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Orithm. Galectin-1 was ranked at the top of this list. We thus took advantage of our own patient-derived glioblastoma xenograft model [25] in order to further decipher the roles of galectin-1 on GBM cell migration features. The system we have developed mitigates the effect of three important confounders from human samples. First, tissue is frozen within one minute of removal, ensuring high quality
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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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He AMPK agonist AICAR inhibits the growth of EGFRvIII-expressing glioblastomas by inhibiting lipogenesis. Proc Natl Acad Sci U S A 2009, 106:12932?2937.doi:10.1186/1476-4598-11-22 Cite this article as: Euw et al.: Antitumor effects of the investigational selective MEK inhibitor TAK733 against cutaneous and uveal melanoma cell lines. Molecular Cancer 2012 11:22.Submit your next manuscript to BioMed
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Thur GA, Hutson TE, Moschos SJ, Flaherty KT, et al: Survival in BRAF V600mutant advanced melanoma treated with vemurafenib. N Engl J Med 2012, 366:707?14. Lin WM, Baker AC, Beroukhim R, Winckler W, Feng W, Marmion JM, Laine E, Greulich H, Tseng H, Gates C, et al: Modeling genomic diversity and tumor dependency in malignant melanoma. Cancer Res 2008, 68:664?73. Haigis KM, Kendall KR, Wang Y, Cheung
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L resection is an important predictor of patient survival [3,4], local therapy for glioblastoma fails because microscopically invasive cells evade resection and eventually proliferate in spite of adjuvant chemoradiotherapy [5,6]. Controlling the invasive nature of this tumor may offer hope for more efficacious local therapy, improved quality of life, and perhaps better response to adjuvant therapi
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Ting allows for harvesting of normal host brain from regions remote from the tumor, which serve as a control for possible contamination of samples microdissected at the tumor-brain interface. Galectin-1 was thus identified in this unsupervised method of analysis as a key marker of glioma invasion, while validating the novel filtering method (used to control for sample contamination) presented in t
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Ed to their corresponding extraction buffer reservoirs. The column-based PicoPure RNA isolation kit (Arcturus, Mountain View, CA) was used to extract RNA from collected cells per manufacturer instructions.Toussaint et al. Molecular Cancer 2012, 11:32 http://www.molecular-cancer.com/content/11/1/Page 3 ofFigure 1 Three geographic tumor regions targeted for RNA isolation. Using laser-capture microdi
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Ed migration and invasion in vitro. In vivo, tumors expressing high galectin-1 levels showed enhanced invasion and decreased host survival. Conclusions: In conclusion, cells at the margin of glioblastoma, in comparison to tumor core cells, have enhanced expression of mediators of invasion. Galectin-1 is likely one such mediator. Previous studies, along with the current one, have proven galectin-1