PCI-32765 abrogates BCR-controlled signaling and adhesion. (A) Namalwa cells pretreated with 1μM PCI-32765 were stimulated with αIgM and immunoblotted for phosphorylated (p) AKT, ERK, and BTK (pY551). Total ERK2 and BTK were used as loading controls. The blots are representative of 4 independent experiments. (B) Namalwa cells pretreated with PCI-32765 were stimulated with αIgM, and phosphorylated phospholipase C-γ2 (PLCγ2-pY759) was measured by flow cytometry (n = 6). (C) Namalwa cells pretreated with PCI-32765 were stimulated with αIgM or PMA and allowed to adhere to fibronectin-coated (n = 13) or VCAM-1–coated (n = 8) surfaces. (D) Namalwa cells pretreated with PCI-32765 (BTK inhibitor), R406 (SYK inhibitor), wortmannin (PI3K inhibitor), or PD-98059 (MEK inhibitor) were stimulated with αIgM and allowed to adhere to fibronectin-coated surfaces (n = 7). (E) Primary CLL cells (patient 898) pretreated with 1μM PCI-32765 were stimulated with αIgM and immunoblotted for pERK. Total ERK2 was used as loading control. Phosphorylated PLCγ2 (pY759) was measured by flow cytometry from the same patient sample. (F) CLL cells pretreated with PCI-32765 were stimulated with αIgM or PMA and allowed to adhere to fibronectin-coated (n = 5 patients) or VCAM-1–coated (n = 6 patients) surfaces. Graphs are presented as normalized mean + SEM (100% = stimulated cells without inhibitors). C indicates control (unstimulated); and MFI, mean fluorescence intensity. *P < .05; **P < .01; ***P < .001.