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Tcaag gacacat, SNAI2 reverse; 5-gttgcagtgagggcaagaa, GAPDH forward; 5-acccagaagactgtggatgg, GAPDH reverse; 5-cagtg agcttcccgttcag.BRAF transfectionResultsScreening of BRAF-mutant specific miRNAsHuman wild-type BRAF cDNA was prepared by PCR using the primers (forward; 5-gtggaattctgcagatataagatggcg gcgctgagcggtgg, reverse; 5-gccactgtgctggatcctttgttgctactct cctgaactctctcactc), which cover full length
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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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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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Ld-type tumors and 15 BRAF-mutant tumors from the TUH and NCCH cohort) and a validation set (30 KRAS/BRAF-wild type tumors and four BRAF-mutant tumors from the TUH cohort) (Table 1). Using the screening set, we found nine up-regulated miRNAs (median, > 1.5-fold) and 13 down-regulated miRNAs (median,
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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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X Ethnicity (n = 555, 336, 219) White/Caucasian (reference) Unknown/Mixed/ Other Aboriginal Asian Obesity Diabetes mellitus Chronic obstructive pulmonary disease Alcohol abuse Chronic kidney disease Day 1 support, physiology, and laboratory values APACHE II score (n = 508, 306, 202) Invasive mechanical ventilation (n = 553, 338, 215) Inotrope or vasopressor Mean arterial pressure (mmHg) (n = 522,
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Rbance values of the other wells. Average corrected absorbance was compared between transfectant and parental cells, using a t-test.ECM attachment assaysThe U87MG human glioma cell line was kept in tissue culture in DMEM (Cellgro Mediatech, Inc.), with 10 fetal bovine serum, and penicillin/streptomycin. For transfection, 2.5x106 cells were plated overnight on a 100 mm round dish. Cells were trans
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Ble cross-hybridizing host genes. The use of our animal model to identify mediators of glioma invasion has the potential pitfall of identifying artifacts of xenografting. That is, human glioma cells confronted with nude mouse brain rather than human brain may express genes specific to this setting. Two arguments can be made against this theory. First, there is no teleological reason for human cell