Anticancer Drugs — MCQs

A 54-year-old woman with metastatic breast cancer comes to the physician for a follow-up examination. She had a mastectomy 6 months ago and received chemotherapy with doxorubicin and paclitaxel. A CT scan of the chest shows new metastases in the lungs and liver. Adjuvant therapy is initiated with a drug that inhibits the formation of deoxythymidine monophosphate and results in the accumulation of deoxyuridine triphosphate. The patient is advised to avoid folic acid supplementation while receiving this drug in order to prevent the toxic effects of this drug. Which of the following drugs was most likely given?

Q525

Which is the most cardiotoxic anti-cancer drug among the following?

Q526

Mechanism of action of Pemetrexed is:-

Q527

Many drugs are used as rescue therapy for preventing the adverse effects of anticancer drugs. Folinic acid is used in:-

Q528

Which of the following is a monoclonal antibody used in cancer treatment?

Q529

Thalidomide acts through -

Q530

Profound mitotic delay occurs when the doses of anticancer drugs are:

Anticancer Drugs Indian Medical PG Practice Questions and MCQs

Question 521: A 52-year-old female patient presents with HER-2 positive breast cancer that has become resistant to trastuzumab treatment. The oncologist is considering the next line of treatment for the patient. Which of the following options would be the most appropriate choice?

A. Vemurafenib
B. Erlotinib
C. Lapatinib (Correct Answer)
D. Sorafenib

Explanation: ***Lapatinib*** - Lapatinib is an oral **dual tyrosine kinase inhibitor** that targets both **HER2** and **EGFR** receptors, specifically approved for **trastuzumab-resistant HER2-positive breast cancer**. - Unlike trastuzumab (a monoclonal antibody that binds the extracellular domain), lapatinib inhibits the **intracellular tyrosine kinase domain** of HER2, providing an **alternative mechanism** to overcome resistance. - Often used in combination with capecitabine for patients who have progressed on trastuzumab-containing regimens. - **Clinical evidence**: The EGF100151 trial demonstrated efficacy in trastuzumab-refractory disease. *Vemurafenib* - Vemurafenib is a **BRAF V600E/K inhibitor** used primarily for **metastatic melanoma** with BRAF mutations. - It has **no activity against HER2** and is not indicated for breast cancer. - Would not provide benefit in this clinical scenario. *Erlotinib* - Erlotinib is a selective **EGFR tyrosine kinase inhibitor** used for **EGFR-mutant non-small cell lung cancer** and **pancreatic cancer** (with gemcitabine). - While it inhibits EGFR (which lapatinib also targets), erlotinib has **insufficient HER2 inhibition** to be effective in HER2-driven breast cancer. - Not approved or effective for trastuzumab-resistant HER2-positive breast cancer. *Sorafenib* - Sorafenib is a **multi-kinase inhibitor** targeting **RAF kinases, VEGFR-2/3, and PDGFR-β**, approved for **hepatocellular carcinoma, renal cell carcinoma, and thyroid cancer**. - It does **not specifically target HER2** signaling and has no established role in HER2-positive breast cancer. - Would not address the mechanism of disease in this patient.

Question 522: What is the MOA of thalidomide?

A. Inhibits factor Xa
B. Prevents folic acid synthesis in bacteria
C. Inhibits leukotrienes
D. Angiogenesis inhibitor (Correct Answer)

Explanation: ***Angiogenesis inhibitor*** - Thalidomide is known to **inhibit angiogenesis** [1] by blocking the formation of new blood vessels, a key mechanism in its anti-cancer effects. - It also has **immunomodulatory** [1], [2], [3] and **anti-inflammatory** properties, affecting cytokine production and immune cell function [1], [3]. *Inhibits factor Xa* - This is the mechanism of action for **direct oral anticoagulants (DOACs)** like rivaroxaban and apixaban, used to prevent blood clot formation. - Thalidomide does not primarily act on the **coagulation cascade** at this step. *Prevents folic acid synthesis in bacteria* - This is the classic mechanism of action for **sulfonamide antibiotics**, which target bacterial enzymes involved in folate metabolism. - Thalidomide is an **immunomodulatory drug** [2], [3], not an antibiotic that interferes with bacterial folic acid synthesis. *Inhibits leukotrienes* - **Leukotriene inhibitors**, such as montelukast and zafirlukast, are used to treat asthma and allergies by blocking inflammatory pathways. - Thalidomide's primary mechanism is not the direct inhibition of **leukotriene synthesis or receptor binding**.

