Tuomela et al. BMC Cancer 2010, 10:596 http://www.biomedcentral.com/1471-2407/10/596 expression of FGF-8, VEGF and clinicopathological find- ings correlate with each other [61]. FGF8b could thus, alone or combined with other markers, be used as a prognostic indicator in cases of prostate cancer. It remains to be studied whether FGF8 expression is able to contribute to development of resistance to radiation and cytotoxic therapies of prostate cancer. Conclusions Our results suggest that while VEGF-increased prostate tumour growth is associated with and most probably caused by increased density and performance of the vas- cular network. Elevated tumour growth in FGF8b expressing xenografts is based on stimulated prolifera- tive activity and increased hypoxia tolerance, which may promote prostate tumour progression to a more aggres- sive phenotype associated with resistance to radiation and cytotoxic therapies. Abbreviations AIGF: androgen-induced growth factor; DMEM: Dulbecco’s modified Eagle’s medium; ECL: enhanced chemiluminescence; EDTA: ethylenediaminetetra- acetic acid; EF5: (2-(2-nitro-1H-imidazol-1-yl)-N-(2,2,3,3,3-pentafluoropropyl)- acetamide); FAS: fatty acid synthetase; FDG: fluoro-2-deoxyglucose; FDG-6-P: fluoro-2-deoxyglucose-6-phosphate; FGF: fibroblast growth factor; FGFR: fibroblast growth factor receptor; GLUT: glucose transport protein; H&E: hematoxylin-eosine; HPLC: high performance liquid chromatography; iFBS: heat-inactivated fetal bovine serum; IHC: immunohistochemistry; PBS: phosphate-buffered saline; PIN: prostatic intraepithelial neoplasia; pO2: partial oxygen pressure; s.c.: subcutaneous; T/B: tumour to blood ratio; VEGF: vascular endothelial growth factor. Acknowledgements We thank Ms. Soili Jussila, Mrs. Pirkko Rauhamäki and Ms. Sanna Auer from the Department of Cell Biology and Anatomy, Veronica Fagerholm, Ph.D., from the Turku PET Centre and Mrs. Seija Lindqvist from the Turku University Central Animal laboratory for excellent technical assistance. Dr. Cameron Koch from the University of Pennsylvania is warmly thanked for collaboration and for providing the EF5 precursor. Finally, we thank Professor Kari Alitalo from the University of Helsinki for providing us with the VEGF gene construct and for his expertise concerning angiogenesis. This work was supported by grants from the Academy of Finland, the Finnish Cancer Societies, the Sigrid Jusélius Foundation, the South-Western Finnish Cancer Societies and the Foundation for the Finnish Cancer Institute. Author details 1Institute of Biomedicine, Department of Cell Biology and Anatomy, University of Turku, Turku, Finland. 2Pharmatest Services Ltd., Turku, Finland. 3Turku PET Centre, MediCity Preclinical Research Laboratory, University of Turku and Åbo Akademi University, Turku, Finland. 4Cell Imaging Core, Turku Centre for Biotechnology, University of Turku and Åbo Akademi University, Turku, Finland. 5Department of Otorhinolaryngology - Head and Neck Surgery, Turku University Hospital, University of Turku, Turku, Finland. 6Turku PET Centre, Radiopharmaceutical Chemistry Laboratory, University of Turku and Åbo Akademi University, Turku, Finland. 7Turku PET Centre, Accelerator Laboratory, MediCity Preclinical Research Laboratory, University of Turku and Åbo Akademi University, Turku, Finland. 8Department of Oncology and Radiotherapy, Turku University Hospital, Turku, Finland. 9Department of Laboratory Medicine, MAS University Hospital, Lund University, Malmö, Sweden. Authors’ contributions JT carried out the cell cultures, RNA isolation, Northern Blot analysis, Western Blot analysis, analysis of morphology and morphometry. Transfection of the Page 12 of 14 PC-3 cell was done by MV and JSe. Tumour experiments were done by JT and TG. Flow cytometric analysis was made by JSa. AS and IK helped with partial oxygen measurement. PM helped with processing the tumours. SF made the radiochemical synthesis of tracers. TG made the analysis of uptake of tracers and statistical analysis. PH, HM and OS participated in the design of the study. JT wrote the first version of the manuscript and all authors helped to process it. All authors have read and approved the final manuscript. PH gave final approval for the manuscript to be submitted. Competing interests The authors declare that they have no competing interests. Received: 1 April 2010 Accepted: 30 October 2010 Published: 30 October 2010 References 1. 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