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Ns including phosphorylation of select sites of CNKSR1, appears in line with our findings of a correlation between the cellular distribution of CNKSR1 and nuclear p-ERK expression levels [30].Fig. 8 Cellular distribution of CNKSR1 is associated with p-ERK expression levels in pancreatic cancer specimens. a p-ERK cellular distribution and nuclear expression levels (scored as 1+, 2+, and 3+) in 86 c
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Nostic marker using multivariate analysis, with patients in the low CNKSR1 expression group having a median OS that is nearly half that of patients with high CNKSR1 expression. In addition, we attempted to determine whether CNKSR1 status might affect the survival difference associated with resection in pancreatic cancer patients. If validated in a larger patient sample, such information might be u
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That is relatively over-expressed at the tumor periphery. These graphical representations of gene expression data compare the relative expression of galectin-1 from the core and edge of tumors to pooled data from normal mouse brain samples. (Graphics from GeneSpringW).created. To ensure that galectin-1 over-expression would not enhance proliferation of the U87MG line (and hence alter the interpret
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On began the day after transfection. When enough GFP-expressing cells were identified, single cell suspensions were sorted under sterile conditions using the GFP filters (488/530 nm excitation/emission) on a FACS Vantage Sorter (Beckton Dickinson Immunocytometry Systems, San Jose, CA). Cells were collected in 96-well plates at a setting of 2 cells / well, after attempts to collect 1 cell per well
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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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S independently with similar results. Statistical significance was determined by one-way ANOVA followed by Bonferroni's post hoc analysis for multiple comparisons. *Significantly different compared with PBStreated control (P
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Ble cross-hybridizing host genes. The use of our animal model to identify mediators of glioma invasion has the potential pitfall of identifying artifacts of xenografting. That is, human glioma cells confronted with nude mouse brain rather than human brain may express genes specific to this setting. Two arguments can be made against this theory. First, there is no teleological reason for human cell
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Ental counterparts. We did not observe, however, distant invasion in U87MG tumors over-expressing galectin-1. The U87MG model is in fact weakly invasive in the brains of immunocompromized mice [33,34], while it is associated with pronounced neoangiogenesis processes [37]. Further work (e.g. viral transduction) with our patient-derivedToussaint et al. Molecular Cancer 2012, 11:32 http://www.molecul