For differentiation, mice were sacrificed at 7 days after the first BrdU injection

ural signature has been proposed for oligodendrogliomas, OG33, OG35, and HOG cells were subjected to phenotype profiling by rtPCR using well-accepted proneural and mesenchymal markers . OG cells did not express the proneural markers CD133, Sox2 or Olig2, but abundantly expressed the mesenchymal markers CD44, BCL2A1, and Wilms Tumor 1. Most importantly, the OG cells expressed platelet-derived growth factor receptor-alpha, a well-accepted OPC marker ; thus, supporting their oligodendroglial origin. DNA mapping for chromosomal copy variation using GeneChip 250K Nsp arrays revealed similar amplifications and deletions in HOG, OG33, and OG35 cells. This analysis confirmed the surgical pathology report of the allelic loss of 1p36/19q13, the most common genetic change in oligodendroglial neoplasms. Principal component analysis with the SNP raw intensity data grouped OG33, OG35, and HOG cells together, indicating similar copy variations, and that these cytogenetic alterations were distinct from mesenchymal or proneural GBM-derived GSCs. Interestingly, the chromosomal alterations in oligodendroglioma-derived cells were more similar to mesenchymal GBM GSCs than proneural GSCs. Although Hs683 cells were established from a GBM, they display typical oligodendroglioma features, including 1p/19 co-deletion, temozolomide sensitivity, abundant integrin 4 and low integrin 1 expression, and only one Notch2 gene copy per diploid cell. However, the copy variations of Hs683 cells are distinct from both oligodendroglioma-derived and GBM-derived cells. IDH mutations are prominent in HC-067047 oligodendrogliomas and appear early in gliomagenesis ; thus, 100% of tumors with complete 1p/19q co-deletion are mutated in IDH1 or IDH2. Therefore, DNA sequencing was undertaken to 15722457 determine whether the OG cells harbored known IDH mutations. PCR of genomic DNA and sequencing of exon 4 containing codon R132 of IDH1 and codon R172 of IDH2 demonstrated that Hs683, OG33, and OG35 cells express wildtype IDH1 and IDH2. HOG cells were previously reported to express wild-type IDH1/2. The wild-type IDH status in OG cells is not surprising given that only a 33% mutation rate is present in tumors bearing variable 1p/19q deletions and the OG cells display the minimal 1p36/19q13 deletion. Finally, immunocytochemical profiling was performed. In SCM, both OG33 and OG35 cells expressed NG2 and PDGFR, two well-accepted markers of OPCs, but 14522929 did not express Sox2 or Olig2. In contrast, the cells abundantly express the mesenchymal marker CD44 and the oligodendrocyte-associated enzyme glutathione Stransferase . In glioma, GST is linked with drug resistance. In DM, the OG cells expressed low levels of CNPase, but failed to express myelin basic protein even when cultured in DM for up to 3 weeks. In contrast, Oli-Neu cells displayed MBP immunoreactivity after 3 days in SATO DM. Collectively, these data support the oligodendroglial origin of OG33 and OG35 cells. GTA induces growth arrest of oligodendroglioma cells, but not neural stem cells Inasmuch as ASPA-mediated NAA catabolism to liberate acetate is reduced in glioma, the effect of GTA-mediated acetate supplementation on the growth and differentiation of established oligodendroglioma cells was tested. Twenty-four hours of treatment with 0.25% GTA induced G0/G1 growth arrest of Hs683 cells, but not HOG cells. While GTA induced a modest G0/G1 growth arrest of Oli-Neu cells in both growth medium and DM, it had no effect on neural stem cells . GTA treatmen