Tumor cell–specific BCR-mediated Syk signaling. (A) Flow cytometry contour plots of FL patient biopsy cells (FL-P10) stimulated by BCR cross-linking alone (α-μ/γ) or by a combination of BCR cross-linking and H₂O₂ (α-μ/γ+ H₂O₂) for various times (4, 16, 30, 60, 90 minutes) or left unstimulated (0 minute). BCR-mediated phosphorylation of Syk was compared in CD20⁺ Bcl-2⁺ FL B cells and CD20⁺ Bcl-2^– nonmalignant B cells (refer to Figure 1). Dark arrows indicate greater Syk signaling in Bcl-2⁺ FL tumor B cells than in nonmalignant host B cells. Light arrows indicate λ isotype B cells that failed to activate Syk in response to BCR cross-linking. (B) Flow cytometry contour plots of FL patient biopsy cells (FL-P10) stimulated by a combination of BCR cross-linking and H₂O₂ (α-μ/γ + H₂O₂) for various times (4, 16, 30, 60, or 90 minutes) or left unstimulated (0 minute). BCR-mediated phosphorylation of Syk was measured in CD20⁺ κ isotype B cells and compared with that in λ isotype nonmalignant B cells (all λ^– cells are κ⁺). Dark arrows indicate sustained Syk signaling in Bcl-2⁺ FL tumor B cells. Light arrows indicate where Syk signaling in λ isotype B cells differed from κ isotype B cells.