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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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The resected specimen and, with the limitations of reviewing small tissue cores on a TMA, was re-confirmed in select cases. No re-classifications of the original grading upon re-review were made. Of the different grading systems the WHO 2010 [WHO Classification] classification was used defining Grade 1 as well differentiated (>95 of tumor composed of glands), Grade 2 moderately differentiated (50
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By the ample amount of normal mouse brain tissue available for dissection. In spite of species differences, cross-hybridization of mouse genetic material to human probes did prove to be a common occurrence. These data made it possible to control, rather stringently, for the potential contamination of tumor edge samples with mouse brain. Of course, there could still be possible contamination ?react
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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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Thanized and their brains removed and either frozen using Optimal Cutting Temperature (OCT) compound (Electron Microscopy Sciences, Fort Washington, PA) in cryomolds placed atop dry ice, or fixed in 10 buffered formalin and paraffin embedded for histopathological analysis. The symptom-free survival of nude mice harboring U87MG parental versus transfected xenografts was compared. Kaplan-Meyer surv
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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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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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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