6 research outputs found

    Additional file 1: Table S1. of Inhibition of IGF1-R overcomes IGFBP7-induced chemotherapy resistance in T-ALL

    No full text
    Probe sets in the IGF1-R signatures that are over-expressed in the high IGF1-R group. Table S2. Probe sets in the IGF1-R signatures that are under-expressed in the high IGF1-R group. (PDF 209 kb

    Combinations of antigens as a surrogate marker for <i>FLT3</i> mutations in ETP-ALL.

    No full text
    <p>Abbreviations:</p>§<p>combination of markers suggested by Hoehn <i>et al.</i><a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0053190#pone.0053190-Hoehn1" target="_blank">[17]</a>,</p>#<p>combination of markers suggested by Paietta <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0053190#pone.0053190-Paietta2" target="_blank">[36]</a>,</p>&<p>combination of markers suggested in this paper. All combinations were adapted to the subgroup of ETP-ALL.</p

    Effects of tyrosine kinase inhibitors on proliferation in T-ALL cell lines transfected with FLT3 expression constructs (A–C).

    No full text
    <p>Fourty-eight hours (hrs) after transfection, cells were seeded and cultured for additionally 48 hrs with tyrosine kinase inhibitors (PKC412, TKI258, and Sorafenib) and chemotherapy (AraC). Cell proliferation was measured using the WST-1 proliferation reagent. The mean optical density (OD) values corresponding to non-treated FLT3-ITD transfected cells were taken as 100%. The results were expressed in percentages of the OD of treated versus untreated control cells. Two experiments were performed in duplicates. For each drug two different doses were used. All results were expressed as means ±S.D. <b>A</b>: Jurkat cells. <b>B</b>: MOLT4 cells. <b>C</b>: BE13 cells.</p
    corecore