Anticancer Drugs — MCQs

Anticancer Drugs Indian Medical PG Practice Questions and MCQs

Question 541: A patient with breast cancer is administered a chemotherapy agent that stabilizes microtubules, preventing their disassembly during mitosis. Which drug is used?

A. Doxorubicin
B. Cyclophosphamide
C. Paclitaxel (Correct Answer)
D. Vincristine

Explanation: ***Paclitaxel*** - **Paclitaxel** is a **taxane** drug that works by binding to **beta-tubulin subunits**, stabilizing microtubules and preventing their depolymerization. - This stabilization arrests cells in the **G2/M phase of mitosis**, leading to apoptotic cell death in rapidly dividing cancer cells. *Doxorubicin* - **Doxorubicin** is an **anthracycline antibiotic** that intercalates into DNA, leading to strand breaks and inhibition of **topoisomerase II**. - Its primary mechanism is DNA damage, not direct microtubule stabilization. *Cyclophosphamide* - **Cyclophosphamide** is an **alkylating agent** that forms covalent bonds with DNA, causing cross-linking and strand breaks. - This DNA damage interferes with replication and transcription, leading to cell cycle arrest and apoptosis. *Vincristine* - **Vincristine** is a **vinca alkaloid** that binds to **tubulin dimers**, preventing their polymerization into microtubules. - Unlike paclitaxel, which stabilizes microtubules, vincristine inhibits their formation and promotes disassembly.

Question 542: Which enzyme is inhibited by the drug methotrexate during cancer treatment?

A. Dihydrofolate reductase (Correct Answer)
B. DNA polymerase
C. Ribonucleotide reductase
D. Thymidylate synthase

Explanation: ***Dihydrofolate reductase*** - **Methotrexate** is a **folate analog** that competitively inhibits **dihydrofolate reductase (DHFR)**, an enzyme essential for converting dihydrofolate to **tetrahydrofolate**. - Inhibition of DHFR blocks the synthesis of **purine nucleotides** and **thymidylate**, thereby impairing DNA synthesis and cell proliferation, particularly in rapidly dividing cancer cells. *DNA polymerase* - **DNA polymerase** is involved in **DNA replication and repair**, but it is not the primary target of methotrexate. - While inhibition of DNA synthesis is an effect of methotrexate, it occurs upstream through the depletion of nucleotide precursors rather than direct inhibition of DNA polymerase. *Ribonucleotide reductase* - **Ribonucleotide reductase** is an enzyme responsible for converting **ribonucleotides to deoxyribonucleotides**, which are necessary for DNA synthesis. - While inhibiting this enzyme would also affect DNA synthesis, it is primarily targeted by drugs like **hydroxyurea**, not methotrexate. *Thymidylate synthase* - **Thymidylate synthase** is an enzyme that catalyzes the methylation of **deoxyuridylate (dUMP)** to **deoxythymidylate (dTMP)**, a crucial precursor for DNA synthesis. - While methotrexate ultimately reduces the supply of **N5, N10-methylenetetrahydrofolate**, a cofactor for thymidylate synthase, it does not directly inhibit the enzyme itself; rather, drugs like **5-fluorouracil** target this enzyme.

Question 543: A patient with HER2-positive breast cancer is resistant to trastuzumab. Which other targeted therapy could be considered?