Question 523: Nivolumab is used as checkpoint inhibitor in

A. Hodgkin's lymphoma (Correct Answer)
B. Medulloblastoma
C. Retinoblastoma
D. Pleuropulmonary blastoma

Explanation: ***Hodgkin's lymphoma*** - **Nivolumab** is an **immune checkpoint inhibitor** targeting **PD-1**. It has shown significant efficacy in treating relapsed or refractory Hodgkin's lymphoma, particularly in patients who have failed prior therapies. - Hodgkin's lymphoma cells, specifically **Reed-Sternberg cells**, often overexpress PD-L1, which allows them to evade the immune system, making PD-1 blockade a rational therapeutic strategy. *Medulloblastoma* - **Medulloblastoma** is a common malignant brain tumor in children, and while immunotherapy research is ongoing, Nivolumab is **not a standard treatment** for this condition. - Treatment typically involves **surgery, radiation, and chemotherapy**, with targeted therapies under investigation. *Retinoblastoma* - **Retinoblastoma** is a malignant tumor of the retina, most commonly affecting young children. Treatment usually involves **chemotherapy, laser therapy, cryotherapy, or enucleation**. - There is **no established role for Nivolumab** or PD-1 inhibitors in the routine management of retinoblastoma. *Pleuropulmonary blastoma* - **Pleuropulmonary blastoma** is a rare, malignant lung tumor of childhood. Treatment primarily consists of **surgery and chemotherapy**. - While experimental, there is **no current evidence** supporting the use of Nivolumab as a standard treatment for pleuropulmonary blastoma.

Question 524: A 54-year-old woman with metastatic breast cancer comes to the physician for a follow-up examination. She had a mastectomy 6 months ago and received chemotherapy with doxorubicin and paclitaxel. A CT scan of the chest shows new metastases in the lungs and liver. Adjuvant therapy is initiated with a drug that inhibits the formation of deoxythymidine monophosphate and results in the accumulation of deoxyuridine triphosphate. The patient is advised to avoid folic acid supplementation while receiving this drug in order to prevent the toxic effects of this drug. Which of the following drugs was most likely given?

A. Leflunomide
B. Capecitabine (Correct Answer)
C. Mycophenolate mofetil
D. Hydroxyurea
E. Azathioprine

Explanation: Capecitabine - Capecitabine is a **prodrug of 5-fluorouracil (5-FU)**, which inhibits **thymidylate synthase**, thereby blocking the formation of **deoxythymidine monophosphate (dTMP)** from deoxyuridine monophosphate (dUMP) [1], [2]. - This leads to the accumulation of **deoxyuridine triphosphate (dUTP)** and depletion of deoxythymidine triphosphate (dTTP), disrupting DNA synthesis [2]. - The instruction to avoid **folic acid supplementation** is important because excessive folate can potentially reduce the drug's efficacy by providing alternative pathways for nucleotide synthesis, though leucovorin (folinic acid) is sometimes given WITH 5-FU to enhance its binding to thymidylate synthase in certain chemotherapy regimens [1], [2]. - Commonly used in **metastatic breast cancer** and colorectal cancer [3]. *Hydroxyurea* - Inhibits **ribonucleotide reductase**, preventing the conversion of ribonucleotides to deoxyribonucleotides needed for DNA synthesis. - Affects all deoxyribonucleotides (not specifically dTMP), and does not cause dUTP accumulation. - Used in **sickle cell disease**, chronic myeloid leukemia, and polycythemia vera. *Mycophenolate mofetil* - An **immunosuppressant** that inhibits **inosine monophosphate dehydrogenase (IMPDH)**, blocking de novo **guanine nucleotide synthesis**. - Does not affect thymidylate synthase or pyrimidine metabolism. - Used to prevent **organ transplant rejection** and in autoimmune diseases. *Leflunomide* - An **immunosuppressant** that inhibits **dihydroorotate dehydrogenase**, blocking de novo **pyrimidine synthesis** at an earlier step than thymidylate synthase. - Does not specifically inhibit dTMP formation or cause dUTP accumulation. - Primarily used in **rheumatoid arthritis**. *Azathioprine* - An **immunosuppressant** that acts as a prodrug for 6-mercaptopurine, interfering with **purine synthesis** (adenine and guanine pathways). - Does not affect pyrimidine metabolism or thymidylate synthase. - Used in transplant recipients and autoimmune diseases.

