HuLuc63 mediates lysis of autologous MM cells resistant to conventional or novel therapies. (A) CD138-purified tumor cells from 9 patients with MM resistant or refractory to conventional therapies were incubated with autologous effector cells, in the presence of serial dilutions of HuLuc63 (■) or control iso IgG1 (□). Shown is mean plus or minus SE of triplicate wells. (B) CD138-purified tumor cells from 4 patients with MM resistant to either bortezomib or 17-AAG were incubated with autologous effector cells, in the presence of HuLuc63 (■) or iso IgG1 (□). Shown is mean plus or minus SE of triplicate wells. (C) PBMC effector cells were preincubated with lenalidomide (0.2 μM) followed by HuLuc63-mediated ADCC against MM1S and MM1R cells as well as primary MM patient cells. Shown is mean plus or minus SE of triplicate wells. (D) MM1R cells were pretreated overnight with U0126 (5 μM), Dex (25 nM), perifosine (5 μM), bortezomib (2 nM), or lenalidomide (0.05, 0.2 μM). HuLuc63-triggered ADCC against pretreated and control MM1R cells was assayed using PBMC effector cells from healthy donors (n = 3). HuLuc63, (■); iso IgG1 (□). *P < .05; **P < .01. (E) HuLuc63-mediated ADCC against MM1S and MM1R lines was performed in the presence or absence of BMSCs. *P < .05.
