1
Rody JR, Rocha FG, Jia XY, Qin LX, D'Angelica MI, DeMatteo RP, et al. A novel survival-based tissue microarray of pancreatic cancer validates MUC1 and Mesothelin as biomarkers. PLoS One. 2012;7(7):10. 5. Jones S, Zhang XS, Parsons DW, Lin JCH, Leary RJ, Angenendt P, Mankoo P, Carter H, Kamiyama H, Jimeno A, et al. Core signaling pathways in human pancreatic cancers revealed by global genomic analy
1
Omprising 255 patients who underwent drug therapy including cytotoxic agents and anti-EGFR antibody, and/or surgery in the Tohoku University Hospital (TUH) between 2004 and 2013, and 59 patients who received anti-EGFR antibody in the National Cancer Center Hospital (NCCH) between 2003 and 2012, were recruited in this study. The clinical information regarding clinical characteristics of patients an
1
E atrophy in these animals. It has been shown that the physical activity and weight bearing on the injured limb, has a significant correlation with collagen production and density of the injured area of the tendon [10,12,24]. Lower DTEC and higher TRDEC together with a higher transverse diameter of the injured area of the ITTs, specifically during the initial weeks after injury, could comprehensiv
1
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
1
Ays. The association between miRNA expression status and the clinical outcome of patients treated with various chemotherapies was analyzed. Results: Within the top five of the miRNAs screened, we validated miRNA-31 (miR-31) and miR-135b as upregulated, while miR-193a-3p was down-regulated in BRAF-mutated cancer. Moreover, miR-193a-3p inhibited cell growth, and invasion of colorectal cancer cells.
1
Y using miRNA microarrayThe genome-wide miRNA expression levels of the 30 colorectal cancers from the screening set were analyzed by the SurePrint G3 Human miRNA Rel. 16.0 microarray (Agilent Technologies, Santa Clara, CA, USA), which covers 1222 human miRNAs, according to the manufacturer's protocol. The microarray data were extracted using the GeneSpring ver. 12.5 (Agilent Technologies). The raw
1
R of proteins either indirectly or directly connected to MAPK/ERK signaling (Ras, ERBB2, Myc) [4, 31]. A limitation of this study was that the dataset did not include all clinical variables, such as complete TNM staging and chemotherapy treatment, and thus we could not evaluate all variables that might impact survival. While the HRs of known clinical (TNM system N and M stage) and pathological var
1
Ioblastoma in general. In conclusion, the orthotopic glioblastoma xenograft model recapitulates not only the invasive phenotype, but also the regional expression profile reported in human samples of glioblastoma multiforme. The value of the model (i.e., abundant tissue, high-quality RNA, andToussaint et al. Molecular Cancer 2012, 11:32 http://www.molecular-cancer.com/content/11/1/Page 10 ofFigure