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Ells stained [24, 25]. CNKSR1 expression was evaluated based on intensity semiquantitatively on a four-tier scale (0 = negative, 1 = weak/background, 2 = moderate/positive, 3 = strongly positive). CNKSRshows minimal expression in lymphoid tissues according to RNA-Seq data and immunohistochemical staining from the Human Protein Atlas (Human Protein Atlas available from www.proteinatlas.org) [26]. S
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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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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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Nostics, INC, New Jersey) along with a human-specific mouse monoclonal anti-vimentin antibody (Dakocytomation,Toussaint et al. Molecular Cancer 2012, 11:32 http://www.molecular-cancer.com/content/11/1/Page 4 ofTrappes, France). After incubation with the provided goat anti-mouse secondary antibody, staining developed with NovaRed Developing Reagent (Vector Laboratories, Burlingame, CA). Sections we
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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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Ed clones were compared to their GFP control counterparts. (Westerns controlled for loading by -actin IB). (D) Over-expression of galectin-1 promotes invasion. All cell counts were normalized to the parental cell line data. (Westerns controlled for loading by -actin IB).our identification of galectin-1 as a mediator of glioma invasion has been corroborated previously as detailed below. While previ
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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