Carlet et al. BMC Cancer 2010, 10:638 http://www.biomedcentral.com/1471-2407/10/638 further work is needed to dissect whether the effects of GC on glucose metabolism are mediated by induction of PFKFB2 (as we hypothesized based on the reported role of PFKFB enzymes) or whether other, perhaps less obvious, pathways are involved. Preliminary experiments addressing this issue suggested that, surprisingly, over- expression of both PFKFB2 splice variants seems to have little, if any, effect on lactate and ATP production, two indicators of glycolytic activity that are reduced after GC treatment. Thus, the current data show that induction of the 2 splice variants of PFKFB2 cannot explain the anti-leukemic GC effects. Whether altera- tions of glucose metabolism by other GC-dependent mechanisms might contribute to GC-induced leukemia apoptosis requires further investigations. Conclusions Our study demonstrated that the heart-specific PFKFB2 isoenzyme is expressed and specifically induced by GC in malignant lymphoid cells, however, functional analysis of this gene in the human T-ALL cell line model CCRF- CEM revealed that its over-expression does not explain the anti-leukemic effects of GC. Additional material Additional file 1: Supplement. Supplementary information consisting of 3 Tables, 4 Figures and additional discussion section. Acknowledgements The authors would like to thank Drs. Stephan Geley and A. Trockenbacher for stimulating discussions, M. Brunner, K. Götsch, D. Grazio, B. Gschirr, A. Kofler, S. Lobenwein, C. Mantinger for technical assistance and M. Kat Occhipinti-Bender for editing the manuscript. Supported by the Austrian Science Fund (SFB-F021, P18747), and ONCOTYROL, a COMET Center funded by the Austrian Research Promotion Agency (FFG), the Tiroler Zukunftsstiftung and the Styrian Business Promotion Agency (SFG). The Tyrolean Cancer Research Institute is supported by the “Tiroler Landeskrankenanstalten Ges.m.b.H. (TILAK)”, the “Tyrolean Cancer Aid Society”, various businesses, financial institutions and the People of Tyrol. Author details 1Division Molecular Pathophysiology, Biocenter, Medical University of Innsbruck, Innsbruck, Austria. 2Tyrolean Cancer Research Institute, Innsbruck, 6020-Austria. 3Department of Hematology and Oncology, Medical University of Innsbruck, Innsbruck, Austria. 4Children’s Cancer Research Institute and St. Anna Kinderspital, Vienna, Austria. 5Department of Pediatrics I, Medical University of Innsbruck, Innsbruck, Austria. 6Department of Pediatrics II, Medical University of Innsbruck, Innsbruck, Austria. 7Institute of Legal Medicine, Medical University Innsbruck, Innsbruck, Austria. Authors’ contributions MC participated in most experiments and contributed to the writing of the manuscript. 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