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Inase suppressor of Ras 1 (CNKSR1)* Correspondence: rudloffu@mail.nih.gov Equal contributors 1 Thoracic and Gastrointestinal Oncology Branch, Gastrointestinal Oncology Section, Investigator Center for Cancer Research, National Cancer Institute, Building 10 - Hatfield CRC, Room 4-5950, Bethesda, MD 20892, USA Full list of author information is available at the end of the article?The Author(s). 201
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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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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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Y intensity of p-ERK immunostaining. Figure 8C shows nuclear p-ERK expression levels (0, 1+, 2+, 3+)) by CNKSR1 cellular distribution (cytoplasmic CNKSR1 expression only vs cytoplasmic and nuclear) in pancreas cancer specimens of the SEER Pancreatic Cancer TMA (Mann Whitney U test; p = 0.017). To test whether expression levels of the two proteins are correlated as well, including if a possible neg
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He presence of higher transverse diameter and temperature in the injured area together with the higher infiltration of the inflammatory cells in the injured area of the treated lesions during the first 14 DPI, suggest that a higher inflammatory reaction has commenced, the healing response has been motivated by the collagen implant and the metabolism of the injured area has increased. At earlier st
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E inflammatory response and tissue remodeling in tendon healing and also it revealed that; although the severe inflammatory reaction has been developed in response to the collagen implant, but this immune response was due to the remodeling effect of the collagen implant, not its rejection. It has been postulated that inflammation has a major role in tendon healing and if immune response does not p
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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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Ental counterparts. We did not observe, however, distant invasion in U87MG tumors over-expressing galectin-1. The U87MG model is in fact weakly invasive in the brains of immunocompromized mice [33,34], while it is associated with pronounced neoangiogenesis processes [37]. Further work (e.g. viral transduction) with our patient-derivedToussaint et al. Molecular Cancer 2012, 11:32 http://www.molecul