Adenoviral E1A-associated protein p300 is involved in acute myeloid leukemia with t(11;22)(q23;q13)

被引:208
|
作者
Ida, K
Kitabayashi, I
Taki, T
Taniwaki, M
Noro, K
Yamamoto, M
Ohki, M
Hayashi, Y
机构
[1] UNIV TOKYO,FAC MED,DEPT PEDIAT,BUNKYO KU,TOKYO 113,JAPAN
[2] NATL CANC CTR,RES INST,DIV RADIOBIOL,CHUO KU,TOKYO 104,JAPAN
[3] KYOTO PREFECTURAL UNIV MED,DEPT INTERNAL MED 3,KAMIGYO KU,KYOTO 602,JAPAN
[4] NIPPON MED COLL,DEPT PEDIAT,BUNKYO KU,TOKYO 113,JAPAN
关键词
D O I
10.1182/blood.V90.12.4699.4699_4699_4704
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
p300, which was originally cloned as a nuclear binding target of the adenovirus E1A oncoprotein, forms a family with cyclic-AMP response element binding protein (CREB)-binding protein (CBP), p300/CBP are considered to be transcriptional coactivators that connect the basal transcriptional machinery to various DNA-binding transcriptional factors. p300/CBP are implicated in both cell differentiation and regulation of cell-cycle. We identify here that the p300 gene is fused to the MLL gene and that in-frame MLL-p300 fusion protein is generated in acute myeloid leukemia (AML) with t(11;22)(q23;q13). These findings suggest that the basis for the leukemogenesis of t(11;22)-AM L is the inability of p300 to regulate cell-cycle and cell differentiation after fusion with MLL. (C) 1997 by The American Society of Hematology.
引用
收藏
页码:4699 / 4704
页数:6
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