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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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Thor(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.Quadri et al. BMC Cancer (2017) 17:Page 2 ofBackground While advances in the understanding of cancer biology, sc
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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]. S
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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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The resected specimen and, with the limitations of reviewing small tissue cores on a TMA, was re-confirmed in select cases. No re-classifications of the original grading upon re-review were made. Of the different grading systems the WHO 2010 [WHO Classification] classification was used defining Grade 1 as well differentiated (>95 of tumor composed of glands), Grade 2 moderately differentiated (50
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Tic cancer, there is considerable heterogeneity in the molecular make-up, MAPK/ERK pathway activation states, and clinical outcome in this disease. We analyzed the expression levels of CNKSR1, a scaffold that influences MAPK/ ERK pathway activity, in clinical pancreas cancer specimens and their impact on survival of patients with pancreatic cancer. Methods: Immunohistochemical staining for CNKSR1
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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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