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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
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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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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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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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Activation of ERK with induction of apoptosis by various chemopreventive and chemotherapeutic agents [39-41]. In fact, oxidants have been shown to activate ERK by taking over the growth factor receptor signaling pathways [42-46]. Moreover, ERK may get activated in response to DNA damage and can phosphorylate p53 in vitro [23,24,47-49]. We found that exposure of Capan-2 or BxPC-3 cells with apoptos
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Mail: Vinzenz Link - link@mpi-cbg.de; Andrej Shevchenko - shevchenko@mpi-cbg.de; Carl-Philipp Heisenberg* - heisenberg@mpi-cbg.de * Corresponding authorPublished: 13 January 2006 BMC Developmental Biology 2006, 6:1 doi:10.1186/1471-213X-6-Received: 28 August 2005 Accepted: 13 JanuaryThis article is available from: http://www.biomedcentral.com/1471-213X/6/1 ?2006 Link et al; licensee BioMed Central