Figure 2
Figure 2. Analysis of expression of NF-κB/Rel subunits in primary ATLL cells by EMSA. Nuclear extracts from leukemic cells of (A) antiviral-sensitive (ATLL-1, ATLL-2, ATLL-3, ATLL-21, ATLL-27) and (B) antiviral-resistant (ATLL-4, ATLL-5, ATLL-6, ATLL-20, ATLL-22, ATLL-25) tumors were incubated with the indicated antibodies specific for the different NF-κB subunits and 32P-labeled oligonucleotide containing a consensus NF-κB–binding sequence and were separated by gel electrophoresis. PBMCs from a healthy subject, isolated CD4+ cells from normal PBMCs, a leukemia patient with CD4+CD25+ mycosis fungoides/CTCL (HTLV-1 negative) (WBCs, 70 × 109/L), and MT-2 cells (c-Rel+, HTLV-1+ line) were used as controls. The NF-κB complex was further characterized by supershifting with several antibody combinations in one patient (ATLL-6). WBC counts over time during induction AZT and IFN-α therapy curves are demonstrated in the selected leukemia patients.

Analysis of expression of NF-κB/Rel subunits in primary ATLL cells by EMSA. Nuclear extracts from leukemic cells of (A) antiviral-sensitive (ATLL-1, ATLL-2, ATLL-3, ATLL-21, ATLL-27) and (B) antiviral-resistant (ATLL-4, ATLL-5, ATLL-6, ATLL-20, ATLL-22, ATLL-25) tumors were incubated with the indicated antibodies specific for the different NF-κB subunits and 32P-labeled oligonucleotide containing a consensus NF-κB–binding sequence and were separated by gel electrophoresis. PBMCs from a healthy subject, isolated CD4+ cells from normal PBMCs, a leukemia patient with CD4+CD25+ mycosis fungoides/CTCL (HTLV-1 negative) (WBCs, 70 × 109/L), and MT-2 cells (c-Rel+, HTLV-1+ line) were used as controls. The NF-κB complex was further characterized by supershifting with several antibody combinations in one patient (ATLL-6). WBC counts over time during induction AZT and IFN-α therapy curves are demonstrated in the selected leukemia patients.

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