Anticancer Drugs Practice Questions

Q: Hydroxyurea's mechanism of action in cancer is by inhibiting which enzyme?

Ribonucleotide diphosphate reductase. **Explanation** **Mechanism of Action** Hydroxyurea is an S-phase specific antimetabolite. Its primary mechanism of action is the inhibition of the enzyme **Ribonucleotide diphosphate reductase (RNR)**. This enzyme is responsible for the rate-limiting step in DNA synthesis: the conversion of ribonucleoside diphosphates (NDPs) to deoxyribonucleoside diphosphates (dNDPs). By inhibiting RNR, hydroxyurea depletes the intracellular pool of deoxyribonucleotides, thereby halting DNA synthesis and repair. **Analysis of Options** * **Option A (Correct):** Ribonucleotide diphosphate reductase is the specific target. Hydroxyurea acts by scavenging the tyrosyl free radical required for the enzyme's catalytic activity. * **Option B:** Ribonucleotide oxidase is not a recognized enzyme in the de novo synthesis of nucleotides. * **Option C & D:** DNA lyase and DNA synthetase (often referred to as DNA Polymerase/Ligase) are involved in the later stages of DNA strand assembly and repair, but they are not the targets of hydroxyurea. **Clinical Pearls for NEET-PG** * **Sickle Cell Anemia:** Hydroxyurea is the drug of choice to reduce the frequency of painful crises. It works by **increasing the levels of Fetal Hemoglobin (HbF)**, which inhibits the polymerization of HbS. * **Myeloproliferative Disorders:** It is used in the management of Chronic Myeloid Leukemia (CML), Polycythemia Vera, and Essential Thrombocythemia to rapidly lower cell counts. * **Radiation Sensitizer:** It is used in cervical and head/neck cancers to synchronize cells in the G1 phase, making them more sensitive to radiotherapy. * **Side Effect:** The most common dose-limiting toxicity is **myelosuppression** (leukopenia). It can also cause macrocytosis and cutaneous ulcers.

Q: Which of the following is a significant cause of alopecia (epilation)?

Doxorubicin. **Explanation:** **Doxorubicin (Option A)** is the correct answer. Alopecia (hair loss) is a common side effect of cytotoxic chemotherapy because these drugs target rapidly dividing cells [1]. Hair follicle matrix cells have a high mitotic index, making them highly susceptible. Doxorubicin, an anthracycline, is notorious for causing **complete and severe alopecia** (often occurring within 2–3 weeks of the first cycle). It works by intercalating DNA and inhibiting Topoisomerase II, leading to significant damage in the hair bulb. **Analysis of Incorrect Options:** * **Docetaxel (Option B):** While taxanes do cause significant alopecia, Doxorubicin is classically associated with the most profound and rapid epilation in pharmacological literature and exams. * **Rituximab (Option C):** This is a monoclonal antibody targeting CD20 on B-cells. Unlike cytotoxic drugs, it does not typically affect hair follicles and rarely causes alopecia. * **Carboplatin (Option D):** While platinum compounds can cause hair thinning [1], the incidence and severity are significantly lower compared to anthracyclines like Doxorubicin. **High-Yield NEET-PG Pearls:** * **"Red Devil":** Doxorubicin is nicknamed the "Red Devil" due to its red color and significant toxicities, including **cardiotoxicity** (dilated cardiomyopathy) and severe alopecia. * **Prevention:** Scalp cooling (cold caps) is used to induce vasoconstriction, reducing the delivery of chemotherapy to hair follicles. * **Other high-alopecia drugs:** Cyclophosphamide, Vincristine, and Paclitaxel. * **Minimal-alopecia drugs:** Methotrexate (low dose), Fluorouracil (5-FU), and Bleomycin.

Q: Toxicity of nitrogen mustards can be decreased by?

GM-CSF. ### Explanation **Correct Answer: C. GM-CSF** **Mechanism and Rationale:** Nitrogen mustards (e.g., Cyclophosphamide, Ifosfamide, Mechlorethamine) are potent alkylating agents. Their most common dose-limiting toxicity is **bone marrow suppression (myelosuppression)**, leading to severe neutropenia and increased risk of infections. **GM-CSF (Granulocyte-Macrophage Colony-Stimulating Factor)**, such as Sargramostim, or G-CSF (Filgrastim), stimulates the production and differentiation of myeloid progenitor cells in the bone marrow. By accelerating the recovery of neutrophil counts, GM-CSF directly mitigates the hematological toxicity caused by nitrogen mustards. **Analysis of Incorrect Options:** * **A. Allopurinol:** While used in cancer patients, it is specifically indicated to prevent **Tumor Lysis Syndrome** (hyperuricemia) resulting from rapid cell kill. It does not reduce the direct cytotoxic damage of nitrogen mustards on healthy tissues. * **B. Folinic acid (Leucovorin):** This is the specific "rescue" agent for **Methotrexate** (a folate antagonist) toxicity. It has no role in reversing the DNA alkylation caused by nitrogen mustards. **High-Yield Clinical Pearls for NEET-PG:** * **Mesna:** Specifically used to prevent **Hemorrhagic Cystitis** caused by the metabolite *Acrolein* during Cyclophosphamide or Ifosfamide therapy. * **Amifostine:** A cytoprotective agent used to reduce renal toxicity from Cisplatin. * **Dexrazoxane:** Used to prevent cardiomyopathy caused by Anthracyclines (Doxorubicin). * **Nitrogen Mustard Mnemonic:** *Mechlorethamine* was the first non-hormonal anticancer drug developed from mustard gas used in WWI.

