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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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Ional role of miRNAs in colorectal cancer, such as miRNA-21 (miR-21), miR-31, miR-34b/c, miR-135b, miR-137, miR-143, miR-145, miR-148a, miR200, and miR-203 [21?9]. Moreover, a few reports have focused on the relationship between BRAF mutations and some miRNA alterations in other cancers, although their miRNA expression profiles were not similar [30?2]. However, whether the BRAF-mutant-specific miR
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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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Tial still remains to be elucidated, and promising molecular targets for therapy against this subtype remain to be identified. microRNAs (miRNAs) are a class of small non-coding RNA, which exert their tumor suppressive and/or oncogenic functions primarily by binding to the 3-untranslated region of the mRNA of target genes. The binding of miRNA to each mRNA leads to the inhibition of translation an
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Chi1, Shin Takahashi1,2, Yasuhide Yamada4, Hideki Shimodaira1,2 and Chikashi Ishioka1,2*AbstractBackground: The aim of this study was to identify miRNAs specifically dysregulated in BRAF-mutated colorectal cancer, which could lead to a better understanding of the molecular mechanisms underlying oncogenesis of this malignant subtype of colorectal cancer. Methods: Candidate dysregulated miRNAs were
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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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R 100 mg/kg Triphala 5 times a week. Our results are consistent with previous studies where Triphala was shown to be effective in suppressing the growth ofPage 10 of(page number not for citation purposes)BMC Cancer 2008, 8:http://www.biomedcentral.com/1471-2407/8/.' .' .' .'0 0.5 1 2 4of cells with DCF fluorescenceS (5. 7KU 7U SS 6HU16 12 8 43 53 FOHDYHGFWLQTPL treatment (hours)1 P0 73/ J PO0.'
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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