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S 1. Lefranc F, Facchini V, Kiss R: Proautophagic drugs: a novel means to combat apoptosis-resistant cancers, with a special emphasis on glioblastomas. Oncologist 2007, 12:1395?403. 2. Stupp R, Hegi ME, Mason WP, van den Bent MJ, Taphoorn MJ, Janzer RC, Ludwin SK, Allgeier A, Fisher B, Belanger K, Hau P, Brandes AA, Gijtenbeek J, Marosi C, Vecht CJ, Mokhtari K, Wesseling P, Villa S, Eisenhauer E,
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X Ethnicity (n = 555, 336, 219) White/Caucasian (reference) Unknown/Mixed/ Other Aboriginal Asian Obesity Diabetes mellitus Chronic obstructive pulmonary disease Alcohol abuse Chronic kidney disease Day 1 support, physiology, and laboratory values APACHE II score (n = 508, 306, 202) Invasive mechanical ventilation (n = 553, 338, 215) Inotrope or vasopressor Mean arterial pressure (mmHg) (n = 522,
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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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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
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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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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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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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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