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The RNaseq data generated by the TCGA Research Network (http://cancergenome.nih.gov/) showed a significant correlation between the expression of both genes (Figure?6A). Interestingly, the silencing of AXL in two MES GSC lines (83 and 1123) decreased the mRNA expression of CD44 (Figure?6B), suggesting a co-regulation of both genes. These data were confirmed at the protein level by immunofluorescent staining of orthotopically see more injected 83 GSCs transduced with shNT or shRNA targeting AXL (shAXL#2) (Figure?6C). Supporting this finding, in orthotopically xenografted tumors derived from patient GSCs, AXL co-expressed with CD44 preferentially in perinecrotic pseudopallisading areas (Figure?S5). Moreover, AXL and CD44 co-expression correlated with the clinical survival time of glioma patients. The data generated by TCGA Research Network, visualized using the GBM-Bio Discovery Portal, shows that the co-upregulation of AXL and CD44 is a predictor of poor survival in GBM patients (Figure?7A). Figure?6 AXL Expression Correlates with CD44 Figure?7 AXL Is Highly Expressed in Clinical High-Grade Glioma Tumors Finally, we assessed the relevance of AXL as a potential therapeutic target for GBM and other tumor entities. Evaluating the Sun et?al. (2006) dataset, elevated AXL expression was observed in glioma compared with non-tumor (n?= 23 non-tumor group; n?= 7 grade II astrocytoma; n?= 19 grade S6 Kinase III astrocytoma; n?= 81 GBM group; p?Lapatinib ic50 and p?