gms | German Medical Science

60. Jahrestagung der Deutschen Gesellschaft für Neuropathologie und Neuroanatomie (DGNN)

Deutsche Gesellschaft für Neuropathologie und Neuroanatomie

26. - 28.08.2015, Berlin

In human GBM myeloid cells contribute to tumor vascularization by homing to the perivascular niche and overexpression of proangiogenic factors

Meeting Abstract

  • corresponding author presenting/speaker Anne Blank - Charité Universitätsmedizin Berlin, Neurosurgery, Berlin, Germany
  • Susan Brandenburg - Charité Universitätsmedizin Berlin, Neurosurgery, Berlin, Germany
  • Ulf Schneider - Charité Universitätsmedizin Berlin, Neurosurgery, Berlin, Germany
  • Peter Vajkoczy - Charité Universitätsmedizin Berlin, Neurosurgery, Berlin, Germany

Deutsche Gesellschaft für Neuropathologie und Neuroanatomie. 60th Annual Meeting of the German Society for Neuropathology and Neuroanatomy (DGNN). Berlin, 26.-28.08.2015. Düsseldorf: German Medical Science GMS Publishing House; 2015. Doc15dgnnP56

doi: 10.3205/15dgnn80, urn:nbn:de:0183-15dgnn802

Veröffentlicht: 25. August 2015

© 2015 Blank et al.
Dieser Artikel ist ein Open-Access-Artikel und steht unter den Lizenzbedingungen der Creative Commons Attribution 4.0 License (Namensnennung). Lizenz-Angaben siehe



Glioblastoma multiforme (GBM), one of the most malignant brain tumors, is characterized by high proliferation rates, strong vascularization and accumulation of microglia/macrophages. The function and phenotype of these immune cells within glioma tissue is highly discussed.

We aimed to analyze the contribution of microglia/macrophages on different grades of astrocytomas. Here, we investigated their activation status and expression of proangiogenic factors, as well as their interaction with the vasculature.

During surgical treatment, tissue samples of 65 patients with astrocytomas (WHO°III and °IV) or epilepsy (control) were obtained. These tissues were either used for immunofluorescence staining or enzymatically homogenization. Prepared cell suspensions were analyzed by FACS concerning activation markers of microglia/macrophages. In addition, CD11b+ cells were isolated by MACS technology and qRT-PCRs regarding proangiogenic factors were performed.

We found altered phenotypes of microglia/macrophages within the different grades of astrocytoma accompanied by remodeling of the tumor vasculature. Tissue of GBM patients showed larger vessel calibers and a high association of microglia/macrophages with tumor blood vessels compared to astrocytomas WHO°III and controls. Additionally, we observed different fractions of myeloid cells by FACS, identifying microglia/macrophages and granulocytes dependent on the grade of malignancy. Here, we established subgroups of GBM patients based on percentage of the granulocyte fraction. The GBM group with high amounts of granulocytes contained microglia/macrophages with upregulated activation markers (CD86, MHCI, MHCII) and also higher expression of CD45 in comparison to controls or WHO°III. Furthermore we detected increased levels of various proangiogenic factors (e.g. VEGF, CXCL8, CXCL2, CD13) in GBM samples.

Our data demonstrate, that cells of the myeloid lineage are able to support vascularization in human GBM. Their proangiogenic potential is defined by localization in the perivascular niche and expression of angiogenic factors. Thus, myeloid cells contribute to tumor progression. Regarding the still insufficient treatment options for GBM patients, myeloid cells may represent an additional therapeutic target to improve the survival.