Question 525: Which is the most cardiotoxic anti-cancer drug among the following?

A. Cyclophosphamide
B. Tamoxifen
C. Imatinib
D. Anthracyclines (Correct Answer)

Explanation: ***Anthracyclines*** - **Anthracyclines** (e.g., doxorubicin, daunorubicin) are notorious for causing **dose-dependent cardiotoxicity**, leading to **irreversible dilated cardiomyopathy** and **heart failure**. - Their cardiotoxic effect is primarily due to the generation of **reactive oxygen species** and interference with cardiac topoisomerase IIβ. *Cyclophosphamide* - Cyclophosphamide can cause cardiotoxicity, particularly at **high doses**, manifesting as **hemorrhagic myocardial necrosis** or **pericarditis**. - However, its cardiotoxicity is generally considered **less frequent and severe** than that of anthracyclines. *Tamoxifen* - Tamoxifen is primarily associated with an **increased risk of thromboembolic events** and **endometrial cancer**. - While some cardiac effects like **QT prolongation** can occur, it is not considered a primary cardiotoxic agent leading to cardiomyopathy. *Imatinib* - Imatinib, a **tyrosine kinase inhibitor**, has been linked to **cardiac dysfunction** including heart failure in some patients. - However, the incidence and severity of cardiotoxicity with imatinib are **lower** compared to anthracyclines, which are broadly cardiotoxic.

Question 526: Mechanism of action of Pemetrexed is:-

A. Topoisomerase inhibitor
B. Dihydrofolate reductase inhibitor
C. Dopamine agonist
D. Thymidylate synthase inhibitor (Correct Answer)

Explanation: ***Thymidylate synthase inhibitor*** - **Pemetrexed** is a **multi-targeted antifolate agent** that primarily inhibits **thymidylate synthase (TS)**, the key enzyme responsible for synthesizing thymidine monophosphate, an essential building block for DNA synthesis. - While pemetrexed also inhibits **dihydrofolate reductase (DHFR)** and **glycinamide ribonucleotide formyltransferase (GARFT)**, its **primary and most clinically significant mechanism** is TS inhibition, making it particularly effective in mesothelioma and non-small cell lung cancer. - This multi-targeted action enhances its cytotoxic effects compared to single-target antifolates. *Dihydrofolate reductase inhibitor* - While pemetrexed does inhibit **DHFR** as part of its multi-targeted mechanism, this is a **secondary action**, not its primary mechanism. - Classical DHFR inhibitors include **methotrexate** and **trimethoprim**, which specifically target this enzyme. - In exam contexts, pemetrexed is best classified by its **primary target: thymidylate synthase**. *Topoisomerase inhibitor* - **Topoisomerase inhibitors** target enzymes that control DNA topology during replication and transcription. - Examples include **irinotecan** and **topotecan** (topoisomerase I inhibitors) and **etoposide** (topoisomerase II inhibitor). - This is not the mechanism of action for pemetrexed. *Dopamine agonist* - **Dopamine agonists** activate dopamine receptors and are used in neurological conditions like Parkinson's disease (e.g., **pramipexole**, **ropinirole**). - This mechanism is completely unrelated to anticancer agents and folate metabolism.

Question 527: Many drugs are used as rescue therapy for preventing the adverse effects of anticancer drugs. Folinic acid is used in:-

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

Explanation: ***Methotrexate toxicity*** - **Folinic acid (leucovorin)** is a reduced folate that bypasses the metabolic block caused by **methotrexate** on dihydrofolate reductase. - It replenishes the body's **folate stores** and protects healthy cells from methotrexate's cytotoxic effects, particularly in the bone marrow and gastrointestinal tract. *Cyclophosphamide toxicity* - **Cyclophosphamide** toxicity, primarily hemorrhagic cystitis, is prevented by **mesna** (2-mercaptoethane sulfonate). - Mesna inactivates the urotoxic metabolite **acrolein** in the urine, preventing bladder damage. *Doxorubicin toxicity* - **Doxorubicin** causes cardiotoxicity, which can be mitigated by the iron-chelating agent **dexrazoxane**. - Dexrazoxane reduces the formation of **free radicals** that contribute to doxorubicin-induced myocardial damage. *Cisplatin toxicity* - **Cisplatin** toxicity, especially nephrotoxicity, is largely prevented by **aggressive hydration** and administration of **diuretics**. - **Amifostine** is another agent that can reduce cisplatin-induced nephrotoxicity, neurotoxicity, and ototoxicity by acting as a cytoprotectant.

