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S. Increased CNKSR1 expression levels were observed in tumor tissues compared to matched normal tissue by Wilcoxon matchedpairs signed rank test (** p = 0.004)Table 1 presents demographic and clinical characteristics of the pancreatic cancer patient specimens used for clinical outcome associations (SEER, UMD, and NIH). Table 2 presents the demographics and tumor characteristics by CNKSR1 expressio
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A, c ?200; b, d ?Quadri et al. BMC Cancer (2017) 17:Page 5 ofFig. 3 Photomicrographs of pancreatic cancer tissue microarray (TMA) cores of p-ERK immunohistochemical staining: a no staining for p-ERK (score 0); b weak p-ERK (score 1+) staining; c moderate p-ERK (score 2+) staining; d strong p-ERK (score 3+) staining. Magnification: a-d: ?70 cases as 2+ (58.3 ), and 16 cases as 3+ (13.3 ) (Fig. 5a).
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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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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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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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File1: Figure S1. Galectin-1 staining correlates with patient survival. Using a tissue microarray created at Mayo Clinic, we stained glioblastoma samples from 34 separate patients using immunohistochemistry for galectin-1. A survival analysis revealed a trend towards shorter survival in those patients harboring galectin-1 positive tumors. Abbreviations ATCC: American type culture collection; ECM:
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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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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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