@article{GuoJuerchottFuetal.2012,
  author    = {Guo, Ke-Tai and J{\"u}rchott, Kathrin and Fu, Peng and Selbig, Joachim and Eigenbrod, Sabina and Tonn, J{\"o}rg-Christian and Schichor, Christian},
  title     = {Isolation and characterization of bone marrow-derived progenitor cells from malignant gliomas},
  series = {Anticancer research : international journal of cancer research and treatment},
  volume    = {32},
  journal   = {Anticancer research : international journal of cancer research and treatment},
  number    = {11},
  publisher = {International Institute of Anticancer Research},
  address   = {Athens},
  issn      = {0250-7005},
  pages     = {4971 -- 4982},
  year      = {2012},
  abstract  = {Background: Malignant gliomas are highly-vascularised tumours. Neoangiogenesis is a crucial factor in the malignant behaviour of tumour and prognosis of patients. Several mechanisms are suspected to lead to neoangiogenesis, one of them is the recruitment of multipotent progenitor cells towards the tumour. Factors such as Vascular endothelial growth factor-A (VEGF-A) were described to recruit bone marrow-derived endothelial progenitor cells (EPCs) to the glioma stroma and vasculature. Little is known about isolating EPCs from normal or malignant tissues. Materials and Methods: In this study, we addressed the topic of characterization of tumour-isolated EPCs and re-defined the clonal relationship between EPCs and hematopoietic stem cells (HSCs) in gliomas. We first checked public gene expression data of glioma for putative marker expression, pointing towards a prevalence of EPCs and HSCs in glioma. Immunohistochemical staining of glioma tissue confirmed the higher expression of these progenitor markers in glioma tissue. EPCs and HSCs were consequently isolated and characterized at the phenotypic and functional levels. We applied a new isolation method, for the first time, to specimen from patients with high grade glioma including seven grade IV glioblastoma, five-grade III astrocytoma, and three grade III oligoastrocytoma. Results: In all samples, we were able to isolate the tumour-derived EPCs, which were positive for characteristic markers: CD31, CD34 and VEGFR2. The EPCs formed capillary networks in vitro and had the ability to take up acetylated low-density lipoprotein. Glioma-derived HSCs were positive for CD34 and CD45, but they were unable to form a capillary network in vitro. These findings on tumour-derived EPCs/HSCs were in concordance with the results, derived from peripheral blood of healthy volunteers. Conclusion: In our study, we established a new method for EPC/HSC isolation from human gliomas, defined the contribution of EPCs and HSCs to the tumour tissue, and highlighted the intense in vivo tumour host interaction.},
  language  = {en}
}
@article{BordagKlieJuerchottetal.2015,
  author    = {Bordag, Natalie and Klie, Sebastian and J{\"u}rchott, Kathrin and Vierheller, Janine and Schiewe, Hajo and Albrecht, Valerie and Tonn, J{\"o}rg-Christian and Schwartz, Christoph and Schichor, Christian and Selbig, Joachim},
  title     = {Glucocorticoid (dexamethasone)-induced metabolome changes in healthy males suggest prediction of response and side effects},
  series = {Scientific reports},
  volume    = {5},
  journal   = {Scientific reports},
  publisher = {Nature Publ. Group},
  address   = {London},
  issn      = {2045-2322},
  doi       = {10.1038/srep15954},
  pages     = {12},
  year      = {2015},
  abstract  = {Glucocorticoids are indispensable anti-inflammatory and decongestant drugs with high prevalence of use at (similar to)0.9\% of the adult population. Better holistic insights into glucocorticoid-induced changes are crucial for effective use as concurrent medication and management of adverse effects. The profiles of 214 metabolites from plasma of 20 male healthy volunteers were recorded prior to and after ingestion of a single dose of 4 mg dexamethasone (+20 mg pantoprazole). Samples were drawn at three predefined time points per day: seven untreated (day 1 midday - day 3 midday) and four treated (day 3 evening - day 4 evening) per volunteer. Statistical analysis revealed tremendous impact of dexamethasone on the metabolome with 150 of 214 metabolites being significantly deregulated on at least one time point after treatment (ANOVA, Benjamini-Hochberg corrected, q < 0.05). Inter-person variability was high and remained uninfluenced by treatment. The clearly visible circadian rhythm prior to treatment was almost completely suppressed and deregulated by dexamethasone. The results draw a holistic picture of the severe metabolic deregulation induced by single-dose, short-term glucocorticoid application. The observed metabolic changes suggest a potential for early detection of severe side effects, raising hope for personalized early countermeasures increasing quality of life and reducing health care costs.},
  language  = {en}
}