Question 528: Which of the following is a monoclonal antibody used in cancer treatment?

A. Cisplatin
B. Rituximab (Correct Answer)
C. 5-fluorouracil
D. Methotrexate

Explanation: ***Rituximab*** - **Rituximab** is a **chimeric monoclonal antibody** that targets the **CD20 protein** found on the surface of normal and malignant **B lymphocytes**. - It is widely used in the treatment of various **lymphomas** and **leukemias**, as well as autoimmune diseases, by inducing the death of CD20-positive B cells. *Cisplatin* - **Cisplatin** is a **platinum-based chemotherapy drug** that works by forming **DNA adducts**, leading to DNA damage and apoptosis of cancer cells. - It is used in various solid tumors but is not a monoclonal antibody; it's a **cytotoxic agent**. *5-fluorouracil* - **5-fluorouracil (5-FU)** is an **antimetabolite chemotherapy drug** that interferes with DNA and RNA synthesis, thereby inhibiting cell division. - It is a **pyrimidine analog** and not a monoclonal antibody. *Methotrexate* - **Methotrexate** is a **folate analog antimetabolite** that inhibits **dihydrofolate reductase**, interfering with DNA synthesis and cell proliferation. - It's a conventional chemotherapy agent and immunosuppressant, not a monoclonal antibody.

Question 529: Thalidomide acts through -

A. Inhibiting angiogenesis (Correct Answer)
B. Inhibiting thymidylate synthase
C. Inhibition of Topo-isomerase I
D. All of the options

Explanation: **Inhibiting angiogenesis** - **Thalidomide** is known for its **anti-angiogenic properties**, making it useful in treating certain cancers and inflammatory conditions by preventing the formation of new blood vessels. - This mechanism is also implicated in its teratogenic effects, as **angiogenesis** is crucial for limb development. *Inhibiting thymidylate synthase* - This mechanism is characteristic of **fluorouracil**, a different class of antineoplastic agents that interfere with DNA synthesis. - **Thalidomide** does not exert its primary therapeutic or toxic effects through **thymidylate synthase inhibition**. *Inhibition of Topo-isomerase I* - Inhibition of **topoisomerase I** is the primary mechanism of action for drugs like **irinotecan** and **topotecan**, which are used in cancer chemotherapy. - **Thalidomide** does not target **topoisomerase I**; its actions are related to immune modulation and **angiogenesis**. *All of the options* - This option is incorrect because **thalidomide** specifically acts as an **anti-angiogenic** and immunomodulatory agent, not through the other mentioned mechanisms. - The other mechanisms (inhibition of **thymidylate synthase** and **topoisomerase I**) belong to different classes of drugs with distinct biological targets.

Question 530: Profound mitotic delay occurs when the doses of anticancer drugs are:

A. No dose effect
B. Smaller
C. Intermediate
D. Larger (Correct Answer)

Explanation: ***Larger*** - **Larger doses** of anticancer drugs cause extensive DNA damage, leading to prolonged activation of cell cycle checkpoints (G2/M checkpoint) [1] - This extensive damage results in **profound mitotic delay** as the cell attempts DNA repair or undergoes apoptosis [1] - High-dose chemotherapy maximally activates checkpoint mechanisms, causing significant and prolonged mitotic arrest [1] *No dose effect* - This option is incorrect because mitotic delay is a well-established dose-dependent phenomenon - Even minimal doses of cytotoxic agents can trigger checkpoint activation and affect mitotic progression *Smaller* - **Smaller doses** cause less severe DNA damage, leading to minimal or transient mitotic delay - Cells can efficiently repair minor damage and resume mitosis relatively quickly - The delay is present but not "profound" *Intermediate* - **Intermediate doses** cause moderate mitotic delay, falling between minimal and profound effects - The checkpoint activation is noticeable but not maximal - This would not be characterized as "profound," which implies extensive and prolonged cell cycle arrest

Practice by Chapter

Principles of Cancer Chemotherapy

Practice Questions

Alkylating Agents

Practice Questions

Antimetabolites

Practice Questions

Antitumor Antibiotics

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Plant Alkaloids

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Topoisomerase Inhibitors

Practice Questions

Hormonal Agents

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Targeted Therapy

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Immunotherapy

Practice Questions

Management of Chemotherapy Side Effects

Practice Questions

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