Fig. 5.

MTT proliferation assays averaged over three experiments including SD. (A) H929 cells treated with increasing concentrations of imatinib (100 nM, 500 nM, and 1 μM) over 72 h. (B) RPMI-8226 cells treated with imatinib under the same conditions as H929. (C) H929 cells treated with 500 nM of various tyrosine kinase inhibitor drugs and the proteasome inhibitor bortezomib over a 96-h period. (D) The biological model for BCR–ABL signaling in H929 MM cells driving proliferation primarily through ERK via binding of the Grb2 adaptor to BCR-ABL and to a lesser degree through AKT via PI3K.