Anticancer Drugs Practice Questions

Q: Which of the following is a highly emetogenic chemotherapy drug?

Cisplatin. **Explanation:** The emetogenic potential of chemotherapy drugs is categorized based on the percentage of patients who experience vomiting without antiemetic prophylaxis. **Correct Answer: D. Cisplatin** Cisplatin is the prototype of **High Emetogenic Risk (>90%)** chemotherapy. It triggers nausea and vomiting through two pathways: 1. **Acute Phase:** Occurs within 24 hours due to serotonin (5-HT3) release from enterochromaffin cells in the GI tract. 2. **Delayed Phase:** Occurs after 24 hours (peak at 48–72h) primarily mediated by Substance P acting on **NK1 receptors** in the brainstem. *Management:* Requires a triple-drug regimen (5-HT3 antagonist + Dexamethasone + NK1 antagonist like Aprepitant). **Incorrect Options:** * **A. 5-Fluorouracil:** Classified as **Low Emetogenic Risk (10–30%)**. It is an antimetabolite primarily associated with mucositis and diarrhea. * **B. Paclitaxel:** Classified as **Low Emetogenic Risk (10–30%)**. Its major dose-limiting toxicity is peripheral neuropathy and hypersensitivity reactions. * **C. Vincristine:** Classified as **Minimal Emetogenic Risk ( 90%):** Cisplatin, Dacarbazine, Cyclophosphamide (>1500 mg/m²). * **Moderately Emetogenic (30–90%):** Carboplatin, Oxaliplatin, Doxorubicin. * **Drug of Choice for Cisplatin-induced vomiting:** * *Acute:* Ondansetron (5-HT3 blocker). * *Delayed:* Aprepitant (NK1 blocker). * **Cisplatin Toxicity Triad:** Nephrotoxicity (prevented by aggressive hydration/Amifostine), Ototoxicity, and severe Emetogenicity.

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: What class of drug is Tamoxifen?

SERM (Selective Estrogen Receptor Modulator). **Explanation:** **Tamoxifen** is the prototypical **Selective Estrogen Receptor Modulator (SERM)** [1]. The core pharmacological concept of SERMs is their **tissue-specific action**: they act as competitive antagonists of estrogen in some tissues while acting as agonists in others [3]. * **Mechanism in Breast:** Tamoxifen acts as an **antagonist** on estrogen receptors in breast tissue, inhibiting the growth of estrogen-receptor-positive (ER+) breast cancer cells [1]. * **Mechanism in Other Tissues:** It acts as a partial **agonist** in the bone (preventing osteoporosis) and the endometrium [4]. **Analysis of Incorrect Options:** * **SSRI (A), SNRI (C), and DNRI (D):** These are classes of **antidepressants** that modulate neurotransmitters (Serotonin, Norepinephrine, and Dopamine) in the synaptic cleft. They have no structural or functional relationship to estrogen receptor modulation. Note: Some SSRIs (like Paroxetine) can actually inhibit the metabolism of Tamoxifen via CYP2D6, potentially reducing its efficacy. **High-Yield Clinical Pearls for NEET-PG:** 1. **Drug of Choice:** Tamoxifen is the gold standard for pre-menopausal women with ER-positive breast cancer [1]. 2. **Metabolism:** It is a prodrug converted to its active metabolite, **Endoxifen**, by the hepatic enzyme **CYP2D6**. 3. **Adverse Effects:** Due to its agonist effect on the endometrium, it increases the risk of **Endometrial Carcinoma** [2]. It also increases the risk of **Thromboembolism** (DVT/PE) and causes "hot flashes" [2]. 4. **Raloxifene:** Another SERM used for osteoporosis; unlike Tamoxifen, it is an *antagonist* in the uterus and does not increase endometrial cancer risk [3], [4].

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).

Question 1

Which of the following is a highly emetogenic chemotherapy drug?

Accepted Answer

Cisplatin

Answer

5–Fluorouracil

Answer

Paclitaxel

Answer

Vincristine

Question 2

Which of the following is NOT included in the management of febrile neutropenic patients receiving anti-cancer therapy?

Accepted Answer

Transfusion of granulocytes

Answer

Colony stimulating factors

Answer

Antibiotic prophylaxis

Answer

Repeated hand washing

Question 3

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 4

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

Accepted Answer

Hydroxyurea

Answer

Bortezomib

Answer

Melphalan

Answer

Cyclophosphamide

Question 5

Which of the following statements regarding the management of iron toxicity in a 3-year-old child presenting with severe GI distress, hematemesis, a shock-like state with marked dehydration, and progressive hemorrhagic gastritis is accurate?

Accepted Answer

Deferoxamine should be administered as soon as possible.

Answer

Gastric lavage should not be attempted due to the risk of aspiration.

Answer

The patient is likely to have a reduced anion gap.

Answer

Urinary alkalization increases the elimination of iron.

Question 6

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 7

Multiple myeloma is treated by all of the following EXCEPT:

Accepted Answer

All of the above

Answer

Lenalidomide

Answer

Bortezomib

Answer

Thalidomide

Question 8

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 9

What class of drug is Tamoxifen?

Accepted Answer

SERM (Selective Estrogen Receptor Modulator)

Answer

SSRI (Selective Serotonin Reuptake Inhibitor)

Answer

SNRI (Serotonin-Norepinephrine Reuptake Inhibitor)

Answer

DNRI (Dopamine-Norepinephrine Reuptake Inhibitor)

Question 10

All of the following are mTOR inhibitors except?

Accepted Answer

Tacrolimus

Answer

Sirolimus

Answer

Everolimus

Answer

Temsirolimus

Anticancer Drugs — MCQs

Anticancer Drugs — MCQs

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