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Rtner and regulator of KSR1 and the MAPK pathway.One of the main functions of the scaffold protein CNKSR1 is the regulation of other cancer-related signaling pathways integrating output to different intracellular signaling cascades upon cellular stimulation by extracellular cues [11, 12, 17?0]. In breast and cervical cancer cell models, a pro-oncogenic potential has been demonstrated through ERK-i
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Pathologists (MM, MA). CNKSR1 low (0 and 1 + expression) versus CNKSR1 high (2+, 3+) comprised 28.3 and 71.7 of cases in the study cohort and 44.1 and 55.9 of cases in the validation cohort suggesting similar expression patterns across the different arrays. In the study cohort 30 of cases also showed some degree of nuclear staining (Fig. 5b). Nuclear staining was lower than cytoplasmic expressi
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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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Time intervals in a time-dependent experiment. Expression and phosphorylation of ERK (Thr-202/Tyr204) and MEK-1 (Ser-217/221) was determined by western blotting. B) The effect of Triphala on the kinase activity of ERK was determined using a kit from Cell Signaling Technology, measuring the phosphorylation of Elk-1 at Ser-383. C, D) Effect of ERK inhibitor on Triphala induced apoptosis and activati
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Ite were true: lowest relative expression value at the tumor edge compared to tumor core and normal brain. The genes meeting this ideal profile were ranked by pvalue (between core and edge).ImmunohistochemistryRaw data from chip hybridization experiments were normalized across chips and across probesets using a fast linear Loess routine [29], known as Fastlo. This normalization routine, in some re
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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
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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
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Or cells, which was due to the activation of ERK and p53. To the best of our knowledge, this is the first study to report the molecular mechanism of the chemotherapeutic effects of Triphala against pancreatic cancer. Reactive oxygen species (ROS) are the known mediators of intracellular signaling cascades. Excessive production of ROS nonetheless leads to oxidative stress, loss of cell function and

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