Figure 3
Figure 3. Differential expression of Ki-67, Bcl-2, c-myc, and p27−kip1 in CLL B cells with ongoing IgG CSR and in their IgM counterpart. (A-B) Flow cytometric analysis, in a representative patient with UM CLL, showing the Ki-67 and Bcl-2 protein expressions, respectively. Values are mean ± SE of mean fluorescence intensity (MFI) of, respectively, Ki-67 and Bcl-2 expression from 6 patients with UM CLL with high AID expression levels. (C-D) Semiquantitative RT-PCR from the cell sorter–isolated subpopulations with c-myc–specific primers (C) and with p27−kip1-specific primers (D) are depicted. GAPDH was amplified in all cases as internal semiquantitative control.

Differential expression of Ki-67, Bcl-2, c-myc, and p27−kip1 in CLL B cells with ongoing IgG CSR and in their IgM counterpart. (A-B) Flow cytometric analysis, in a representative patient with UM CLL, showing the Ki-67 and Bcl-2 protein expressions, respectively. Values are mean ± SE of mean fluorescence intensity (MFI) of, respectively, Ki-67 and Bcl-2 expression from 6 patients with UM CLL with high AID expression levels. (C-D) Semiquantitative RT-PCR from the cell sorter–isolated subpopulations with c-myc–specific primers (C) and with p27−kip1-specific primers (D) are depicted. GAPDH was amplified in all cases as internal semiquantitative control.

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