t(4;11) leukemias display addiction to MLL-AF4 but not to AF4-MLL.
t(4;11) leukemias display addiction to MLL-AF4 but not to AF4-MLL.
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DOI：
10.1016/j.leukres.2010.08.011
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发表时间：
2011-03
影响因子：
2.7
通讯作者：
Kersey JH
中科院分区：
文献类型：
--
作者：
Kumar AR;Yao Q;Li Q;Sam TA;Kersey JH
The most frequent MLL-gene rearrangement found in leukemia is a reciprocal translocation with AF4 on chromosome 4 resulting in the formation of the MLL-AF4 and the AF4-MLL fusion genes. The oncogenic role of MLL-AF4 is documented but the significance of the reciprocal product - AF4-MLL in leukemia is less clear. In the human leukemia cell lines – RS4;11 and SEMK2-M1, both of which express MLL-AF4 and AF4-MLL, we knocked down the expression of AF4-MLL using siRNA. Loss of AF4-MLL had no effect on the growth of either RS4;11 or SEMK2-M1 cells. Furthermore, in SEMK2-M1 cells there were no changes in cell cycle or apoptosis with loss of AF4-MLL. In contrast, knockdown of MLL-AF4 significantly inhibited growth of both RS4;11 and SEMK2-M1. Additionally, in SEMK2-M1 cells, loss of MLL-AF4 led to G2/M cell cycle arrest and increased apoptosis. Overall, these results demonstrate that in t(4;11) leukemia, the MLL-AF4 fusion protein is critical for leukemia cell proliferation and survival while the AF4-MLL fusion product is dispensable.
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影响因子：
50.3
作者：
Armstrong, SA;Kung, AL;Korsmeyer, SJ
通讯作者：
Korsmeyer, SJ
影响因子：
20.3
作者：
Chen, Weili;Li, Quanzhi;Kersey, John H.
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Kersey, John H.
影响因子：
16
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Milne, TA;Briggs, SD;Hess, JL
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Hess, JL
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20.3
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Li, QZ;Frestedt, JL;Kersey, JH
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Kersey, JH
影响因子：
11.8
作者：
Ernst, P;Fisher, JK;Korsmeyer, SJ
通讯作者：
Korsmeyer, SJ