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Previous studies, prospectively evaluated and validated nomograms on surgical outcome of pancreas cancer have shown that, by far, M and N stage, as captured in our study, are the strongest predictors of outcome [32, 33]. In addition, data regarding systemic therapy was not available, though nearly all cases were diagnosed prior to the routine use of FOLFIRINOX or Gemcitabine/nab-Paclitaxel. We con
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Erved association of CNKSR1 expression and survival outcome suggests scaffolding proteins of the RAS-MAPK pathway may account, in part, for the observed heterogeneity of PDAC biology, and clinically may aid in improved future patient stratification.MethodsStudy participants and tissue microarray (TMA) compositionDe-identified cancer tissues included in this analysis were confirmed to be pancreatic
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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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Radial migration assay was performed as previously described [30,31]. In a blinded fashion, various U87Gal-1 clones were analyzed and compared to U87GFP controls and parental U87MG cells. Of each clone, 2500 cells were allowed to sediment through a cooled manifold onto laminin-coated cell culture wells (Creative Scientific Methods, Inc., Phoenix, AZ). The manifold and slide were incubated together
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Nostics, INC, New Jersey) along with a human-specific mouse monoclonal anti-vimentin antibody (Dakocytomation,Toussaint et al. Molecular Cancer 2012, 11:32 http://www.molecular-cancer.com/content/11/1/Page 4 ofTrappes, France). After incubation with the provided goat anti-mouse secondary antibody, staining developed with NovaRed Developing Reagent (Vector Laboratories, Burlingame, CA). Sections we
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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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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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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