Gene expression profiling of Bangpungtongseong-san (Bofutsushosan) and Bangkihwangki-tang (Boiogito) administered individuals


Few studies on the biologic and molecular properties of pediatric glioblastoma have been performed. Until now,
differential genomic analysis of CD133+ve and CD133-ve fractions has not been described in pediatric glioma. We
hypothesize not only that the presence of CD133 could be the source of tumor resistance but also that
maintenance of this molecule by hypoxia dictates cellular and molecular behavior. From a series of human
glioblastoma biopsies investigated, only one, IN699 (from a pediatric glioblastoma), generated greater than 4%
of the total cell volume as CD133+ve cells. Using this pediatric glioblastoma, containing unprecedented high levels
of the putative brain tumor stem cell marker CD133, as a study model, we report biologic and molecular
characteristics of the parent culture and of CD133+ve and CD133-ve populations derived therefrom under
atmospheric and hypoxic culture conditions. Immunocytochemistry and flow cytometry were performed with
antigenic markers known to characterize neural stem cells and associated glioma behavior. Behavioral analysis
was carried out using proliferation, adhesion, migration, and invasion assays. Cell cycle analysis and array
comparative genomic hybridization were used to assess copy number profiles for parental cells and CD133+ve
and CD133-ve fractions, respectively. With regard to invasion and proliferation, CD133+ve and CD133-ve fractions
were inversely proportional, with a significant increase in invasive propensity within the CD133-ve cells (P < .005)
and a significant increase in proliferation within CD133+ve cells (P < .005). Our observations indicate identical
genomic imbalances between CD133+ve and CD133-ve fractions. Furthermore, our research documents a direct
link between decreasing oxygen tension and CD133 expression.


Laura K Donovan,1 Nicola E Potter,2 Tracy Warr,3 and Geoffrey J Pilkington1

  • 1. Cellular and Molecular Neuro-oncology Group, Institute of Biomedical and Biomolecular Sciences, School of Pharmacy and Biomedical Sciences, University of Portsmouth, Portsmouth, UK
  • 2. Department of Molecular Neuroscience, Institute of Neurology, University College London, National Hospital for Neurology and Neurosurgery, London, UK
  • 3. Brain Tumour UK Neuro-oncology Research Group, Research Institute in Healthcare Sciences, School of Applied Sciences, University of Wolverhampton, Wolverhampton, UK


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