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Ics, tumor characteristics, and treatment by CNKSR1 expression statusCNKSR1 Low (N = 34) Age group
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Filtering algorithm. This algorithm was designed to minimize the effect of potential contamination of the edge samples with normal mouse brain cells. Relative expression values for each gene from tumor core, tumor edge, and normal mouse brain samples were compared. Genes of interest were identified that met three criteria: a) low expression at tumor core; b) relatively increased expression at tumo
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Ained parallel sections with a pooled IgG control. This protein-level confirmation of our microarray data gave us the impetus to pursue functional in vitro and in vivo assays with galectin-1 over-expressing GBM cells.Extracellular matrix attachmentResultsIdentification of galectin-1 as a potential mediator of glioma invasionThe quantity of RNA obtained from various xenograft tumors was highly vari
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Ase) makes it a resource for identification, as well as preclinical targeting, of novel mediators of glioma invasion. Galectin-1 was identified in this manner, and has proven in vitro and in vivo to be important in the migration and invasion of glioblastoma cells. Previous work suggests an even greater role of galectin-1 in GBM neoangiogenesis, chemo- and radioresistence, and immune privilege. Tar
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Ase) makes it a resource for identification, as well as preclinical targeting, of novel mediators of glioma invasion. Galectin-1 was identified in this manner, and has proven in vitro and in vivo to be important in the migration and invasion of glioblastoma cells. Previous work suggests an even greater role of galectin-1 in GBM neoangiogenesis, chemo- and radioresistence, and immune privilege. Tar
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Ioblastoma in general. In conclusion, the orthotopic glioblastoma xenograft model recapitulates not only the invasive phenotype, but also the regional expression profile reported in human samples of glioblastoma multiforme. The value of the model (i.e., abundant tissue, high-quality RNA, andToussaint et al. Molecular Cancer 2012, 11:32 http://www.molecular-cancer.com/content/11/1/Page 10 ofFigure
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Ns were transferred to nitrocellulose and these membranes were incubated with primary antibody for 60 minutes (anti-Gal1 from Research Diagnostics, Flanders, New Jersey, anti-beta actin from Sigma, St. Louis, Missouri). After washing and incubation with secondary antibody (Goat Anti-Mse IgG-HRP, Pierce, Rockford, IL), developing solution was added to the membrane (Supersignal West Femto Substrate,
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Tin S, Mathieu V, Kiss R, Lefranc F: Galectins and gliomas. Brain Pathol 2010, 20:17?7. Mariani L, Beaudry C, McDonough WS, Hoelzinger DB, Kaczmarek E, Ponce F, Coons SW, Giese A, Seiler RW, Berens ME: Death-associated protein 3 (Dap3) is overexpressed in invasive glioblastoma cells in vivo and in glioma cell lines with induced motility phenotype in vitro. Clin Cancer Res 2001, 7:2480?489. Mariani

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