How does fluorouracil work as a chemotherapy agent?

Fluorouracil is primarily recognized for its mechanism of action as an antineoplastic agent, specifically through the inhibition of thymidylate synthase. Thymidylate synthase is an enzyme crucial for the synthesis of thymidine monophosphate (dTMP), which is a necessary precursor for DNA synthesis. By inhibiting this enzyme, fluorouracil effectively reduces the availability of dTMP, leading to a disruption in DNA synthesis and ultimately impairing the ability of rapidly dividing tumor cells to proliferate.

This mechanism of action is particularly significant because it specifically targets tumor cells that are highly reliant on rapid DNA synthesis for growth and division. Fluorouracil's effectiveness in blocking DNA synthesis is one of the reasons it is utilized in the treatment of various cancers, including colorectal and breast cancer.

In the context of the other options, apoptosis induction is a separate mechanism that can occur through various agents, but it is not the primary action of fluorouracil. Enhancing tumor immunogenicity refers to assuring that the immune system can better recognize and attack the tumor, which is not directly relevant to fluorouracil's mechanism. Additionally, increasing metabolic activity in cancer cells would typically suggest promoting growth rather than inhibiting