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Nostic marker using multivariate analysis, with patients in the low CNKSR1 expression group having a median OS that is nearly half that of patients with high CNKSR1 expression. In addition, we attempted to determine whether CNKSR1 status might affect the survival difference associated with resection in pancreatic cancer patients. If validated in a larger patient sample, such information might be u
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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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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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Aging revealed a similar hazard ratio (HR) of 1.91 (95 CI: 1.20 to 3.05; data not shown). Other statistically significant variables in the model were, as expected and known from previous clinicopathological multivariate outcome models of pancreas cancer, no resection compared to any resection (HR = 3.78, 95 CI: 2.to 6.85), TNM staging indicating regional lymph nodes (HR = 1.89, 95 Cl: 1.21 to 2
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Pathologists (MM, MA). CNKSR1 low (0 and 1 + expression) versus CNKSR1 high (2+, 3+) comprised 28.3 and 71.7 of cases in the study cohort and 44.1 and 55.9 of cases in the validation cohort suggesting similar expression patterns across the different arrays. In the study cohort 30 of cases also showed some degree of nuclear staining (Fig. 5b). Nuclear staining was lower than cytoplasmic expressi
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Ning (scored by 0, 1+, 2+, and 3+ intensity levels) compared to pancreatic cancers with cytoplasmic CNKSR1 staining only (Mann Whitney U test; 2-tailed). d Cytoplasmic CNKSR1 expression levels (scored semiquantitatively as 0, 1+, 2+, and 3+) and nuclear p-ERK expression levels (scored as positive cells) (Pearson's correlation coefficient test; 2-tailed). e Kaplan-Meier survival analysis of pancr
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Ained parallel sections with a pooled IgG control. This protein-level confirmation of our microarray data gave us the impetus to pursue functional in vitro and in vivo assays with galectin-1 over-expressing GBM cells.Extracellular matrix attachmentResultsIdentification of galectin-1 as a potential mediator of glioma invasionThe quantity of RNA obtained from various xenograft tumors was highly vari