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Zhang, Weizhou; Kater, Arnon P.; Widhopf, George F.; Chuang, Han-Yu; Enzler, Thomas; James, Danelle F.; Poustovoitov, Maxim; Tseng, Ping-Hui; Janz, Siegfried; Hoh, Carl; Herschman, Harvey; Karin, Michael; Kipps, Thomas J.
Proceedings of the National Academy of Sciences - PNAS, 11/2010, Letnik: 107, Številka: 44Journal Article
Mice bearing a v-Myc myelocytomatosis viral oncogene homolog (c-Myc) transgene controlled by an Ig-alpha heavy-chain enhancer (iMyc Cα mice) rarely develop lymphomas but instead have increased rates of memory B-cell turnover and impaired antibody responses to antigen. We found that male progeny of iMyc Cα mice mated with mice transgenic (Tg) for CD257 (B-cell activating factor, BAFF) developed CD5⁺ B-cell leukemia resembling human chronic lymphocytic leukemia (CLL), which also displays a male gender bias. Surprisingly, leukemic cells of Myc/Baff Tg mice expressed higher levels of c-Myc than did B cells of iMyc Cα mice. We found that CLL cells of many patients with progressive disease also expressed high amounts of c-MYC, particularly CLL cells whose survival depends on nurse-like cells (NLC), which express highlevels of BAFF. We find that BAFF could enhance CLL-cell expression of c-MYC via activation the canonical IκB kinase (IKK)/NF-κB pathway. Inhibition of the IKK/NF-κB pathway in mouse or human leukemia cells blocked the capacity of BAFF to induce c-MYC or promote leukemia-cell survival and significantly impaired disease progression in Myc/Baff Tg mice. This study reveals an important relationship between BAFF and c-MYC in CLL which may affect disease development and progression, and suggests that inhibitors of the canonical NF-κB pathway may be effective in treatment of patients with this disease.
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JCR | SNIP | JCR | SNIP | JCR | SNIP | JCR | SNIP |
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in: SICRIS
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