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Ite were true: lowest relative expression value at the tumor edge compared to tumor core and normal brain. The genes meeting this ideal profile were ranked by pvalue (between core and edge).ImmunohistochemistryRaw data from chip hybridization experiments were normalized across chips and across probesets using a fast linear Loess routine [29], known as Fastlo. This normalization routine, in some re
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Few of our U87 galectin1 clones. Parental U87MG cells, along with galectin-1 and acGFP-only clones were injected into the right caudate/putamen complex of nude mice. Tumors overexpressing galectin-1 shortened survival of their hosts compared to their parental counterparts (Figure 5). A few animals (7/20) bearing tumors expressing acGFP alone eventually exhibited neurological symptoms. The examinat
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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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Ss microarray chip platforms when hybridizing the same sample RNA [32]. Additionally,Toussaint et al. Molecular Cancer 2012, 11:32 http://www.molecular-cancer.com/content/11/1/Page 8 ofFigure 4 (A) Galectin-1 transfection does not alter U87MG attachment to fibronectin. Attachment to fibronectin-coated 96-well plates was quantitated with an MTT assay with and without a media change in the middle of
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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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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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Or cells, which was due to the activation of ERK and p53. To the best of our knowledge, this is the first study to report the molecular mechanism of the chemotherapeutic effects of Triphala against pancreatic cancer. Reactive oxygen species (ROS) are the known mediators of intracellular signaling cascades. Excessive production of ROS nonetheless leads to oxidative stress, loss of cell function and
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Of each cell colony over 24 hours was calculated. Data for each cell line was averaged over 10 wells and compared between parental, control transfected, and galectin-1 transfected cells. A t-test was applied to compare means.In vitro invasion assay6.8 pg +/- 4.2 pg. In spite of this variability, the quality of the RNA was consistently high with a mean RNA integrity number of 8.13 ?0.74. Expression