A. Bevacizumab
B. Lapatinib (Correct Answer)
C. Imatinib
D. Cetuximab

Explanation: ***Lapatinib*** - **Lapatinib** is a dual tyrosine kinase inhibitor that targets both **HER1 (EGFR)** and **HER2**, providing an alternative mechanism of action that can be effective in some trastuzumab-resistant cases. - Its ability to inhibit the intracellular phosphorylation of these receptors helps to overcome resistance pathways that may develop with trastuzumab, which primarily targets the extracellular domain of HER2. *Bevacizumab* - **Bevacizumab** is a **monoclonal antibody** that targets **VEGF (vascular endothelial growth factor)**, inhibiting angiogenesis. - It is used in certain types of cancer but does not directly target HER2 or HER1 pathways, making it less effective for trastuzumab-resistant HER2-positive breast cancer. *Cetuximab* - **Cetuximab** is a monoclonal antibody that targets the **epidermal growth factor receptor (EGFR or HER1)**, but not HER2. - While it targets a related receptor, its specificity for HER1 means it would not be an appropriate choice for HER2-positive breast cancer, particularly in a trastuzumab-resistant setting. *Imatinib* - **Imatinib** is a **tyrosine kinase inhibitor** primarily used in **chronic myeloid leukemia (CML)** and **gastrointestinal stromal tumors (GIST)**. - It targets the **BCR-ABL fusion protein** and **KIT (CD117)**, which are not relevant therapeutic targets in HER2-positive breast cancer.

Question 544: Which chemotherapeutic agent is primarily associated with cardiotoxicity, particularly manifesting as dilated cardiomyopathy?

A. Methotrexate
B. Vincristine
C. Cisplatin
D. Doxorubicin (Correct Answer)

Explanation: ***Doxorubicin*** - **Doxorubicin** is a well-known **anthracycline chemotherapeutic agent** with a significant risk of **dose-dependent cardiotoxicity**. - This cardiotoxicity primarily manifests as **dilated cardiomyopathy**, leading to progressive heart failure and ventricular dysfunction. *Vincristine* - **Vincristine** is a **vinca alkaloid** primarily associated with **neurotoxicity**, causing peripheral neuropathies, muscle weakness, and autonomic dysfunction. - While it can have some cardiac effects, **dilated cardiomyopathy** is not its primary or most common cardiotoxic manifestation. *Methotrexate* - **Methotrexate** is an **antimetabolite** primarily associated with toxicity to rapidly dividing cells, leading to **mucositis**, **myelosuppression**, and **hepatotoxicity**. - Although rare, it can cause pericardial effusion or myocarditis, but not typically **dilated cardiomyopathy**. *Cisplatin* - **Cisplatin** is a **platinum-based chemotherapeutic agent** primarily associated with **nephrotoxicity**, **ototoxicity**, and **neurotoxicity**. - While it can rarely cause electrolyte disturbances that indirectly affect cardiac function, **dilated cardiomyopathy** is not a primary or direct cardiotoxic effect.

Question 545: Which class of chemotherapy drugs inhibits the enzyme topoisomerase I, resulting in DNA damage and cancer cell death?

A. Vinca alkaloids
B. Taxanes
C. Topoisomerase II inhibitors
D. Topoisomerase I inhibitors (Correct Answer)

Explanation: ***Topoisomerase I inhibitors*** - **Topoisomerase I inhibitors** like **irinotecan** and **topotecan** specifically target and inhibit **DNA Topoisomerase I**, preventing it from rejoining single-strand breaks. - This inhibition leads to the accumulation of **single-strand DNA breaks**, which are converted into lethal **double-strand breaks** during DNA replication, inducing **apoptosis** in cancer cells. *Vinca alkaloids* - **Vinca alkaloids** (e.g., **vincristine**, **vinblastine**) are **microtubule-targeting agents** that bind to **tubulin** and inhibit its polymerization, thus disrupting spindle formation during mitosis. - Their primary mechanism is **mitotic arrest** at the metaphase stage, not direct inhibition of topoisomerase enzymes. *Taxanes* - **Taxanes** (e.g., **paclitaxel**, **docetaxel**) are also **microtubule-targeting agents** that, unlike vinca alkaloids, stabilize microtubules and prevent their depolymerization. - This stabilization gums up the cell's machinery, leading to **mitotic arrest** and subsequent **apoptosis**. *Topoisomerase II inhibitors* - **Topoisomerase II inhibitors** (e.g., **etoposide**, **doxorubicin**) target and inhibit **DNA Topoisomerase II**, an enzyme that creates and reseals **double-strand DNA breaks**. - While they do cause DNA damage, their mechanism is distinct from Topoisomerase I inhibitors as they interfere with the religation step of **double-strand breaks**, not single-strand breaks.

