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Blood, Vol. 113, Issue 24, 6193-6205, June 11, 2009 This Article Abstract Full Text Services Email this article to a friend Alert me to new issues of the journal Rights and Permissions Citing Articles Citing Articles via CrossRef Identification of AML1-ETO modulators by chemical genomics Blood Corsello et al. 113: 6193 Supplemental materials for: Corsello et al Files in this Data Supplement: Figure S7. Leucovorin rescues the effects of pyrimethamine in Kasumi-1 and SKNO-1 cells (JPG, 545 KB) - Kasumi-1 (A) and SKNO-1 (B) cells were treated with the indicated concentrations of pyrimethamine. Rescue was performed with 1 µM leucovorin. Cellular viability was assessed at three days (left panel) and at 6 days (right panel) with an ATP-based assay and plotted as a ratio relative to control cells. Error bars depict the standard deviation across 6 replicates. Figure S8. RU486 rescues the effects of dexamethasone in Kasumi-1 and SKNO-1 cells (JPG, 138 KB) - Kasumi-1 (A) and SKNO-1 (B) cells were treated with the indicated concentrations of dexamethasone. Rescue was performed with 1 µM RU486. Cellular viability was assessed at 72 hours with an ATP-based assay and plotted as a ratio relative to control cells. Samples were evaluated in replicate of 7. Error bars depict the standard deviation across the 7 replicates. Figure S9. Early decrease in AML1-ETO protein abundance upon corticosteroid treatment for 24 hours (JPG, 87.5 KB) - Kasumi-1 immunoblot with anti-AML antibody. AML1-ETO protein loss was seen with methylprednisolone (MPD) or dexamethasone (DEX) for 24 hours. AML1-ETO protein was not decreased with methotrexate at this time point. Induction of AML1-ETO in U937 cells was included as a positive control. Figure S10. Decreased AML1-ETO protein abundance and viability with methylprednisolone in primary patient AML blasts (JPG, 121 KB) - Primary patients AML1-ETO positive cells were treated with methylprednisolone for 48 hours and AML1-ETO protein level evaluated by immunoblotting with an anti-ETO antibody (A and B). In both samples, there is a decrement in AML1-ETO protein level with methylprednisolone treatment. In A, cellular viability was also assessed at 72 hours after methylprednisolone treatment in a 2-fold dilution series and measured with an ATP based assay. Viability is plotted as a ratio relative to control cells. Sample were evaluated in replicate of five and error bars denote the standard deviation across these measurements. Figure S11. Methylprednisolone and methotrexate attenuate colony formation in Kasumi-1 cells (JPG, 204 KB) - The ability of Kasumi-1 to form colonies in methylcellulose with methylprednisolone or methotrexate was assessed in duplicate biological replicate. Colony number was counted on day 14 using an inverted microscope (Nikon Eclipse TE200) at 400× magnification. Both compounds inhibited colony formation compared to a vehicle control. Figure S12. Methylprednisolone inhibits Kasumi-1 and SKNO-1 viability with a synergistic interaction in combination with either daunorubicin or cytosine arabinoside (JPG, 691 KB) - (A) Kasumi-1 cells were treated in combination with daunorubicin and methylprednisolone for three days or cytosine arabinoside and methylprednisolone for five days and viability measured by an ATP-based assay. Studies were performed in duplicate. The percent inhibition of cell viability compared to control cells is shown. (B) SKNO-1 cells were treated in combination with daunorubicin and methylprednisolone for five days or cytosine arabinoside and methylprednisolone for five days and viability measured by an ATP-based assay. Studies were performed in duplicate. The percent inhibition of cell viability compared to control cells is shown. This Article Abstract Full Text Services Email this article to a friend Alert me to new issues of the journal Rights and Permissions Citing Articles Citing Articles via CrossRef

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