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AdeQuadri et al. BMC Cancer (2017) 17:Page 6 ofFig. 5 a Comparison of CNKSR1 expression of study cohort and secondary validation cohort. b Cellular distribution pattern of CNKSR1 showed primarily cytoplasmic expression in pancreatic cancer specimens. Nuclear staining of CNKSR1 was not associated with cytoplasmic CNKSR1 expression levels (0, 1+ vs 2+, 3+; p = 0.22; chi square test, 2-tailed)tumors
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Pathologists (MM, MA). CNKSR1 low (0 and 1 + expression) versus CNKSR1 high (2+, 3+) comprised 28.3 and 71.7 of cases in the study cohort and 44.1 and 55.9 of cases in the validation cohort suggesting similar expression patterns across the different arrays. In the study cohort 30 of cases also showed some degree of nuclear staining (Fig. 5b). Nuclear staining was lower than cytoplasmic expressi
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Cts that pancreatic cancer will rank second of all cancer-related mortalities by the year 2030 [1, 2]. Neither current chemotherapy nor molecular therapy provides patients with an extension of survival measured by more than a few months, or the hope for sustained tumor regressions. Even in the minority of patients who are able to undergo surgical resection, median overall survival remains poor [3]
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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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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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Rbance values of the other wells. Average corrected absorbance was compared between transfectant and parental cells, using a t-test.ECM attachment assaysThe U87MG human glioma cell line was kept in tissue culture in DMEM (Cellgro Mediatech, Inc.), with 10 fetal bovine serum, and penicillin/streptomycin. For transfection, 2.5x106 cells were plated overnight on a 100 mm round dish. Cells were trans
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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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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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