Through double-immunohistochemical staining for platelet-derived growth factor receptor α (PDGFRα) and glial fibrillary acidic protein (GFAP), this study explored the intercase variability among 45 human GBM samples regarding density of GFAP+ peritumoral astrocytes and a subset of GFAP+ peritumoral astrocyte-like cells also expressing PDGFRα.
In this study, we observed that TAM-GBM cell hybrids existed in human GBM specimens as demonstrated by co-expression of glioma biomarkers (GFAP, IDH1<sup>R132H</sup> and PDGFRA) and macrophage biomarkers (CD68 and CD14).
Previous studies indicated that Glial fibrillary acidic protein (<i>GFAP</i>) might play an important role in the aggressiveness of GBM and also contributed to its poor overall survival.
Knockdown of EPHA2 and EPHA3 together led to increased expression of differentiation marker GFAP and blocked clonogenic and tumorigenic potential, promoting significantly higher survival <i>in vivo</i> Treatment of rGBM with a bispecific antibody against EPHA2/A3 reduced clonogenicity <i>in vitro</i> and tumorigenic potential of xenografted recurrent GBM <i>in vivo</i> via downregulation of AKT and ERK and increased cellular differentiation.
We used samples of human glioblastoma (GBM) and rat neurospheres transfected with GFAP mutations to analyse GFAP and NG2 expression after differentiation.
We find that GBM induced in neural stem-cell-like glial fibrillary acidic protein (GFAP)-expressing cells in the subventricular zone of adult mice shows accelerated tumor development and produces more malignant GCs (mGC1<sub>GFAP</sub>) that are less resistant to cancer drugs, compared with those originating from more differentiated nestin- (mGC2<sub>NES</sub>) or 2,'3'-cyclic nucleotide 3'-phosphodiesterase (mGC3<sub>CNP</sub>)-expressing cells.
Here we show a significant downregulation of <i>GFAP</i>α in grade IV astrocytoma compared to grade II and III, resulting in an increased GFAPδ/<i>α</i> ratio.
Comparing each individual pair, five different 'EMT groups' within our glioblastoma collective were identified according to the regulation of mRNA expression of GFAP, desmoplakin, Snail1, Snail2, Twist1 and vimentin.
Gliosarcoma is a rare glioblastoma variant characterized by a biphasic tissue pattern with alternating areas that display either glial (glial fibrillary acidic protein-positive) or mesenchymal (reticulin-positive) differentiation.
The second tumor exhibited a high degree of cellularity, atypical mitosis, pseudo-palisading and microvascular proliferation, and was immunohistologically positive for GFAP and was diagnosed as a glioblastoma.
The biotoxin cholera toxin is capable of inducing differentiation of U87-MG human glioblastoma cells, which is characterized by morphological changes to astrocytic phenotype, increase in differentiation marker protein GFAP and decrease in proliferation.
Histologically, the tumors demonstrated typical features of glioblastoma but additionally contained areas consisting of glial fibrillary acidic protein (GFAP)-positive astrocytic tumor cells resembling adipocytes, that is, containing large intracellular lipid vacuoles.
The therapy employed, in a single baculoviral vector, a glial fibrillary acidic protein (GFAP) gene promoter and the repeated target sequences of three miRNAs that are enriched in astrocytes but downregulated in glioblastoma cells to control the expression of the herpes simplex virus thymidine kinase (HSVtk) gene.
Moreover, the cells derived from a majority of glioblastomas (7 out of 8), as well as GFAP+NNP, showed features of mesenchymal differentiation when exposed to medium with serum.
We confirmed contactin overexpression in glioblastomas at the protein level, and localized contactin to the surface of glial fibrillary acidic protein (GFAP)-expressing glioblastoma cells.
These data indicate that acquisition of a highly anaplastic glioblastoma phenotype with marked proliferative activity and lack of glial fibrillary acidic protein expression is associated with loss of a putative tumor suppressor gene on 10q25-qter.