ALL-1/MLL1, a homologue of Drosophila TRITHORAX, modifies chromatin and is directly involved in infant acute leukaemia.
ALL-1/MLL1, a homologue of Drosophila TRITHORAX, modifies chromatin and is directly involved in infant acute leukaemia.
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DOI：
10.1038/sj.bjc.6601639
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发表时间：
2004-02-23
影响因子：
8.8
通讯作者：
Mazo, A
中科院分区：
文献类型：
--
作者：
Canaani, E;Nakamura, T;Rozovskaia, T;Smith, S T;Mori, T;Croce, C M;Mazo, A
ALL-1/MLL 1基因的重排是大多数婴儿急性白血病的基础，也是接受拓扑异构酶II抑制剂（如VP 16和多柔比星）治疗的癌症患者中发生的治疗相关白血病的基础。这种重排将ALL-1融合到50个以上的伴侣基因中的任何一个或自身。在这里，我们描述了ALL-1相关白血病的独特功能，以及最近在理解ALL-1蛋白及其果蝇同源物TRITHORAX的活性所涉及的分子机制方面的进展。
Rearrangements of the ALL-1/MLL1 gene underlie the majority of infant acute leukaemias, as well as of therapy-related leukaemias developing in cancer patients treated with inhibitors of topoisomerase II, such as VP16 and doxorubicin. The rearrangements fuse ALL-1 to any of >50 partner genes or to itself. Here, we describe the unique features of ALL-1-associated leukaemias, and recent progress in understanding molecular mechanisms involved in the activity of the ALL-1 protein and of its Drosophila homologue TRITHORAX.