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Ancer, particularly in BRAF-mutated colorectal cancer. Keywords: Colorectal cancer, BRAF, miRNA, miR-193a-3p, Anti-EGFR therapyBackground RAF family kinases, including BRAF and RAF1, function downstream of RAS as critical regulators of the MEK-ERK MAP kinase signaling pathway [1]. This RAS-RAF-MEKERK cascade is a key pathway, which contributes to human oncogenesis controlling the cell cycle, proli
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Is transcriptionaly regulated by ERK in response to Triphala treatment suggesting ERK as an upstream regulator of p53 in Capan-2 cells. We also observed that Triphala induce apoptosis by ERK activation in BxPC-3 cells, which has mutated p53. This is in part consistent with the observation that activated ERK lead to apoptosis after DNA damage in a p53 independent manner [49]. On the other hand, Tri
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Mas. Sem Oncol 2003, 30:10?4. 4. McGirt MJ, Chaichana KL, Gathinji M, Attenello FJ, Than K, Olivi A, Weingart JD, Brem H, Quinones-Hinojosa AR: Independent association of extent of resection with survival in patients with malignant brain astrocytomas. J Neurosurg 2009, 110:156?62.Toussaint et al. Molecular Cancer 2012, 11:32 http://www.molecular-cancer.com/content/11/1/Page 11 of5.6.7. 8. 9.10.11.
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With a narrow tip, the yolk cell can be disrupted. A buffer of low osmolarity facilitated the dissolving of the yolk. The deyolking efficiency was further increased by two additional wash steps. By removing the yolk proteins this method efficiently decreased the total protein amount per embryo more than 10 fold from 55 to 3 per embryo (Fig. 2A and 2B). However, recovery of cellular proteins rema
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Ant, and the Mayo Clinic Clinician Investigator Training Program (LGT). Author details 1 The Texas Brain and Spine Institute, 8441 St. Hwy 47, Suite 4300, Bryan, TX 77807, USA. 2Department of Neuroscience and Experimental Therapeutics, Texas A M HSC College of Medicine, 2006 MREB, 8447 St. Hwy 47, Bryan, TX 77807, USA. 3Department of Neurology, Mayo Clinic, Rochester, MN, USA. 4 Division of Biomed
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Few of our U87 galectin1 clones. Parental U87MG cells, along with galectin-1 and acGFP-only clones were injected into the right caudate/putamen complex of nude mice. Tumors overexpressing galectin-1 shortened survival of their hosts compared to their parental counterparts (Figure 5). A few animals (7/20) bearing tumors expressing acGFP alone eventually exhibited neurological symptoms. The examinat
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Ase) makes it a resource for identification, as well as preclinical targeting, of novel mediators of glioma invasion. Galectin-1 was identified in this manner, and has proven in vitro and in vivo to be important in the migration and invasion of glioblastoma cells. Previous work suggests an even greater role of galectin-1 in GBM neoangiogenesis, chemo- and radioresistence, and immune privilege. Tar
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Few of our U87 galectin1 clones. Parental U87MG cells, along with galectin-1 and acGFP-only clones were injected into the right caudate/putamen complex of nude mice. Tumors overexpressing galectin-1 shortened survival of their hosts compared to their parental counterparts (Figure 5). A few animals (7/20) bearing tumors expressing acGFP alone eventually exhibited neurological symptoms. The examinat