Dietary uridine supplementation decreases tumor number in Apc(Min/+) mice (829.11) Academic Article uri icon


  • Colorectal cancer affects 1.23 million people and accounts for more than 600,000 deaths each year worldwide. Deficiency of methyl donors including folate and methionine has been linked to increased colon cancer risk in experimental and epidemiological studies. The Apc(Min/+) mouse model is a powerful tool for studying the genetic and dietary mechanisms which contribute to intestinal cancer phenotypes. A previous study showed that Apc(Min/+) mice also lacking one copy of the Shmt1 gene, which results in perturbed de novo thymidylate (dTMP) synthesis, displayed increased intestinal tumor number that was exacerbated by folate deficiency. dTMP is the only nucleotide that is synthesized at the replication fork as needed for DNA replication and repair. dTMP can either be synthesized de novo from the folatedependent reductive methylation of deoxyuridylate (dUMP) to dTMP through a multienzyme complex or can be generated by phosphorylating thymidine to dTMP by the salvage pathway enzyme thymidine kinase (TK1). In this study, we sought to determine whether dietary supplementation of dTMP precursors (thymidine, deoxyuridine or uridine) could modify tumor number in the Apc(Min/+) model. Surprisingly, dietary uridine supplementation reduced intestinal tumor number and tumor burden by 40% (p<0.05) relative to the control diet; neither thymidine nor deoxyuridine affected tumor number.Grant Funding Source: Supported by NIH R37DK58144

published proceedings

  • The FASEB Journal

author list (cited authors)

  • Field, M., & Stover, P.

citation count

  • 0

complete list of authors

  • Field, Martha||Stover, Patrick

publication date

  • April 2014