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R clinical stage and proximal location compared to those within the NCCH cohort.DNA and RNA extractionDNA was extracted from a 5 m- or 10 m-thick formalin-fixed paraffin-embedded (FFPE) tissue of each patient with colorectal cancer through the use of QIAmp DNA FFPE tissue kit (Qiagen, Valencia, CA, USA). Total RNA including miRNA fraction was extracted from the FFPE tissue of each colorectal cance
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Ability was randomly developed and the peri-tendinous fibroblasts proliferated not only in the injured area, but also they randomly invaded into the peri-tendinous tissues such as skin, subcutaneous fascia and muscle and proliferated and manufactured a haphazard granulation tissue throughout these structures. Thus, the potential of the healing response of the ICTs was divided into different region
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S unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(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 otherwis
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Xpressing tumors, patients did not show any difference in survival when stratified by resection status whereas patients with high CNKSR1 expression levels who underwent resection had significantly improved outcome compared to non-resected patients in this group. Combination of CNKSR1 expression levels with current clinicopathological prognostic features might improve risk stratification and treatm
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Ribution of CNKSR1 and nuclear p-ERK expression levels, possibly indicating regulation of MAPK pathway signaling less connected to absolute CNKSR1 expression levels. In addition, the SEER TMA studied has been used in multiple previous biomarker studies, several of which have been validated in additional larger cohorts [4, 22]. CNKSR1 may represent an additional prognostic marker in pancreatic canc
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E of patients with colorectal cancer and even other cancers harboring BRAF mutations. In this study, we aimed to identify miRNAs that are specifically dysregulated in BRAF-mutant colorectal cancer using a genome-wide miRNA expression analysis, and to clarify whether these miRNAs play a role in colorectal tumorigenesis as an oncogene or a tumor-suppressor through functional assays using colorectal
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Ics, tumor characteristics, and treatment by CNKSR1 expression statusCNKSR1 Low (N = 34) Age group
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Ed by the current ones, highlight a major role for galectin-1 in GBM invasiveness. The characteristic malignant phenotype of glioblastoma extends beyond aggressive invasion. This tumor develops resistance to chemo- and radio-therapy, it promotes neoangiogenesis, and it seems to benefit from immune privilege. Interestingly, galectin-1 may play a role in promoting each of these phenotypes. While gal