ALL-1/MLL1, a homologue of Drosophila TRITHORAX, modifies chromatin and is directly involved in infant acute leukaemia
- PMID: 14970849
- PMCID: PMC2410188
- DOI: 10.1038/sj.bjc.6601639
ALL-1/MLL1, a homologue of Drosophila TRITHORAX, modifies chromatin and is directly involved in infant acute leukaemia
Abstract
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.
References
-
- Armstrong SA, Staunton JE, Silverman LB, Pieters R, den Boer ML, Minden MD, Sallan SE, Lander ES, Golub TR, Korsmeyer SJ (2002) MLL translocations specify a distinct gene expression profile that distinguishes a unique leukemia. Nat Genet 30: 41–47 - PubMed
-
- Ayton PM, Cleary ML (2001) Molecular mechanisms of leukemogenesis mediated by MLL fusion proteins. Oncogene 20: 5695–5707 - PubMed
-
- Bender W, Fitzgerald DP (2002) Transcription activates repressed domains in the Drosophila bithorax complex. Development 129: 4923–4930 - PubMed
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