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Man T lymphocytes. J Immunol 1998, 161:2114?119. 47. Rubinstein N, Alvarez M, Zwirner NW, Toscano MA, Ilarregui JM, Bravo A, Mordoh J, Fainboim L, Podhajcer OL, Rabinovich GA: Targeted inhibition of galectin-1 gene expression in tumor cells results in heightened T cellmediated rejection; A potential mechanism of tumor-immune privilege. Cancer Cell 2004, 5:241?51. 48. Kuppner MC, Hamou MF, Sawamura
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Opathol Exp Neurol 2008, 67:456?69. Le Mercier M, Fortin S, Mathieu V, Roland I, Spiegl-Kreinecker S, Haibe-Kains B, Bontempi G, Decaestecker C, Berger W, Lefranc F, Kiss R: Galectin-1 proangiogenic and promigratory effects in the Hs683 oligodendroglioma25.26.27.28.29.30.31. 32.33.34.35.36.37.38.39.40.41.42. 43. 44.model are partly mediated through the control of BEX2 expression. Neoplasia 2009, 1
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Ble cross-hybridizing host genes. The use of our animal model to identify mediators of glioma invasion has the potential pitfall of identifying artifacts of xenografting. That is, human glioma cells confronted with nude mouse brain rather than human brain may express genes specific to this setting. Two arguments can be made against this theory. First, there is no teleological reason for human cell
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Or his help with radial migration assays. Reagents used in preliminary pilot assays were kindly provided by Yoel Kloog Authors' contributions LGT and JHU conceived of the study and designed the assays. LGT performed tumor xenografting, cell culture, and laser capture microdissection. LGT, FL, and RK wrote and edited the manuscript. AN designed and performed all DNA vector construction and sequenci
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Tion into the brain through modifications to the actin cytoskeleton and the levels of expression of small GTPases. J Neuropathol Exp Neurol 2002, 61:585?97. Camby I, Decaestecker C, Lefranc F, Kaltner H, Gabius HJ, Kiss R: Galectin-1 knocking down in human U87 glioblastoma cells alters their gene expression pattern. Biochem Biophys Res Commun 2005, 335:27?5. Jung TY, Jung S, Ryu HH, Jeong YI, Jin
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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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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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Ing glioblastoma cells to apoptosis. J Clin Oncol 2005, 23: 2411?422. Paulus W, Baur I, Beutler AS, Reeves SA: Diffuse brain invasion of glioma cells requires beta 1 integrins. Lab Invest 1996, 75:819?26. Uhm JH, Gladson CL, Rao JS: The role of integrins in the malignant phenotype of gliomas. Front Biosci 1999, 4:D188 199. Lipinski CA, Tran NL, Bay C, Kloss J, McDonough WS, Beaudry C, Berens ME, L