Inhibition of Mer expression results in increased chemosensitivity in B-ALL cells. (A) Mer knockdown (shMer1, shMer4) and shControl 697 and REH cells were treated with 30 nM methotrexate (+) or equivalent concentration of PBS (−) (vehicle control) for 48 hours, then washed, resuspended in cRPMI medium in equal numbers, and cultured for 6 days. Similarly, cells were treated with (B) 0.2 nM vincristine or PBS, (C) 50 nM dexamethasone for 697 and 10 µm dexamethasone for REH or ethanol, and (D) 3 IU/mL l-asparaginase or ethanol. At the end of 6 days, the concentration of viable cells was determined. Mean values and SEs derived from at least 3 independent experiments are shown. (A-B) Rebound growth of 697 and REH cells after methotrexate or vincristine treatment was abrogated by Mer inhibition compared with shControl cells. (C) Rebound growth of 697 cells after treatment with dexamethasone was abrogated by Mer inhibition although Mer inhibition did not affect steroid resistance in REH cells. (D) Rebound growth of 697 cells after treatment with l-asparaginase was abrogated by Mer inhibition. A similar trend was observed for REH cells, although both knockdowns were not statistically significant. *P < .05; **P < .01; ***P < .001.