Alkylating agent** (Nitrogen mustard). Historically, Melphalan + Prednisolone was the gold standard. Today, high-dose Melphalan is the standard conditioning regimen used before Autologous Stem Cell Transplantation (ASCT) in MM patients. * **Cyclophosphamide:** Another **Alkylating agent** frequently used in MM, especially in combination regimens (e.g., CyBorD: Cyclophosphamide + Bortezomib + Dexamethasone) or for patients with renal impairment. **3. Clinical Pearls for NEET-PG:** * **Mnemonic for MM Drugs:** "**ABCD-M**" — **A**lkylators (Melphalan/Cyclophosphamide), **B**ortezomib (Proteasome inhibitors), **C**orticosteroids (Dexamethasone), **D**aratumumab (Anti-CD38), **I**mmunomodulators (Thalidomide/Lenalidomide). * **Bortezomib Side Effect:** Peripheral neuropathy and Herpes Zoster reactivation (prophylactic Acyclovir is required). * **Thalidomide/Lenalidomide:** Act by binding to **Cereblon** (E3 ubiquitin ligase). * **Drug of Choice for MM:** Triple therapy (Bortezomib + Lenalidomide + Dexamethasone) is currently preferred.

Q: What is the mechanism of action of bevacizumab?

Inhibitor of VEGF. **Explanation:** **Bevacizumab** is a recombinant humanized monoclonal antibody that acts as a potent **angiogenesis inhibitor**. Its primary mechanism of action is binding to and neutralizing **Vascular Endothelial Growth Factor (VEGF-A)**. By preventing VEGF from binding to its receptors (VEGFR-1 and VEGFR-2) on endothelial cells, bevacizumab inhibits the formation of new blood vessels (angiogenesis), thereby "starving" the tumor of the blood supply and nutrients required for growth and metastasis. **Analysis of Options:** * **Option A (Inhibitor of HER-2/neu):** This describes **Trastuzumab**. It is used primarily in HER-2 positive breast cancer and gastric cancer. * **Option B (Inhibitor of VEGF):** **Correct.** Bevacizumab specifically targets the VEGF ligand. * **Option C (Inhibitor of c-kit):** This describes **Imatinib**, a tyrosine kinase inhibitor used in Chronic Myeloid Leukemia (CML) and Gastrointestinal Stromal Tumors (GIST). **High-Yield NEET-PG Clinical Pearls:** 1. **Clinical Uses:** Bevacizumab is used in metastatic colorectal cancer, non-small cell lung cancer (NSCLC), renal cell carcinoma, and glioblastoma multiforme. 2. **Ocular Use:** It is frequently used "off-label" via intravitreal injection for **Age-related Macular Degeneration (ARMD)** and diabetic retinopathy to reduce neovascularization. 3. **Adverse Effects:** The most characteristic side effects include **hypertension**, proteinuria, impaired wound healing, and an increased risk of arterial thromboembolism or gastrointestinal perforation. 4. **Contraindication:** It should be avoided for at least 28 days before or after major surgery due to its impact on wound healing.

Q: Multiple myeloma is treated by all of the following EXCEPT:

All of the above. **Explanation:** Multiple Myeloma (MM) is a plasma cell dyscrasia that has seen a paradigm shift in treatment with the introduction of Immunomodulatory drugs (IMiDs) and Proteasome inhibitors. **1. Why "All of the above" is correct:** The management of Multiple Myeloma typically involves a combination of different classes of drugs to achieve remission. All three listed drugs—Lenalidomide, Bortezomib, and Thalidomide—are cornerstone FDA-approved therapies for MM. **2. Analysis of Options:** * **Thalidomide (Option C):** Historically used as a sedative, it is now a first-line agent for MM. It acts by inhibiting TNF-α and has potent anti-angiogenic properties. * **Lenalidomide (Option A):** A more potent derivative of thalidomide with fewer side effects (less peripheral neuropathy). It is currently a standard of care for both induction and maintenance therapy in MM. * **Bortezomib (Option B):** A reversible inhibitor of the **26S proteasome**. By inhibiting the degradation of pro-apoptotic proteins and blocking the NF-κB pathway, it leads to the death of malignant plasma cells. **3. High-Yield Clinical Pearls for NEET-PG:** * **Mechanism of IMiDs:** Thalidomide and Lenalidomide bind to a protein called **Cereblon**, leading to the degradation of transcription factors (Ikaros/Aiolos) essential for myeloma cell survival. * **Side Effects:** * **Thalidomide:** Highly teratogenic (**Phocomelia**) and causes significant peripheral neuropathy. * **Lenalidomide:** Main dose-limiting toxicity is **myelosuppression** (neutropenia/thrombocytopenia). * **Bortezomib:** Associated with **Herpes Zoster reactivation** (prophylactic acyclovir is often given) and peripheral neuropathy. * **Other MM Drugs:** Daratumumab (Anti-CD38 monoclonal antibody) and Dexamethasone are also frequently used in combination regimens (e.g., VRd: Velcade/Bortezomib, Revlimid/Lenalidomide, dexamethasone).

