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Assays of GBM cells stably transfected to over-express galectin-1, perfectly fit in with the previous studies mentioned above and highlight the importance of galectin-1 in the biologically aggressive behavior of experimental GBMs. While there was no enhancement of proliferation or change inattachment to fibronectin, galectin-1 upregulation induced more rapid two-dimensional migration and enhanced
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File1: Figure S1. Galectin-1 staining correlates with patient survival. Using a tissue microarray created at Mayo Clinic, we stained glioblastoma samples from 34 separate patients using immunohistochemistry for galectin-1. A survival analysis revealed a trend towards shorter survival in those patients harboring galectin-1 positive tumors. Abbreviations ATCC: American type culture collection; ECM:
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By the ample amount of normal mouse brain tissue available for dissection. In spite of species differences, cross-hybridization of mouse genetic material to human probes did prove to be a common occurrence. These data made it possible to control, rather stringently, for the potential contamination of tumor edge samples with mouse brain. Of course, there could still be possible contamination ?react
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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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Expression profile of glioblastoma multiforme invasive phenotype points to new therapeutic targets. Neoplasia 2005, 7:7?6. Zagzag D, Salnikow K, Chiriboga L, Yee H, Lan L, Ali MA, Garcia R, Demaria S, Newcomb EW: Downregulation of major histocompatibility complex antigens in invading glioma cells: stealth invasion of the brain. Lab Invest 2005, 85:328?41. Camby I, Belot N, Rorive S, Lefranc F, Mau
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Tin S, Mathieu V, Kiss R, Lefranc F: Galectins and gliomas. Brain Pathol 2010, 20:17?7. Mariani L, Beaudry C, McDonough WS, Hoelzinger DB, Kaczmarek E, Ponce F, Coons SW, Giese A, Seiler RW, Berens ME: Death-associated protein 3 (Dap3) is overexpressed in invasive glioblastoma cells in vivo and in glioma cell lines with induced motility phenotype in vitro. Clin Cancer Res 2001, 7:2480?489. Mariani
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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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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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