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Nonevent. All cases with missing information were included in proportional hazard ratio calculations after performing a sensitivity analysis which showed negligible effects of excluding missing data.ImmunohistochemistryImmunohistochemical staining for CNKSR1 (mouse monoclonal antibody CNKSR1 (clone 46), Santa Cruz Biotechnology, TX, USA, #sc-135,870; dilution 1:200) was performed on a Leica BOND-M
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Ge, stage, grade, race, resection and radiation. Sensitivity analyses were performed after excluding casesQuadri et al. BMC Cancer (2017) 17:Page 4 ofFig. 1 Representative photomicrographs of pancreatic cancer tissue microarray (TMA) cores illustrating intensities of CNKSR1 immunohistochemical staining scored as low: a, b no staining for CNKSR1 (score 0); c, d weak CNKSR1 (score 1+) staining; only
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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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Normal brain) and totalRNA was eluted at the final step into a final volume of 11 microliters. One microliter of each eluted RNA sample was used for quantitation with the RiboGreen (Molecular Probes, Eugene, OR) assay kit. These total RNA samples were analyzed for integrity by obtaining electropherograms on an Agilent 2100 Bioanalyzer chip. Samples of acceptable quality based on RNA integrity numb
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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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Ss microarray chip platforms when hybridizing the same sample RNA [32]. Additionally,Toussaint et al. Molecular Cancer 2012, 11:32 http://www.molecular-cancer.com/content/11/1/Page 8 ofFigure 4 (A) Galectin-1 transfection does not alter U87MG attachment to fibronectin. Attachment to fibronectin-coated 96-well plates was quantitated with an MTT assay with and without a media change in the middle of
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S independently with similar results. Statistical significance was determined by one-way ANOVA followed by Bonferroni's post hoc analysis for multiple comparisons. *Significantly different compared with PBStreated control (P
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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