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Ibed above. With phosphorylation of extracellular-signalregulated kinase (ERK) inducing nuclear translocation staining was predominantly nuclear with a few cases also showing cytoplasmic staining. Scoring of p-ERK1/2 was done blinded to the CNKSR1 results using standard intensity scores above (0 = no staining, 1 = weak staining, 2 = moderate staining, 3 = strong staining). In addition, the percent
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Ecent studies using phosphomimetic mutants of CNKSR1 have identified phosphorylation sites in the scaffold critical for nuclear translocation and activation of MAPK pathway genes [21]. However, to date all CNKSR1 analysis in the context of pancreatic cancer has been performed at a molecular level with no translational or clinically oriented application. Using pancreatic tumor tissues from three in
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On by age, race, gender, grade, resection status, the TNM variables lymph node status (N0; No regional lymph node metastasis, N1; Regional lymph node metastasis, and NX;Quadri et al. BMC Cancer (2017) 17:Page 3 ofRegional lymph nodes cannot be assessed) and distant metastasis (M0; No distant metastasis, and M1; Distant metastasis), SEER stage (localized, regional, and distant), radiation, and prim
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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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S N1) 65+ Years at Diagnosis Male Moderately Differentiated Poorly Differentiated Non-Palliative Radiation White AsianaHazard Ratio 1.611 Hazard Ratio 2.146 3.783 2.834 1.893 1.550 1.233 1.014 0.a95 Confidence Limits 1.057?.457 95 Confidence Limits 1.341?.434 2.089?.852 1.584?.069 1.206?.972 1.018?.359 0.821?.851 0.580?.772 0.508?.356 0.370?.231 0.288?.298 0.268?.p value 0.0.0014
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Erved association of CNKSR1 expression and survival outcome suggests scaffolding proteins of the RAS-MAPK pathway may account, in part, for the observed heterogeneity of PDAC biology, and clinically may aid in improved future patient stratification.MethodsStudy participants and tissue microarray (TMA) compositionDe-identified cancer tissues included in this analysis were confirmed to be pancreatic
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Or cells, which was due to the activation of ERK and p53. To the best of our knowledge, this is the first study to report the molecular mechanism of the chemotherapeutic effects of Triphala against pancreatic cancer. Reactive oxygen species (ROS) are the known mediators of intracellular signaling cascades. Excessive production of ROS nonetheless leads to oxidative stress, loss of cell function and
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That is relatively over-expressed at the tumor periphery. These graphical representations of gene expression data compare the relative expression of galectin-1 from the core and edge of tumors to pooled data from normal mouse brain samples. (Graphics from GeneSpringW).created. To ensure that galectin-1 over-expression would not enhance proliferation of the U87MG line (and hence alter the interpret