Abstract
For more than 40 years, fluorouracil has been the mainstay of treatment for advanced colorectal cancer, the second leading cause of cancer-related death in the United States. The drug is thought to act primarily by inhibiting the enzyme thymidylate synthase, thereby blocking the synthesis of DNA. In about 20 percent of patients who receive fluorouracil, the measurable tumor decreases by more than 50 percent. These patients are thought to survive longer than patients whose tumors do not respond to fluorouracil. Debate continues about the best way to administer fluorouracil; a “loading” regimen (consisting of an intravenous bolus of the drug . . .

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