Figure 4
Figure 4. Attenuated BCR signaling in p-ERK–positive CLL cells. (A) One phospho-ERK–positive patient was either untreated, or stimulated with anti-IgM or PMA, and analyzed for ERK1/2 phosphorylation (top panels), or total ERK2 protein levels (bottom panels) by Western blot analysis. Densitometric analysis is reported in the right part of the panel. (B) CLL cells from one phospho-ERK–negative patient were either untreated, or stimulated with anti-IgM or PMA, and analyzed for ERK1/2 phosphorylation (top panels), or total ERK2 protein levels (bottom panels) by Western blot analysis. Densitometric analysis is reported in the right part of the panel. (C) Densitometric analysis of 5 p-ERK+ and 4 p-ERK− patients before and after anti-IgM treatment. Data are expressed as average of fold induction and SD. t test was performed between p-ERK+ and p-ERK− samples; *P < .05.

Attenuated BCR signaling in p-ERK–positive CLL cells. (A) One phospho-ERK–positive patient was either untreated, or stimulated with anti-IgM or PMA, and analyzed for ERK1/2 phosphorylation (top panels), or total ERK2 protein levels (bottom panels) by Western blot analysis. Densitometric analysis is reported in the right part of the panel. (B) CLL cells from one phospho-ERK–negative patient were either untreated, or stimulated with anti-IgM or PMA, and analyzed for ERK1/2 phosphorylation (top panels), or total ERK2 protein levels (bottom panels) by Western blot analysis. Densitometric analysis is reported in the right part of the panel. (C) Densitometric analysis of 5 p-ERK+ and 4 p-ERK patients before and after anti-IgM treatment. Data are expressed as average of fold induction and SD. t test was performed between p-ERK+ and p-ERK samples; *P < .05.

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