Q: All are true statements about anticancer drugs except?

Irinotecan is a topoisomerase II inhibitor. **Explanation:** The correct answer is **B**, as Irinotecan is a **Topoisomerase I inhibitor**, not a Topoisomerase II inhibitor. 1. **Why Option B is the correct answer (False statement):** Topoisomerase inhibitors are classified based on the enzyme they target. **Irinotecan** and **Topotecan** (Camptothecin derivatives) inhibit Topoisomerase I, which is responsible for single-strand DNA breaks. In contrast, Topoisomerase II inhibitors include **Etoposide**, **Teniposide**, and **Anthracyclines** (like Doxorubicin), which facilitate double-strand DNA breaks. 2. **Analysis of other options (True statements):** * **Option A:** **Vincristine** is famously known as a "marrow-sparing" drug. Unlike most cytotoxic agents, its dose-limiting toxicity is peripheral neuropathy rather than myelosuppression. * **Option C:** **L-asparaginase** is unique because it interferes with protein synthesis. Its classic side effects include **acute pancreatitis**, hyperglycemia (due to insulin deficiency), and clotting factor deficiencies. * **Option D:** **Anthracyclines** (Doxorubicin, Daunorubicin) are notorious for causing **cardiotoxicity** (dilated cardiomyopathy) mediated by free radical generation. This can be mitigated by the iron-chelating agent **Dexrazoxane**. **High-Yield Clinical Pearls for NEET-PG:** * **Mnemonic for Topoisomerase II inhibitors:** "**ET**" (**E**toposide, **T**eniposide). * **Mnemonic for Topoisomerase I inhibitors:** "**I** can **Top**" (**I**rinotecan, **Top**otecan). * **Vincristine vs. Vinblastine:** Vincristine spares the marrow (**C**risps the nerves), while Vin**b**lastine **b**lasts the marrow (causes myelosuppression). * **Bleomycin** and **Busulfan** are known for causing pulmonary fibrosis. * **Cyclophosphamide** is associated with hemorrhagic cystitis (prevented by **MESNA**).

Q: All of the following are mTOR inhibitors except?

Tacrolimus. ### Explanation The Mammalian Target of Rapamycin (mTOR) is a protein kinase that regulates cell growth, proliferation, and survival. mTOR inhibitors are a class of drugs used primarily as immunosuppressants and in the treatment of certain malignancies (like renal cell carcinoma). **Why Tacrolimus is the correct answer:** While **Tacrolimus** (FK506) and Sirolimus both bind to the same intracellular protein—the **FK-binding protein (FKBP-12)**—their downstream mechanisms differ significantly. The Tacrolimus-FKBP complex inhibits **Calcineurin**, a phosphatase required for the activation of NFAT (Nuclear Factor of Activated T-cells), thereby preventing IL-2 transcription. It does **not** inhibit the mTOR pathway. **Analysis of incorrect options (mTOR Inhibitors):** * **Sirolimus (Rapamycin):** The prototype mTOR inhibitor. The Sirolimus-FKBP complex binds to and inhibits mTOR, blocking the cell cycle transition from G1 to S phase. * **Everolimus:** A derivative of sirolimus with better oral bioavailability. It is used in drug-eluting stents and for treating advanced renal cell carcinoma and breast cancer. * **Temsirolimus:** An intravenous prodrug of sirolimus specifically indicated for advanced renal cell carcinoma. **High-Yield Clinical Pearls for NEET-PG:** * **Side Effects:** Unlike Calcineurin inhibitors (Tacrolimus/Cyclosporine), mTOR inhibitors are **not nephrotoxic**. However, they commonly cause **hyperlipidemia**, thrombocytopenia, and impaired wound healing. * **Mnemonic:** Remember the **"Limus"** family. While all end in "-limus," **Tacrolimus** is the "odd one out" as a Calcineurin inhibitor, while **S**irolimus, **E**verolimus, and **T**emsirolimus (**SET**) are mTOR inhibitors. * **Drug-Eluting Stents:** Sirolimus and Everolimus are frequently used to prevent neointimal hyperplasia (restenosis).

