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Enhancer of the Kinase Suppressor of Ras-1), a regulator and binding partner of KSR1, is another scaffolding protein which is less understood. Its role in pancreatic cancer biology, or as a biomarker, remains to be explored. Current data suggests that CNKSR1 has multiple roles cancer biology, with some reports demonstrating that CNKSR1 interacts with tumor suppressors and othersdescribe its scaffo
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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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Ning (no staining for p-ERK (score 0); weak p-ERK (score 1+), moderate p-ERK (score 2+), and strong p-ERK (score 3 +) staining) in Fig. 3. Staining intensities were grouped as dichotomous variables, defining scores 0? as low and 2? as high expression levels [25]. Evaluation of staining was carried out independently by two pathologists (MM and MA) blinded to patients' outcome and pathological stage
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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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Patients for individualized clinical decision-making would fill an unmet clinical need. Activating somatic KRAS mutations are nearly omnipresent and a hallmark in the genetic make-up of pancreatic ductal adenocarcinoma (PDAC) [5]. While KRAS mutations themselves have been associated as prognostic markers, there is considerable and significant heterogeneity in the activation states of the downstrea
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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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Ics, tumor characteristics, and treatment by CNKSR1 expression statusCNKSR1 Low (N = 34) Age group
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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