Figure 5
Figure 5. K252a induces apoptosis of primary AML cells. Cell viability was analyzed using the annexin-V assay. Results are presented as the percentage of living cells in the presence of K252a (100% value derived from untreated control). (A) Cells were from patient T72 expressing TRKB and BDNF, both patients T10 and T29 expressing TRKs (TRKA, TRKB, and TRKC) and BDNF, and T0 (only TRKs). Patients T17 and T56 were negative for TRKs and NTs. Results presented for T10 (K 200 nM) and T29 (K 400 nM) are the mean plus or minus SD of 2 independent experiments. Note that treatment schedule was not completely applied to all patients tested due to limited number of cells. The concentrations of K252a that we used have been well documented for TRK inhibition in the literature.17,49,50 K indicates K252a. (B) Flow cytometric diagram of apoptosis of blasts from patient T17 and T29, cultured with K252a for 18 hours before analysis.

K252a induces apoptosis of primary AML cells. Cell viability was analyzed using the annexin-V assay. Results are presented as the percentage of living cells in the presence of K252a (100% value derived from untreated control). (A) Cells were from patient T72 expressing TRKB and BDNF, both patients T10 and T29 expressing TRKs (TRKA, TRKB, and TRKC) and BDNF, and T0 (only TRKs). Patients T17 and T56 were negative for TRKs and NTs. Results presented for T10 (K 200 nM) and T29 (K 400 nM) are the mean plus or minus SD of 2 independent experiments. Note that treatment schedule was not completely applied to all patients tested due to limited number of cells. The concentrations of K252a that we used have been well documented for TRK inhibition in the literature.17,49,50  K indicates K252a. (B) Flow cytometric diagram of apoptosis of blasts from patient T17 and T29, cultured with K252a for 18 hours before analysis.

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