Q: Which of the following is an antifolate cancer drug?

Methotrexate. ### Explanation **Correct Option: A. Methotrexate** Methotrexate is the prototypical **antifolate** antimetabolite. It acts by competitively inhibiting the enzyme **Dihydrofolate Reductase (DHFR)**. This inhibition prevents the conversion of dihydrofolate to tetrahydrofolate (THF), the active form of folic acid required for the synthesis of thymidylate and purines. Consequently, DNA synthesis is halted, leading to "thymineless death" of rapidly dividing cancer cells. **Analysis of Incorrect Options:** * **B. Azathioprine:** This is a **purine analog** (a prodrug of 6-mercaptopurine). While it is an antimetabolite used as an immunosuppressant, it does not target folate metabolism. * **C. Cyclosporin:** This is a **calcineurin inhibitor**. It acts by inhibiting T-cell activation via the suppression of IL-2 production. It is not a cytotoxic anticancer drug but an immunosuppressant. * **D. Vincristine:** This is a **Vinca alkaloid** that acts as a mitotic inhibitor. It binds to tubulin and prevents microtubule polymerization, arresting the cell cycle in the M-phase. **High-Yield Clinical Pearls for NEET-PG:** * **Rescue Therapy:** High-dose Methotrexate toxicity is managed with **Leucovorin (Folinic acid)**, which bypasses the inhibited DHFR enzyme to provide a source of active folate. * **Adverse Effects:** Notable for causing **mucositis**, bone marrow suppression, and nephrotoxicity (due to crystalluria). * **Resistance:** Often occurs due to decreased drug uptake or increased synthesis of the DHFR enzyme. * **Other Antifolates:** Pemetrexed and Pralatrexate are newer agents in this class.

Q: Which monoclonal antibody is known to cause cardiomyopathy?

Trastuzumab. **Explanation:** **Trastuzumab** is a humanized monoclonal antibody targeting the **HER2/neu (ErbB2) receptor**, primarily used in HER2-positive breast cancer [1]. The underlying mechanism for its cardiotoxicity lies in the fact that HER2 receptors are also expressed on cardiomyocytes, where they play a vital role in cell survival and repair pathways. Inhibition of these receptors leads to **Type II Chemotherapy-Induced Cardiac Dysfunction (CICD)**. * **Why Trastuzumab is correct:** Unlike anthracyclines (Type I), Trastuzumab-induced cardiomyopathy is **not dose-dependent**, does not involve structural damage (no biopsy changes), and is usually **reversible** upon discontinuation of the drug [1]. * **Why other options are incorrect:** * **Infliximab, Adalimumab, and Etanercept:** These are TNF-alpha inhibitors used in autoimmune conditions like Rheumatoid Arthritis. While they are contraindicated in patients with pre-existing severe heart failure (NYHA Class III/IV) because they may worsen outcomes, they are not primary causes of de novo cardiomyopathy. **High-Yield Clinical Pearls for NEET-PG:** 1. **Monitoring:** Baseline and periodic evaluation of **LVEF (Left Ventricular Ejection Fraction)** via ECHO or MUGA scan is mandatory for patients on Trastuzumab [2]. 2. **Synergy:** The risk of cardiotoxicity increases significantly when Trastuzumab is used concurrently with **Anthracyclines** (e.g., Doxorubicin) [1]. 3. **Reversibility:** Trastuzumab toxicity is characterized by "myocardial stunning" rather than permanent myocyte death.

