LT SUVmax SB-590885 site uptake in the CaP group was comparable to the control group. On day 1 the uptake of FLT SUVmean ratio was lower in the CaP compared with the control group. At all other time points no difference was observed between the treatment and control group. the difference was not statistically significant. In the treatment group HK1 expression was 794% compared to 1008% in the control group on day 8 which was statistically significant . No differences in expression of HK2, Ki67 and TK1 were observed between the treatment and control groups on day 8. Discussion In this study we describe the non-invasive imaging of glucose uptake and cell proliferation for early assessment of treatment response in a pre-clinical mouse model of human ovarian cancer treated with a combination of carboplatin and paclitaxel. Glucose uptake and cell proliferation were visualized by FDG and FLT PET respectively. The A2780 cell line was used for generation of xenograft tumors in mice. This tumor model responded well to the combination therapy with carboplatin and paclitaxel measured as a reduction in tumor Gene expression of GLUT1, HK1, HK2, Ki67 and TK1 The two most stably expressed reference genes were betaglucuronidase and hypoxanthine phosphoribosyltransferase 1. The levels of the GOIs were therefore normalized to the geometric mean of GUSB and HPRT. In the treatment group GLUT1 expression was 6710% compared to 10016% in the control group on day 8; however, 5 FDG and FLT PET Imaging of CaP Treatment doi: 10.1371/journal.pone.0085126.g003 size as compared with a control group on day 8 after start of treatment. On day 4 after start of treatment with carboplatin and paclitaxel, uptake of FDG was significantly lower in the treatment compared to the control group and uptake remained low on day 8. 1659286 The decrease in FDG uptake was paralleled by decreases in GLUT1 and HK1 expression, whereas no change in HK2 expression was observed suggesting that GLUT1 and HK1 are involved in the FDG uptake in this tumor model. We observed an early but transient decrease in cell proliferation measured by FLT PET after treatment initiation of responding A2780 tumors with the combination of 2578618 carboplatin and paclitaxel. A difference in FLT uptake between the treatment and control group was already observed on day 1 after treatment start. In contrast, FLT uptake was not different between the treatment and control mice on day 4 and 8 after treatment start. The identical cell proliferation in the treatment and control group measured by FLT PET on day 8 was supported by gene expression measurements of Ki67 and TK1 which showed no difference in Ki67 and TK1 expression between the treatment and control group on day 8. In other studies, no change in FLT uptake, despite treatment with an effective anti-cancer therapy, has also been observed. The unchanged FLT uptake late in the treatment course could be due to several factors. The anti-cancer treatment may result in feedback activation of the de novo pathway of DNA synthesis resulting in unchanged or even increased FLT uptake despite decreased cell proliferation. This phenomenon has for example been observed during treatment with 5-FU. The relation between the pyrimidine salvage pathway and the de novo pathway of DNA synthesis in tumors has a great influence on the uptake of FLT and different tumors have variable contributions of the two pathways. Some tumors rely mainly on de novo synthesis of DNA precursors which will result in low baseline F