More recent studies using global integrin phenotyping identified ��3��1 as the predominant integrin mediating the dispersal of glioma cells and that treating U251 glioma cells with neutralizing antibodies to ��3��1 prior to injection into nude mice inhibited invasion into brain tissue. These data suggest that ��5��1-fibronectin interaction may not necessarily be of fundamental importance to glial cell migration. However, previous studies from our group have shown that activating��5 integrin function in cell lines lacking capacity for fibronectin matrix assembly consistently reduced tumor cell dispersal and migration. Dexamethasone, a drug routinely used to treat brain tumor-related edema, is highly effective inactivating FNMA in human SSR128129E fibrosarcoma, rat prostate cancer cells, and various GBM cell lines. Thus, a strategy of pharmacologically activating fibronectin matrix assembly consistently gave rise to reduced respective of cell type. Other studies from our group demonstrated that irrespective of the strength of cell-ECM adhesion, a modest increase in cell-cell cohesion was sufficient to significantly reduce dispersal. In 3Dspheroid cultures, an increase in FNMA would effectively cross-link cells together to increase bulk-cohesion of the spheroid. Previous studies using U87-MG, a GBM cell line developed nearly 50years ago, showed that Dex-treatment resulted in markedly increased cohesion and reduced dispersal velocity. Of note, is that the pattern of dispersal was affected by Dex treatment. The Teriflunomide advancing edge of untreated aggregates dispersed as single cells, whereas the leading edge of Dex-treated aggregates advanced as a sheet. Cells at the advancing front were tightly adherent to one another, suggesting that the Dex-mediated decrease in DV arose as a consequence of increased cell-cell cohesion. These previous studies implicated FNMA as a potential mediator of GBM dispersal but were limited by the fact that they were based entirely on cells that may no longer be comparable to GBM cells in an actual tumor. Little is known as to whether reduced capacity for FNMA exists within relevant clinical samples, or whether freshly-excised primary GBM cells would respond to Dex treatment in a manner similar to that observed for immortalized GBM cells.