Each neurosphere is derived from a single stem cell that, by asymmetrical division, gives rise to another stem cell and one progenitor cell. The progenitor cells, in turn, give rise only to other progenitor cells. In this way, only a small fraction of the neurosphere corresponds to genuine stem cells. Here we use the terminology neural precursor cells to describe both cell types within the neurosphere. Despite the advances in stem cell studies, comparatively less effort has been devoted to determine the ideal culture medium for NPC expansion in vitro. Neurospheres are usually cultured in medium containing the mitogens FGF-2 and EGF. Acquisition of EGF responsiveness by neural precursor cells is promoted by FGF-2 in the early development in vitro. Extensive evidence has shown that EGF and FGF-2 promote proliferation while retaining the cells in an undifferentiated state. We suggest that the removal of growth factors EGF and FGF-2 from the medium provokes the neurospheres to start the differentiation process even in suspension. Here we tested the hypothesis that the removal of these mitogens in whole neurospheres prior to plating influences the plasticity of human NPC. The chemical induction test suggested an absence of temperate bacteriophages and the DNA sequence and proteomic analysis confirmed the lytic character of the bacteriophages and the absence of toxin genes. Transmission electron microscopy confirmed the phage particle intactness and expected morphology as well as the absence of cellular debris. The host specificity of the phages could be established by means of electron microscopy as well. Data documenting the BFC-1 production process and the certified quality control tests on the final product were compiled into a batch record file. An industrial pharmacist certified the conformity of this file to the product information file. Gangwal et al. conducted a ChIP-chip promoter wide analysis of EWS-FLI1 binding sites and reported that the regulation of other EWS-FLI1 targets may also rely on such microsatellite sequences. So far, the search for EWS-FLI1 targets has been restricted to promoter regions and the precise in vivo significance of GGAA microsatellites with respect to expression modulation remains elusive. In an attempt to decipher a general EWS-FLI1 DNA binding mechanism and to identify candidate XL-184 direct target genes in the Ewing tumor context, we have combined high throughput sequencing of EWS-FLI1 bound DNA fragments and analysis of EWS-FLI1-induced gene expression modulation. Our approach demonstrates binding of EWS-FLI1 to GGAA-repeat sequences in vivo and further shows a binding preference for tracts of 9 repeats or more. We also extend the repertoire of EWS-FLI1 bound GGAA microsatellites and show that, although these sites may be distant from transcription start sites, they are significantly enriched in regions encoding EWS-FLI1 regulated genes. Such results point out the large contribution of GGAA-microsatellite elements to EWS-FLI1 regulation of targets.