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For the 34 CNKSR1 low cases (logrank test, p = 0.03). Table 3 presents the unadjusted and adjusted hazard ratios for pancreatic cancer cases by CNKSR1 expression status. In the unadjusted model, cases with CNKSR1 low tumors had an increased risk of death compared to those with CNKSR1 high tumors with a hazard ratio (HR) of 1.61 (95 CI: 1.06 to 2.46). In a model that adjusted for resection, TNM st
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Previous studies, prospectively evaluated and validated nomograms on surgical outcome of pancreas cancer have shown that, by far, M and N stage, as captured in our study, are the strongest predictors of outcome [32, 33]. In addition, data regarding systemic therapy was not available, though nearly all cases were diagnosed prior to the routine use of FOLFIRINOX or Gemcitabine/nab-Paclitaxel. We con
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E study targeted larval stages 48 or 72 hpf (hours post fertilization), when the yolk to cell mass ratio is already decreased [5], however, without identifying the proteins. Therefore, it remains unclear whether at this stage analysis without deyolking provides satisfactory information about cellular proteins. Thus, the develop-ment of a reliable method to remove the interfering yolk from cells on
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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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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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Rbance values of the other wells. Average corrected absorbance was compared between transfectant and parental cells, using a t-test.ECM attachment assaysThe U87MG human glioma cell line was kept in tissue culture in DMEM (Cellgro Mediatech, Inc.), with 10 fetal bovine serum, and penicillin/streptomycin. For transfection, 2.5x106 cells were plated overnight on a 100 mm round dish. Cells were trans
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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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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