Identification of a potential role for POU2AFI and BTG4 in the deletion of 11q23 in chronic lymphocytic leukemia
Identification of a potential role for POU2AFI and BTG4 in the deletion of 11q23 in chronic lymphocytic leukemia
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DOI：
10.1002/gcc.20159
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发表时间：
2005-05-01
影响因子：
3.7
通讯作者：
Cotter, FE
中科院分区：
文献类型：
--
作者：
Auer, RL;Starczynski, J;Cotter, FE
慢性淋巴细胞白血病（CLL）中11q基因缺失通常与疾病进展和预后不良相关。在CLL患者中，在先前确定的I I q最小区域内发现了一种新的易位。断点在POU2AFI和BTG4基因之间。POU2AFI是b细胞特异性转录共激活因子，BTG4是细胞周期负调节因子BTG家族的成员，两者都是11q-CLL发病机制的良好候选基因。在没有突变的情况下，POU2AFI在CLL患者细胞中的表达与在正常B细胞中的表达存在差异。这可能反映了CLL细胞中持续的刺激和活跃的辅助信号。BTG4可能在单倍体功能不全失活后参与CLL发病。(c) 2005 Wiley-Liss, Inc。
Deletions of 11q in chronic lymphocytic leukemia (CLL) are usually associated with progressive disease and poor prognosis. A novel translocation within the previously identified I I q minimal region has been defined in a patient with CLL. The breakpoint is between genes POU2AFI and BTG4. POU2AFI is a B-cell-specific transcriptional coactivator, and BTG4 is a member of the BTG family of negative regulators of the cell cycle, making both of them good candidate genes for the pathogenesis of 11q-CLL. POU2AFI was observed to be differentially expressed in the cells of patients with CLL compared to its expression in normal B cells in the absence of mutations. This may reflect ongoing stimulation and active accessory signaling in CLL cells. BTG4 could contribute to CLL pathogenesis following inactivation by haploinsufficiency. (c) 2005 Wiley-Liss, Inc.