Question 546: A patient with chronic myeloid leukemia (CML) is being treated with a drug that specifically inhibits the BCR-ABL tyrosine kinase. Which of the following drugs was the FIRST tyrosine kinase inhibitor approved for first-line treatment of this condition?

A. Imatinib (Correct Answer)
B. Dasatinib
C. Nilotinib
D. All of the options

Explanation: ***Imatinib*** - **Imatinib** was the **first tyrosine kinase inhibitor (TKI)** specifically targeting the **BCR-ABL fusion protein** in CML, approved in 2001. - It revolutionized CML treatment by significantly improving patient outcomes and converting a previously fatal disease into a manageable chronic condition. - While second-generation TKIs are now also approved as first-line options, imatinib holds the distinction of being the **original breakthrough drug** for CML. *Dasatinib* - **Dasatinib** is a **second-generation TKI** approved later (2006) for CML. - Now approved as a first-line option alongside imatinib, but was **not the first** TKI developed for this indication. - Often preferred in patients with high-risk disease or specific mutations. *Nilotinib* - **Nilotinib** is also a **second-generation TKI** approved after imatinib (2007). - Currently approved as a first-line alternative to imatinib, particularly effective with fewer progression events. - However, it was **not the original** first-line TKI for CML. *All of the options* - While all three drugs are now accepted as **first-line treatment options** in current guidelines, the question asks which was the **FIRST** TKI approved. - **Imatinib** holds the unique historical distinction of being the pioneering drug that transformed CML therapy.

Question 547: A patient with cancer is administered a chemotherapy drug that inhibits topoisomerase I, resulting in DNA strand breaks. Which drug is used?

A. Doxorubicin
B. Vincristine
C. Etoposide
D. Irinotecan (Correct Answer)

Explanation: This is an excellent question that tests your knowledge of chemotherapy mechanisms. Let’s break down each option: ***Irinotecan*** - **Irinotecan** is a **topoisomerase I inhibitor**, which prevents DNA unwinding, leading to **DNA strand breaks** and ultimately cell death. - It is a **camptothecin derivative** commonly used in the treatment of **colorectal cancer**. *Doxorubicin* - **Doxorubicin** is an **anthracycline antibiotic** that intercalates into DNA, inhibiting topoisomerase II and generating free radicals. - While it affects topoisomerase, its primary mechanism involves **topoisomerase II inhibition**, not topoisomerase I. *Vincristine* - **Vincristine** is a **vinca alkaloid** that works by binding to **tubulin**, thereby inhibiting microtubule formation and disrupting the mitotic spindle. - Its mechanism is entirely different from topoisomerase inhibition, as it primarily targets **microtubule dynamics** during cell division. *Etoposide* - **Etoposide** is a **topoisomerase II inhibitor**, meaning it interferes with the enzyme responsible for relaxing supercoiled DNA by breaking and rejoining both DNA strands. - While it does cause **DNA strand breaks**, it specifically targets **topoisomerase II**, not topoisomerase I.

Question 548: A patient is treated with a chemotherapy agent that inhibits microtubule assembly and disrupts cell division. Which drug is appropriate?

A. Vincristine (Correct Answer)
B. Cyclophosphamide
C. Doxorubicin
D. Cisplatin

Explanation: ***Correct: Vincristine*** **Vincristine** is a **vinca alkaloid** that works by **inhibiting microtubule assembly**, which is crucial for the formation of the mitotic spindle during cell division. By binding to **tubulin**, vincristine prevents microtubule polymerization, thereby arresting cells in **metaphase** and disrupting mitosis. This leads to cell cycle arrest and apoptosis in rapidly dividing cancer cells. *Incorrect: Cyclophosphamide* **Cyclophosphamide** is an **alkylating agent** that forms covalent bonds with DNA, causing **DNA cross-linking and strand breaks**. It primarily interferes with DNA replication and transcription, rather than affecting microtubule assembly or function. *Incorrect: Doxorubicin* **Doxorubicin** is an **anthracycline antibiotic** that works by **intercalating into DNA** and inhibiting **topoisomerase II**. It also generates **free radicals** causing oxidative damage. Its primary mechanism involves DNA damage and interference with DNA synthesis, not microtubule disruption. *Incorrect: Cisplatin* **Cisplatin** is a **platinum-based alkylating agent** that forms **intrastrand and interstrand DNA cross-links**. These DNA adducts inhibit DNA replication and transcription, leading to apoptosis. It does not directly target microtubules or affect microtubule assembly.

