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This article has been peer reviewed. It is the authors' final version prior to publication in British Journal of Cancer.

Volume 90, Issue 4, February 2004, Pages 756-60.

The published version is available at DOI: 10.1038/sj.bjc.6601639. Copyright © Nature


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.

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