Anticancer Drugs Practice Questions

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.

Q: Which of the following drugs act by inhibiting DNA replication?

6-Mercaptopurine. ***6-Mercaptopurine*** - This drug is a **purine analog** that acts as an **antimetabolite**, directly interfering with the **synthesis of purine nucleotides** required for DNA replication. - By inhibiting enzymes like **PRPP amidotransferase** and getting incorporated into DNA as a fraudulent nucleotide, it blocks the **de novo synthesis** pathway, preventing normal DNA replication. - This represents **direct inhibition of DNA synthesis** at the nucleotide building block level. *Mitomycin C* - This agent is an **alkylating agent** that **cross-links DNA** strands, causing DNA damage that prevents strand separation. - While it does prevent DNA replication, its mechanism is through **DNA damage and structural disruption** rather than inhibition of the DNA synthesis machinery itself. - It acts by damaging already-formed DNA rather than preventing new DNA synthesis. *Actinomycin D* - Actinomycin D is an **intercalating agent** that inserts itself between DNA base pairs, primarily **inhibiting RNA synthesis** by blocking RNA polymerase movement. - While it binds to DNA, its primary therapeutic action is on **transcription (RNA synthesis)**, not direct inhibition of DNA replication. *Asparaginase* - Asparaginase is an enzyme that **depletes asparagine** from the blood, which is an essential amino acid for certain cancer cells (e.g., leukemic cells). - Its mechanism is to starve cancer cells of asparagine, leading to **inhibition of protein synthesis**, not DNA replication.

Q: Which antineoplastic agent is known to cause hemorrhagic cystitis?

Cyclophosphamide. ***Cyclophosphamide*** - Cyclophosphamide is an **alkylating agent** that forms highly reactive metabolites, such as **acrolein**, which is excreted in the urine and causes direct irritation and damage to the bladder urothelium, leading to **hemorrhagic cystitis**. - This toxicity can be mitigated by co-administration of **mesna** (2-mercaptoethane sulfonate sodium), which inactivates acrolein in the bladder, and aggressive intravenous hydration. *Methotrexate* - Methotrexate is a **folate antagonist** primarily known for causing **myelosuppression**, **mucositis**, and **hepatotoxicity**. - While it can cause renal toxicity at high doses due to precipitation in renal tubules, it is not typically associated with hemorrhagic cystitis. *Cisplatin* - Cisplatin is a **platinum-based chemotherapy agent** with significant **nephrotoxicity** and **ototoxicity** as its dose-limiting toxicities. - It also commonly causes profound nausea and vomiting but is not a primary cause of hemorrhagic cystitis. *Vincristine* - Vincristine is a **vinca alkaloid** that interferes with microtubule formation, primarily known for causing **peripheral neuropathy** (e.g., foot drop, paresthesias, constipation due to autonomic neuropathy) and is a vesicant. - It does not typically cause hemorrhagic cystitis; its bone marrow toxicity is generally less severe compared to other chemotherapeutic agents.

Question 1

Mechanism of action of Pemetrexed is:-

Accepted Answer

Thymidylate synthase inhibitor

Answer

Topoisomerase inhibitor

Answer

Dihydrofolate reductase inhibitor

Answer

Dopamine agonist

Question 2

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 3

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

Accepted Answer

Rituximab

Answer

Cisplatin

Answer

5-fluorouracil

Answer

Methotrexate

Question 4

Thalidomide acts through -

Accepted Answer

Inhibiting angiogenesis

Answer

Inhibiting thymidylate synthase

Answer

Inhibition of Topo-isomerase I

Answer

All of the options

Question 5

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

Accepted Answer

Larger

Answer

No dose effect

Answer

Smaller

Answer

Intermediate

Question 6

Secondary leukemias are caused by

Accepted Answer

Alkylating agents

Answer

Antimetabolites

Answer

Vinca alkaloids

Answer

Actinomycin D

Question 7

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

Accepted Answer

Methotrexate

Answer

Cisplatin

Answer

5-FU

Answer

Adriamycin

Question 8

Which of the following statements is not true about tamoxifen?

Accepted Answer

Tamoxifen is useful in post-menopausal and aromatase inhibitors in premenopausal patients.

Answer

It can cause endometrial carcinoma.

Answer

It is used for visceral metastasis.

Answer

Dose is 20 mg for 5 years.

Question 9

Which of the following drugs act by inhibiting DNA replication?

Accepted Answer

6-Mercaptopurine

Answer

Mitomycin C

Answer

Actinomycin D

Answer

Asparaginase

Question 10

Which antineoplastic agent is known to cause hemorrhagic cystitis?

Accepted Answer

Cyclophosphamide

Answer

Methotrexate

Answer

Cisplatin

Answer

Vincristine

Anticancer Drugs — MCQs

Anticancer Drugs — MCQs

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