Conclusion
TP not only plays a role in sensitivity and resistance to anticancer drugs, but also has a clear angiogenic activity, resulting from its enzymatic activity. TP levels in tumors may be prognostic, but also guide the clinician towards effective therapies. TP may reduce thymidine salvage thereby enhancing the effects of anticancer drugs, which inhibit de nova thymidylate synthesis, such as fluoropyrimidines and folate-based TS inhibitors. The induction of TP by cytokines and other agents can potentiate toxicity of TS inhibitors.
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Peters, G.J. et al. (2002). Thymidine Phosphorylase in Angiogenesis and Drug Resistance. In: Zoref-Shani, E., Sperling, O. (eds) Purine and Pyrimidine Metabolism in Man X. Advances in Experimental Medicine and Biology, vol 486. Springer, Boston, MA. https://doi.org/10.1007/0-306-46843-3_57
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DOI: https://doi.org/10.1007/0-306-46843-3_57
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