Q: Which of the following drugs can cause delayed bone marrow suppression leading to sustained neutropenia?

Carmustine. **Explanation:** The correct answer is **Carmustine (Option D)**. **1. Why Carmustine is correct:** Carmustine (BCNU) and Lomustine (CCNU) are **Nitrosoureas**, a class of alkylating agents. Unlike most cytotoxic drugs that cause a nadir (lowest point of blood counts) at 7–14 days, Nitrosoureas are notorious for causing **delayed and cumulative bone marrow suppression**. The neutropenia and thrombocytopenia typically occur **4 to 6 weeks** after administration and can be prolonged. This delay is due to their action on early hematopoietic stem cells rather than rapidly dividing committed progenitors. **2. Analysis of Incorrect Options:** * **Vincristine (A):** A Vinca alkaloid known for being **"bone marrow sparing."** Its dose-limiting toxicity is peripheral neuropathy (paresthesia, foot drop), not myelosuppression. * **Carboplatin (B):** While it causes significant thrombocytopenia, the suppression is typically not "delayed" in the 6-week timeframe characteristic of Nitrosoureas. * **Melphalan (C):** An alkylating agent used in Multiple Myeloma. While it causes myelosuppression, it follows a more standard recovery timeline compared to the profound delay seen with Carmustine. **3. High-Yield Clinical Pearls for NEET-PG:** * **Nitrosoureas (Carmustine/Lomustine):** Highly lipid-soluble; they cross the Blood-Brain Barrier (BBB) and are the drugs of choice for **Glut-4/Brain tumors (Gliomas)**. * **Busulfan:** Another alkylating agent known for "prolonged" marrow suppression and a specific side effect called **"Busulfan Tan"** (skin hyperpigmentation) and pulmonary fibrosis. * **Marrow Sparing Drugs:** Remember the mnemonic **"VBC"** — Vincristine, Bleomycin, and Cisplatin (Cisplatin is more nephrotoxic/emetogenic than myelotoxic).

Q: Which of the following agents is known to cause epilation?

Adriamycin. **Explanation:** **Adriamycin (Doxorubicin)**, an anthracycline antibiotic, is notorious for causing significant **alopecia (epilation)**. The underlying mechanism involves the drug’s interference with rapidly dividing cells. Hair follicles have a high mitotic index; Adriamycin inhibits Topoisomerase II and generates free radicals, leading to DNA damage in the hair bulb. This results in an "anagen effluvium," where hair loss is often complete and occurs within 1–3 weeks of treatment. **Analysis of Incorrect Options:** * **5-Fluorouracil (5-FU):** While it can cause thinning of hair, its hallmark toxicity is **Hand-Foot Syndrome** (palmar-plantar erythrodysesthesia) and GI mucosal ulceration. * **Cisplatin:** This platinum compound is primarily known for its dose-limiting **nephrotoxicity** and severe **emetogenicity**. It causes minimal hair loss compared to anthracyclines. * **Methotrexate:** An antimetabolite that primarily causes **myelosuppression** and **mucositis**. While it can cause some hair thinning, it rarely leads to the total epilation characteristic of Adriamycin. **High-Yield Clinical Pearls for NEET-PG:** 1. **Anthracycline Toxicity:** Apart from epilation, the most specific side effect is **Cardiotoxicity** (dilated cardiomyopathy). This is mediated by iron-dependent superoxide free radicals. 2. **Dexrazoxane:** An iron chelator used to prevent Adriamycin-induced cardiotoxicity. 3. **Radiation Recall:** Adriamycin can cause inflammatory skin reactions in previously irradiated areas. 4. **Red Urine:** Patients should be counseled that Adriamycin can cause harmless red discoloration of urine (not hematuria).

Q: Which of the following chemotherapeutic drugs has selective action on hypoxic tumor cells?

