Expression data from murine brain tumors

There is evidence that brain tumor cells may hijack self-renewal mechanism that regulate stem cell maintenance during normal development. Notch signaling is fundamental for maintaining normal neural stem cells in an undifferentiated state and has been implicated in in the maintenance of brain tumor stem cells as well. We used microarrays to detail the global gene expression program in murine brain tumors lacking RBPjk, an indispensable mediator of the Notch signaling pathway in the cell nucleus. PDGF+p53-/- tumors were induced in p53 floxed mice by combined over-expression of PDGF-B and Cre-recombinase (Cre) from a PDGF-IRES-Cre retroviral construct. PDGF-gain and p53 loss simulate mutations found in human glioblastoma. PDGF+p53-/-RBPjk-/- tumors were induced with the PDGF-IRES-Cre retrovirus in mice carrying floxed p53 and RBPjk alleles. p53-/-RBPjk-/- tumors were induced by conditional deletion of floxed p53 and RBPjk alleles in Hes5+ cells using an Hes5::CreERT2 transgenic mouse line.