8 research outputs found
Additional file 4: Figure S4. of Improving nelarabine efficacy in T cell acute lymphoblastic leukemia by targeting aberrant PI3K/AKT/mTOR signaling pathway
The combination of nelarabine and ZSTK-474 is synergistic in CEM-R cells, which overexpress P-gp. Cell viability assay of CEM-R cell line treated for 48 h with increasing concentrations of nelarabine alone or combined with the pan PI3K p110 inhibitor ZSTK-474. One representative of two different experiments is shown
Additional file 5: Figure S5. of Improving nelarabine efficacy in T cell acute lymphoblastic leukemia by targeting aberrant PI3K/AKT/mTOR signaling pathway
Specific effects of nelarabine on PI3K/AKT and MEK/ERK1/2 pathways. Western blotting analyses for the expression of p-AKT and p-ERK in resistant T-ALL cell lines treated with the specific inhibitors LY294002 (PI3K inhibitor), CCI-779 (mTOR allosteric inhibitor) or trametinib (MEK1/2 inhibitor) alone or in combination with nelarabine. Thirty micrograms of protein was blotted to each lane. Antibody to β-actin served as a loading control. Molecular weights are indicated on the right. CTRL: untreated cells; Nela and N: nelarabine at 10 μM; LY: LY294002 at 10 μM; CCI: CCI-779 at 100 nM; Tram: trametinib at 1 μM. Cells were treated for 48 h
Additional file 3: Figure S3. of Improving nelarabine efficacy in T cell acute lymphoblastic leukemia by targeting aberrant PI3K/AKT/mTOR signaling pathway
Bcl2 expression in T-ALL cell lines. Western blotting analyses for the basal expression of Bcl2 in untreated T-ALL cell lines. Twenty micrograms of protein was blotted to each lane. Antibody to ÃŽË›-actin served as a loading control. Molecular weights are indicated on the right. Densitometric analysis was performed using a Chemidoc 810 Imager with the appropriate software (UVP, Upland, CA, USA), and for each cell line, Bcl2 protein expression is indicated relatively to ÃŽË›-actin expression
Additional file 4: Figure S2. of Hh/Gli antagonist in acute myeloid leukemia with CBFA2T3-GLIS2 fusion gene
Cell cycle analysis. Flow cytometric analysis of PI-stained AML cell lines negative to CBFA2T3-GLIS2 fusion gene after 48 h of treatment with GANT61. NT: sample treated with vehicle alone (DMSO). (TIF 183 kb
Additional file 5: Figure S3. of Hh/Gli antagonist in acute myeloid leukemia with CBFA2T3-GLIS2 fusion gene
Western blotting analysis of GLI1/2 protein in cell lines either positive or negative for GLIS2 fusion gene treated with GANT61. NT, untreated cells. One representative of three independent experiments is shown. (TIF 205 kb
Additional file 3: Table S1. of Hh/Gli antagonist in acute myeloid leukemia with CBFA2T3-GLIS2 fusion gene
Genetic features of control AML cell lines. * Data provided by DSMZ and by literature. (XLSX 11 kb
Additional file 1: of Hh/Gli antagonist in acute myeloid leukemia with CBFA2T3-GLIS2 fusion gene
Materials and methods. (DOCX 22 kb
Additional file 6: Figure S4. of Hh/Gli antagonist in acute myeloid leukemia with CBFA2T3-GLIS2 fusion gene
Cytotoxic effect of either GANT61, or MK-0457 or of GANT61 in association with MK-0457 on A) M07e and in B) WSU-AML cell lines. (TIF 369 kb