Anticancer Drugs Practice Questions

Q: Nivolumab is used as checkpoint inhibitor in

Hodgkin's lymphoma. ***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.

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

Anthracyclines. ***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.

Q: Mechanism of action of Pemetrexed is:-

Thymidylate synthase inhibitor. ***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.

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

Methotrexate toxicity. ***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.

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

Rituximab. ***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.

Q: Thalidomide acts through -

Inhibiting angiogenesis. **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.

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

Larger. ***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

Q: Secondary leukemias are caused by

Alkylating agents. ***Alkylating agents*** - **Alkylating agents**, such as **cyclophosphamide**, **chlorambucil**, **melphalan**, and **busulfan**, are highly associated with the development of secondary leukemias, particularly **acute myeloid leukemia (AML)** and **myelodysplastic syndrome (MDS)**. - They cause **DNA damage** by forming covalent bonds with DNA, leading to mutations and chromosomal aberrations (especially deletions of chromosomes 5 and 7) that can promote leukemogenesis. - The latency period is typically **5-7 years** after exposure, and the risk is dose-dependent. *Antimetabolites* - **Antimetabolites**, like **methotrexate** and **5-fluorouracil**, interfere with **DNA replication** and repair but are less frequently linked to secondary leukemias compared to alkylating agents. - While they can cause bone marrow suppression, their mechanism of action typically involves disrupting nucleotide synthesis rather than directly inducing the specific chromosomal changes seen in secondary leukemias. *Vinca alkaloids* - **Vinca alkaloids**, such as **vincristine** and **vinblastine**, primarily target **microtubule formation** and inhibit cell division, often used in cancer chemotherapy. - They are not a significant cause of secondary leukemias; instead, they primarily cause **neurotoxicity** and bone marrow suppression as side effects. *Actinomycin D* - **Actinomycin D** (dactinomycin) acts by intercalating into **DNA** and inhibiting RNA synthesis, making it an **antitumor antibiotic**. - While it is a potent chemotherapy agent with various side effects, it is not a primary cause of **secondary leukemias**, which are predominantly associated with alkylating agents and topoisomerase II inhibitors.

Q: Leucovorin is used for side effect reduction in which anticancer drug?

Methotrexate. ***Methotrexate*** - **Leucovorin rescue** is a critical adjunct therapy for **methotrexate** to prevent severe toxicity. - Methotrexate is a **folate antagonist**, and leucovorin (folinic acid) provides a reduced folate form that bypasses the blocked enzyme, restoring normal cellular function and protecting healthy cells. - This is true **"rescue therapy"** - leucovorin protects normal cells from methotrexate toxicity. *Cisplatin* - **Cisplatin** is a platinum-based chemotherapy drug primarily associated with **nephrotoxicity** and **ototoxicity**. - Its side effects are managed with **hydration, amifostine**, and antiemetics, not leucovorin. *5-FU* - **5-FU (5-fluorouracil)** is a pyrimidine analog that can cause severe **myelosuppression** and **gastrointestinal toxicity**. - While leucovorin is used WITH 5-FU (e.g., in colorectal cancer regimens), it serves to **enhance/potentiate** 5-FU's cytotoxic effect through biochemical modulation, NOT to rescue from toxicity. - This is the key distinction: leucovorin + 5-FU = **potentiation**; leucovorin + methotrexate = **rescue**. *Adriamycin* - **Adriamycin (doxorubicin)** is an **anthracycline antibiotic** known for causing **cardiotoxicity** and **myelosuppression**. - **Dexrazoxane** is used to prevent Adriamycin-induced cardiotoxicity, not leucovorin.

Question 1

Nivolumab is used as checkpoint inhibitor in

Accepted Answer

Hodgkin's lymphoma

Answer

Medulloblastoma

Answer

Retinoblastoma

Answer

Pleuropulmonary blastoma

Question 2

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?

Accepted Answer

Capecitabine

Answer

Leflunomide

Answer

Mycophenolate mofetil

Answer

Hydroxyurea

Answer

Azathioprine

Question 3

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

Accepted Answer

Anthracyclines

Answer

Cyclophosphamide

Answer

Tamoxifen

Answer

Imatinib

Question 4

Mechanism of action of Pemetrexed is:-

Accepted Answer

Thymidylate synthase inhibitor

Answer

Topoisomerase inhibitor

Answer

Dihydrofolate reductase inhibitor

Answer

Dopamine agonist

Question 5

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

Accepted Answer

Methotrexate toxicity

Answer

Cyclophosphamide toxicity

Answer

Doxorubicin toxicity

Answer

Cisplatin toxicity

Question 6

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

Accepted Answer

Rituximab

Answer

Cisplatin

Answer

5-fluorouracil

Answer

Methotrexate

Question 7

Thalidomide acts through -

Accepted Answer

Inhibiting angiogenesis

Answer

Inhibiting thymidylate synthase

Answer

Inhibition of Topo-isomerase I

Answer

All of the options

Question 8

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

Accepted Answer

Larger

Answer

No dose effect

Answer

Smaller

Answer

Intermediate

Question 9

Secondary leukemias are caused by

Accepted Answer

Alkylating agents

Answer

Antimetabolites

Answer

Vinca alkaloids

Answer

Actinomycin D

Question 10

Leucovorin is used for side effect reduction in which anticancer drug?

Accepted Answer

Methotrexate

Answer

Cisplatin

Answer

5-FU

Answer

Adriamycin

Anticancer Drugs — MCQs

Anticancer Drugs — MCQs

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