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Rotein expression levels in pancreatic tumors compared to matched, uninvolved controls (p = 0.004).CNKSR1 expression levels are heterogeneous in pancreatic adenocarcinomaTo examine if CNKSR1 expression is dysregulated in pancreas cancer we first compared CNKSR1 expression measured by intensity of immunostaining in 13 randomly chosen matched tumor and normal pancreaticCombining cases from all three
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Xpressing tumors, patients did not show any difference in survival when stratified by resection status whereas patients with high CNKSR1 expression levels who underwent resection had significantly improved outcome compared to non-resected patients in this group. Combination of CNKSR1 expression levels with current clinicopathological prognostic features might improve risk stratification and treatm
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For the 34 CNKSR1 low cases (logrank test, p = 0.03). Table 3 presents the unadjusted and adjusted hazard ratios for pancreatic cancer cases by CNKSR1 expression status. In the unadjusted model, cases with CNKSR1 low tumors had an increased risk of death compared to those with CNKSR1 high tumors with a hazard ratio (HR) of 1.61 (95 CI: 1.06 to 2.46). In a model that adjusted for resection, TNM st
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Ays. The association between miRNA expression status and the clinical outcome of patients treated with various chemotherapies was analyzed. Results: Within the top five of the miRNAs screened, we validated miRNA-31 (miR-31) and miR-135b as upregulated, while miR-193a-3p was down-regulated in BRAF-mutated cancer. Moreover, miR-193a-3p inhibited cell growth, and invasion of colorectal cancer cells.
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Manuscript. Ethics approval and consent to participate The pancreatic TMA as well as pancreatic cancer biospecimens transferred under a Material Transfer Agreement (MTA) to NCI was approved by the Office of Human Subjects Research at the NIH and was found exempt from IRB review because it contained patient de-identified information. Consent for publication Not applicable. Competing interests The a
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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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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

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