Mitomycin C. **Explanation:** **Mitomycin C** is the correct answer because it acts as a **bioreductive alkylating agent**. It is a prodrug that requires enzymatic activation (reduction) to form a highly reactive DNA-crosslinking species. This activation process is significantly more efficient in **hypoxic environments** (low oxygen levels) compared to well-oxygenated tissues. Since the core of solid tumors is often poorly vascularized and hypoxic, Mitomycin C exhibits selective toxicity toward these cells, making it a unique tool in treating solid tumors like those of the stomach, pancreas, and bladder. **Analysis of Incorrect Options:** * **B. Cisplatin:** A platinum compound that causes DNA cross-linking. Its efficacy is actually **reduced** in hypoxic conditions because hypoxia can lead to decreased drug uptake and slower cell cycling. * **C. Doxorubicin:** An anthracycline that inhibits Topoisomerase II and generates free radicals. Its free-radical-mediated damage requires **oxygen**, making it less effective in hypoxic tumor zones. * **D. 5-Fluorouracil (5-FU):** An antimetabolite (pyrimidine analog) that inhibits thymidylate synthase. It is most effective against rapidly dividing cells in the S-phase and does not have a selective mechanism for hypoxia. **High-Yield Clinical Pearls for NEET-PG:** * **Dose-Limiting Toxicity:** Mitomycin C causes delayed and prolonged **bone marrow suppression** (thrombocytopenia and leukopenia). * **Specific Side Effect:** It is associated with **Hemolytic Uremic Syndrome (HUS)** and pulmonary fibrosis. * **Clinical Use:** Often used intravesically for superficial bladder cancer to prevent recurrence. * **Concept:** Tumors with high hypoxic fractions are generally resistant to radiotherapy; Mitomycin C is often used as a "hypoxic cell sensitizer" to bridge this gap.

Q: Bevacizumab is:

Monoclonal antibody against VEGF. **Explanation:** **Bevacizumab** is a recombinant humanized monoclonal antibody that acts as a potent **angiogenesis inhibitor**. It works by specifically binding to and neutralizing **Vascular Endothelial Growth Factor (VEGF-A)**. By preventing VEGF from binding to its receptors (VEGFR-1 and VEGFR-2) on the surface of endothelial cells, it inhibits the formation of new blood vessels (neovascularization), thereby "starving" the tumor of oxygen and nutrients required for growth and metastasis. **Analysis of Incorrect Options:** * **Option B (Anti-IL-2):** Drugs like **Daclizumab** and **Basiliximab** are monoclonal antibodies against the IL-2 receptor (CD25), primarily used as immunosuppressants in renal transplants. * **Option C (Anti-FGFR):** While Fibroblast Growth Factor Receptor (FGFR) inhibitors exist (e.g., **Erdafitinib**), they are typically small molecule tyrosine kinase inhibitors rather than widely used monoclonal antibodies in standard NEET-PG curricula. * **Option D (Anti-EGFR):** Monoclonal antibodies against the Epidermal Growth Factor Receptor (EGFR) include **Cetuximab** and **Panitumumab**, commonly used in colorectal and head/neck cancers. **High-Yield Clinical Pearls for NEET-PG:** 1. **Clinical Uses:** Bevacizumab is used in metastatic colorectal cancer, non-small cell lung cancer (NSCLC), glioblastoma, and renal cell carcinoma. 2. **Ocular Use:** It is frequently used **off-label** (intravitreal injection) for **Wet Age-Related Macular Degeneration (ARMD)** and diabetic retinopathy to reduce macular edema. 3. **Key Side Effects:** The most characteristic adverse effects include **hypertension**, impaired wound healing, arterial thrombosis, and **proteinuria**. 4. **Suffix Tip:** Monoclonal antibodies ending in **"-umab"** are human, while **"-ximab"** are chimeric.

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.

Question 1

Hydroxyurea's mechanism of action in cancer is by inhibiting which enzyme?

Accepted Answer

Ribonucleotide diphosphate reductase

Answer

Ribonucleotide oxidase

Answer

DNA lyase

Answer

DNA synthetase

Question 2

Which of the following is a significant cause of alopecia (epilation)?

Accepted Answer

Doxorubicin

Answer

Docetaxel

Answer

Rituximab

Answer

Carboplatin

Question 3

Toxicity of nitrogen mustards can be decreased by?

Accepted Answer

GM-CSF

Answer

Allopurinol

Answer

Folinic acid

Answer

All

Question 4

Which of the following drugs can cause delayed bone marrow suppression leading to sustained neutropenia?

Accepted Answer

Carmustine

Answer

Vincristine

Answer

Carboplatin

Answer

Melphalan

Question 5

Which of the following agents is known to cause epilation?

Accepted Answer

Adriamycin

Answer

5-Flurouracil

Answer

Cisplatin

Answer

Methotrexate

Question 6

Which of the following chemotherapeutic drugs has selective action on hypoxic tumor cells?

Accepted Answer

Mitomycin C

Answer

Cisplatin

Answer

Doxorubicin

Answer

5-Fluorouracil

Question 7

Bevacizumab is:

Accepted Answer

Monoclonal antibody against VEGF

Answer

Anti-IL-2 monoclonal antibody

Answer

Monoclonal antibody against FGFR

Answer

Monoclonal antibody against EGFR

Question 8

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

Accepted Answer

Methotrexate

Answer

Procarbazine

Answer

Vincristine

Answer

Mechlorethamine

Question 9

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 10

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

Accepted Answer

Hydroxyurea

Answer

Bortezomib

Answer

Melphalan

Answer

Cyclophosphamide

Anticancer Drugs — MCQs

Anticancer Drugs — MCQs

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