Thymidine phosphorylase (TP), a key enzyme in the pyrimidine nucleoside salvage pathway, catalyses the reversible phosphorylation of thymidine, thereby ...
Eur J Nucl Med Mol Imaging (2014) 41:1327–1335 DOI 10.1007/s00259-014-2712-z
Thymidine phosphorylase influences [18F]fluorothymidine uptake in cancer cells and patients with non-small cell lung cancer Seung Jin Lee & Jeong Seok Yeo & Haeng Jung Lee & Eun Jung Lee & Seog Young Kim & Se Jin Jang & Jong Jin Lee & Jin-Sook Ryu & Dae Hyuk Moon
Received: 28 August 2013 / Accepted: 20 January 2014 / Published online: 22 February 2014 # Springer-Verlag Berlin Heidelberg 2014
Abstract Purpose Thymidine phosphorylase (TP), a key enzyme in the pyrimidine nucleoside salvage pathway, catalyses the reversible phosphorylation of thymidine, thereby generating thymine and 2-deoxy-D-ribose-1-phosphate. By regulating the levels of endogenous thymidine, TP may influence [18F]fluorothymidine ([18F]FLT) uptake. We investigated the effect of TP activity on [18F]FLT uptake by tumours. Methods Uptake of [3H]FLT and [3H]thymidine ([3H]Thd) and the activities of TP, thymidine kinase 1 (TK1), and equilibrative nucleoside transporter 1 (ENT1) were determined in exponentially growing A431, A549, HT29, HOP92, ACHN, and SKOV3 cells in the presence or absence of tipiracil hydrochloride, a TP inhibitor. Eighty-five non-small cell lung Seung Jin Lee and Jeong Seok Yeo contributed equally to this work. Electronic supplementary material The online version of this article (doi:10.1007/s00259-014-2712-z) contains supplementary material, which is available to authorized users. S. J. Lee College of Pharmacy, Gachon University, Incheon, Republic of Korea J. S. Yeo Department of Nuclear Medicine, Dongguk University Ilsan Hospital, Goyang-si, Republic of Korea H. J. Lee : E. J. Lee : S. Y. Kim Institute for Innovative Cancer Research, Asan Medical Center, Seoul, Republic of Korea S. J. Jang Department of Pathology, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Republic of Korea J. J. Lee : J.