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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 pancreati
I:10.1371/journal.pone.0127641. PubMed PMID: 26011708; PMCID: PMC4444265. 40. Li X, Zhang Z, Yu M, Li L, Du G, Xiao W, Yang H. Involvement of miR-20a in promoting gastric cancer progression by targeting early growth response 2 (EGR2). Int J Mol Sci. 2013;14(8):16226-39. doi:10.3390/ijms140816226. PubMed PMID: 23924943; PMCID: PMC3759908. 41. Yin P, Navarro A, Fang F, Xie A, Coon JS, Richardson C,
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 downstre
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 scaff
Cts that pancreatic cancer will rank second of all cancer-related mortalities by the year 2030 [1, 2]. Neither current chemotherapy nor molecular therapy provides patients with an extension of survival measured by more than a few months, or the hope for sustained tumor regressions. Even in the minority of patients who are able to undergo surgical resection, median overall survival remains poor [3
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-
Ells stained [24, 25]. CNKSR1 expression was evaluated based on intensity semiquantitatively on a four-tier scale (0 = negative, 1 = weak/background, 2 = moderate/positive, 3 = strongly positive). CNKSRshows minimal expression in lymphoid tissues according to RNA-Seq data and immunohistochemical staining from the Human Protein Atlas (Human Protein Atlas available from www.proteinatlas.org) [26].
Low CNKSR1 expression (p = 0.3666). Pancreatic tumors with nuclear in addition to cytoplasmic CNKSR1 staining (32/107) showed increased nuclear phospho-ERK expression compared to tumor with cytoplasmic CNKSR1 staining only (p = 0.017). Conclusion: CNKSR1 expression is increased in pancreatic tissue specimens and was found to be an independent prognostic marker of overall survival. CNKSR1 may help


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