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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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Ic cancer, there have been less than a dozen studies which correlated putative markers with survival outcome [31]. Similar to the hazard ratio (HR) estimates for death reported for CNKSR1 in this study, the majority of previously described prognostic biomarker studies reported HRs for death ranging from 1.5 to 4 [31]. Exceptions to these studies are, among others, the recently reported study of 13
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Manuscript. Ethics approval and consent to participate The pancreatic TMA as well as pancreatic cancer biospecimens transferred under a Material Transfer Agreement (MTA) to NCI was approved by the Office of Human Subjects Research at the NIH and was found exempt from IRB review because it contained patient de-identified information. Consent for publication Not applicable. Competing interests The a
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Action of the tumor [22,36]. Indeed, abrogating galectin-1 expression renders tumor cells more susceptible to temozolamide treatment [22,41]. Finally, galectin-1 induces apoptosis of activated T-cells [42-46], prevents host animals from mounting tumor vaccine-induced immunity [47], and may cooperate with TGF-beta in GBM-induced immunosuppression [48,49]. In sum, galectin-1 expression may inversely
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Ioblastoma in general. In conclusion, the orthotopic glioblastoma xenograft model recapitulates not only the invasive phenotype, but also the regional expression profile reported in human samples of glioblastoma multiforme. The value of the model (i.e., abundant tissue, high-quality RNA, andToussaint et al. Molecular Cancer 2012, 11:32 http://www.molecular-cancer.com/content/11/1/Page 10 ofFigure
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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