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Galectin-1 transfectants. A population of GFP-sorted cells (the "Gal-1" bars in Figure 4A) was compared to its parental counterpart. The number of metabolically-active cells attached to fibronectin was no different between the two lines at eight hours. Changing the media at four hours reduced the number of cells left for labeling, but the effect was equal in both groups, suggesting a similar rate
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Ed clones were compared to their GFP control counterparts. (Westerns controlled for loading by -actin IB). (D) Over-expression of galectin-1 promotes invasion. All cell counts were normalized to the parental cell line data. (Westerns controlled for loading by -actin IB).our identification of galectin-1 as a mediator of glioma invasion has been corroborated previously as detailed below. While previ
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Esthesia. At the onset of neurological symptoms, animals were sacrificed in accordance with the Mayo Clinic IACUC. Survival curves were generated from those animals (38 of 40) developing tumors (7 of 20 acGFP-only).xenograft lines is necessary to characterize completely the in vivo phenotypic alterations that accompany overexpression of galectin-1.Our model system has identified galectin-1 as a ma
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Ed clones were compared to their GFP control counterparts. (Westerns controlled for loading by -actin IB). (D) Over-expression of galectin-1 promotes invasion. All cell counts were normalized to the parental cell line data. (Westerns controlled for loading by -actin IB).our identification of galectin-1 as a mediator of glioma invasion has been corroborated previously as detailed below. While previ
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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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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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L resection is an important predictor of patient survival [3,4], local therapy for glioblastoma fails because microscopically invasive cells evade resection and eventually proliferate in spite of adjuvant chemoradiotherapy [5,6]. Controlling the invasive nature of this tumor may offer hope for more efficacious local therapy, improved quality of life, and perhaps better response to adjuvant therapi
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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