Question 549: A 55-year-old woman is undergoing chemotherapy for breast cancer and experiences severe nausea and vomiting. Which antiemetic, recognized for its minimal extrapyramidal side effects, would be appropriate for her condition?

A. Metoclopramide
B. Ondansetron (Correct Answer)
C. Promethazine
D. Prochlorperazine

Explanation: ***Ondansetron*** - **Ondansetron** is a 5-HT3 receptor antagonist, highly effective against chemotherapy-induced nausea and vomiting (CINV) due to its action on serotonin receptors in the **chemoreceptor trigger zone** and **gastrointestinal tract**. - It is known for its favorable side effect profile, with **minimal to no extrapyramidal symptoms**, making it a preferred choice in patients where such effects are a concern. *Metoclopramide* - While effective against nausea and vomiting, **metoclopramide** (a D2 receptor antagonist) can cause **extrapyramidal symptoms** such as **dystonia** and **tardive dyskinesia**, especially with prolonged use or higher doses. - Its mechanism of action includes both prokinetic effects and central antiemetic action, but its side effect profile makes it less ideal when avoiding extrapyramidal symptoms is a priority. *Promethazine* - **Promethazine** is a first-generation antihistamine with antiemetic properties, but it can cause significant **sedation** and has some **anticholinergic side effects**. - Although its extrapyramidal risk is lower than some other drugs, it's not the primary choice for chemotherapy-induced nausea due to its sedative effects and generally less potent antiemetic action for CINV compared to 5-HT3 antagonists. *Prochlorperazine* - **Prochlorperazine** is a phenothiazine antipsychotic with strong antiemetic effects, acting primarily as a **dopamine receptor antagonist**. - It carries a significant risk of **extrapyramidal side effects**, including **acute dystonia** and **parkinsonism**, making it less suitable when such side effects must be strictly avoided.

Question 550: All-trans retinoic acid is primarily used in the treatment of which of the following tumors?

A. BCR-ABL
B. PML-RARA (Correct Answer)
C. CMYC
D. CEBPA

Explanation: ***PML-RARA*** - **All-trans retinoic acid (ATRA)** is a cornerstone treatment for **acute promyelocytic leukemia (APML)**, which is characterized by the **PML-RARA fusion gene**. - ATRA works by inducing differentiation of leukemic promyelocytes, overcoming the maturation block caused by the **PML-RARA** oncoprotein. *BCR-ABL* - The **BCR-ABL fusion gene** is characteristic of **chronic myeloid leukemia (CML)**, and sometimes in acute lymphoblastic leukemia (ALL). - The primary treatment for **BCR-ABL positive leukemias** involves **tyrosine kinase inhibitors (TKIs)**, such as imatinib, not ATRA. *CMYC* - **CMYC** is an oncogene whose dysregulation is frequently implicated in various cancers, including **Burkitt lymphoma** and some forms of acute myeloid leukemia (AML). - There is no direct therapeutic role for ATRA specifically targeting tumors driven by **CMYC overexpression**. *CEBPA* - **CEBPA** mutations are found in a subset of **acute myeloid leukemia (AML)**, often leading to a favorable prognosis. - While ATRA can be used in some AML subtypes, it is not specifically indicated or primarily effective for AML characterized solely by **CEBPA mutations**; its role is specific to **PML-RARA**.

Practice by Chapter

Principles of Cancer Chemotherapy

Practice Questions

Alkylating Agents

Practice Questions

Antimetabolites

Practice Questions

Antitumor Antibiotics

Practice Questions

Plant Alkaloids

Practice Questions

Topoisomerase Inhibitors

Practice Questions

Hormonal Agents

Practice Questions

Targeted Therapy

Practice Questions

Immunotherapy

Practice Questions

Management of Chemotherapy Side Effects

Practice Questions

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