A Therapeutically Targetable Mechanism of BCR-ABL-Independent Imatinib Resistance in Chronic Myeloid Leukemia
Excerpt:
we derived K562 cell lines that over expressed PRKCH (K562/PRKCH cells) to varying degrees. In several K562/PRKCH cell lines, PKCη levels were comparable to those found in IMSG KD K562 cells (fig. S7A). The elevated PRKCH expression resulted in a 10–20-fold increase in IM resistance (Fig. 3B).