Figure 3
Figure 3. CXCR4/C1013G mutation drives dissemination of WM cells in vivo. WM cells harboring the C1013G/CXCR4 variant present with changes at the mRNA level, together with increased cell adhesion and cell proliferation. SCID/Bg mice injected IV with C1013G/CXCR4 variant-harboring WM cells presented with significant involvement of (A) BM, (B) lymph nodes, (C) liver, (D) lung, (E) kidneys (×4, ×10, and ×20 magnifications). Quantification of human CD20 and CXCR4 staining is shown in supplemental Figure 4. (F) Kaplan-Meier curve showing decreased survival in C1013G/CXCR4 cell–injected mice vs control vector cell–injected mice (n = 7/group). Death for control vector cell–injected mice was observed at days 37, 48, and 62. (G-H) C1013G/CXCR4 variant increased adhesion and proliferation of WM cells either alone or in the context of BM-MSCs. Bars indicate standard deviation. P indicates P values.

CXCR4/C1013G mutation drives dissemination of WM cells in vivo. WM cells harboring the C1013G/CXCR4 variant present with changes at the mRNA level, together with increased cell adhesion and cell proliferation. SCID/Bg mice injected IV with C1013G/CXCR4 variant-harboring WM cells presented with significant involvement of (A) BM, (B) lymph nodes, (C) liver, (D) lung, (E) kidneys (×4, ×10, and ×20 magnifications). Quantification of human CD20 and CXCR4 staining is shown in supplemental Figure 4. (F) Kaplan-Meier curve showing decreased survival in C1013G/CXCR4 cell–injected mice vs control vector cell–injected mice (n = 7/group). Death for control vector cell–injected mice was observed at days 37, 48, and 62. (G-H) C1013G/CXCR4 variant increased adhesion and proliferation of WM cells either alone or in the context of BM-MSCs. Bars indicate standard deviation. P indicates P values.

Close Modal

or Create an Account

Close Modal
Close Modal