1. BCMab1 confers Fc-FcγR–dependent antitumor activity through both macrophages and NK cells.
BCMab1 confers Fc-FcγR–dependent antitumor activity through both macrophages and NK cells. A and B, immunohistochemical quantitation of F4/80+ macrophages (A) or NKp46 NK cells (B) in tumor tissues of mice bearing established T24 tumors treated with control mIgG or BCMab1. Graphs, mean F4/80+ and NKp46+ cells in tumor areas, respectively; **, P < C, depletion of macrophages or NK cells attenuates antitumor activity in vivo. Tumor growth in macrophage or NK cell depleted nude mice bearing established tumors from T24 cells (left) or primary human bladder cancer cells (right) treated with BCMab1 or control mIgG; **, P < D, BCMab1 enhances macrophage-mediated ADCP of T24 cells (left) and primary human bladder cancer cells (right) in the presence of human macrophages; ND, not detectable; **, P < E, BCMab1 promotes NK cell–mediated ADCC of T24 cells (left) and primary human bladder cancer cells (right) in the presence of IL2-activated human NK cells. Graphs, specific lysis against target cells following treatment with BCMab1, control mIgG, or FcγR blockade; **, P < Patient primary tumor cells represent at least four bladder cancer samples.
Chong Li et al. Clin Cancer Res 2014;20:
©2014 by American Association for Cancer Research