QCM : Classical Anticancer Agents Overview — 9 questions

Explication

Vinca alkaloids (e.g., vincristine, vinblastine) inhibit tubulin polymerization, preventing microtubule formation and arresting cells at metaphase. Taxanes (e.g., paclitaxel, docetaxel) stabilize microtubules, preventing their disassembly, which also halts mitosis.

Explication

Classical anticancer agents mainly target S-phase, where DNA synthesis occurs, making them effective at disrupting DNA replication.

Explication

Alkylating agents form covalent bonds with DNA, creating intra- and inter-strand crosslinks. These crosslinks prevent DNA replication and transcription, leading to cell death. They do not intercalate DNA or inhibit topoisomerases or tubulin.

Explication

Alkylating agents work by forming covalent DNA crosslinks, which prevent the DNA from unwinding and separating, leading to DNA damage and cell death.

Explication

Antimetabolites, such as methotrexate and 5-fluorouracil, specifically target the S-phase by inhibiting enzymes involved in DNA synthesis. Methotrexate inhibits dihydrofolate reductase (DHFR), and 5-FU inhibits thymidylate synthase, both leading to impaired DNA replication.

Explication

Folate antagonists such as methotrexate inhibit DHFR, an enzyme essential for nucleotide synthesis, thereby blocking DNA replication.

Explication

P-gp is an efflux transporter that actively exports drugs from cancer cells, leading to multidrug resistance by decreasing intracellular drug concentrations.

Explication

Microtubule inhibitors, such as vinca alkaloids and taxanes, disrupt microtubule dynamics essential for mitosis, resulting in cell cycle arrest at metaphase.

Explication

Topoisomerases relieve coiling and supercoiling of DNA strands during replication and transcription, and are targeted by certain antibiotics including topoisomerase inhibitors.