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S N1) 65+ Years at Diagnosis Male Moderately Differentiated Poorly Differentiated Non-Palliative Radiation White AsianaHazard Ratio 1.611 Hazard Ratio 2.146 3.783 2.834 1.893 1.550 1.233 1.014 0.a95 Confidence Limits 1.057?.457 95 Confidence Limits 1.341?.434 2.089?.852 1.584?.069 1.206?.972 1.018?.359 0.821?.851 0.580?.772 0.508?.356 0.370?.231 0.288?.298 0.268?.p value 0.0.0014
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Pathologists (MM, MA). CNKSR1 low (0 and 1 + expression) versus CNKSR1 high (2+, 3+) comprised 28.3 and 71.7 of cases in the study cohort and 44.1 and 55.9 of cases in the validation cohort suggesting similar expression patterns across the different arrays. In the study cohort 30 of cases also showed some degree of nuclear staining (Fig. 5b). Nuclear staining was lower than cytoplasmic expressi
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Pathologists (MM, MA). CNKSR1 low (0 and 1 + expression) versus CNKSR1 high (2+, 3+) comprised 28.3 and 71.7 of cases in the study cohort and 44.1 and 55.9 of cases in the validation cohort suggesting similar expression patterns across the different arrays. In the study cohort 30 of cases also showed some degree of nuclear staining (Fig. 5b). Nuclear staining was lower than cytoplasmic expressi
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Erulescens green fluorescent protein; FACS: Flow-assisted cell sorting; SDS: Sodium dodecyl sulfate; MTS: 3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2(4-sulfophenyl)-2 H-tetrazolium; MTT: 3-(4,5-Dimethylthiazol-2-yl)-2,5diphenyltetrazolium bromide; CCD: Charge-coupled device. Competing interests None of the listed authors have competing interests related to the publication of this man
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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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Ant, and the Mayo Clinic Clinician Investigator Training Program (LGT). Author details 1 The Texas Brain and Spine Institute, 8441 St. Hwy 47, Suite 4300, Bryan, TX 77807, USA. 2Department of Neuroscience and Experimental Therapeutics, Texas A M HSC College of Medicine, 2006 MREB, 8447 St. Hwy 47, Bryan, TX 77807, USA. 3Department of Neurology, Mayo Clinic, Rochester, MN, USA. 4 Division of Biomed
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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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O the culture media markedly and specifically increased cell migration levels in human neoplastic astrocytes, and that these effects were related to striking modifications in the organization of the actin cytoskeleton and an increase in small GTPase RhoA expression [33]. Conversely, knocking down galectin-1 expression in U87MG GBM cells by stable transfection with antisense galectin-1 mRNA, the co

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