Q: All the following drugs are used in the treatment of metastatic breast cancer except?

Sunitinib. **Explanation:** The correct answer is **Sunitinib**. **1. Why Sunitinib is the correct answer:** Sunitinib is a multi-targeted receptor tyrosine kinase inhibitor (TKI) that primarily inhibits VEGF receptors, PDGF receptors, and c-KIT [2]. It is the standard of care for **Metastatic Renal Cell Carcinoma (mRCC)**, Gastrointestinal Stromal Tumors (GIST), and Pancreatic Neuroendocrine Tumors (pNETs) [2]. It has no established role or FDA approval for the treatment of metastatic breast cancer. **2. Analysis of incorrect options:** * **Ixabepilone:** An **Epothilone B analog** that stabilizes microtubules (similar to taxanes but binds to a different site). It is specifically indicated for metastatic or locally advanced breast cancer, especially in patients resistant to anthracyclines and taxanes. * **Abemaciclib & Ribociclib:** These are **CDK 4/6 inhibitors**. They inhibit the cell cycle transition from G1 to S phase. Both are first-line treatments for Hormone Receptor (HR)-positive, HER2-negative metastatic breast cancer, usually in combination with aromatase inhibitors (e.g., Letrozole). **3. High-Yield Clinical Pearls for NEET-PG:** * **CDK 4/6 Inhibitors:** Palbociclib, Ribociclib, and Abemaciclib. *Mnemonic: "PAR" for Breast Cancer.* * **Ixabepilone:** Unique because it remains active in cells that overexpress P-glycoprotein (MDR1 gene), making it effective in taxane-resistant breast cancer. * **Sunitinib Side Effect:** Characteristically causes **Hand-Foot Syndrome** and yellowing of the skin/depigmentation of hair. * **Trastuzumab/Pertuzumab:** Targeted therapy for HER2-positive breast cancer [1], [2].

Question 1

All of the following drugs are components of the MOPP cancer chemotherapy regimen EXCEPT:

Accepted Answer

Methotrexate

Answer

Procarbazine

Answer

Vincristine

Answer

Mechlorethamine

Question 2

What is the mechanism by which Tamoxifen reduces breast cancer?

Accepted Answer

It competes with the estrogen receptor in breast tissue.

Answer

It decreases the blood supply to the tumor.

Answer

It is a directly acting anticancer drug.

Answer

It augments radiation therapy.

Question 3

All of the following drugs are used in the treatment of Multiple myeloma, EXCEPT?

Accepted Answer

Hydroxyurea

Answer

Bortezomib

Answer

Melphalan

Answer

Cyclophosphamide

Question 4

What is the mechanism of action of bevacizumab?

Accepted Answer

Inhibitor of VEGF

Answer

Inhibitor of HER-2/Neu

Answer

Inhibitor of c-kit

Answer

None of the above

Question 5

Multiple myeloma is treated by all of the following EXCEPT:

Accepted Answer

All of the above

Answer

Lenalidomide

Answer

Bortezomib

Answer

Thalidomide

Question 6

All are true statements about anticancer drugs except?

Accepted Answer

Irinotecan is a topoisomerase II inhibitor

Answer

Vincristine is a marrow sparing anticancer drug

Answer

L-asparaginase can cause acute pancreatitis

Answer

Anthracyclines cause cardiotoxicity

Question 7

All of the following are mTOR inhibitors except?

Accepted Answer

Tacrolimus

Answer

Sirolimus

Answer

Everolimus

Answer

Temsirolimus

Question 8

Which of the following is an antifolate cancer drug?

Accepted Answer

Methotrexate

Answer

Azathioprine

Answer

Cyclosporin

Answer

Vincristine

Question 9

Which monoclonal antibody is known to cause cardiomyopathy?

Accepted Answer

Trastuzumab

Answer

Infliximab

Answer

Etanercept

Answer

Adalimumab

Question 10

All the following drugs are used in the treatment of metastatic breast cancer except?

Accepted Answer

Sunitinib

Answer

Ixabepilone

Answer

Abemaciclib

Answer

Ribociclib

Anticancer Drugs — MCQs

Anticancer Drugs — MCQs

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