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.
ALL-1/MLL1, a homologue of Drosophila TRITHORAX, modifies chromatin and is directly involved in infant acute leukaemia
Eli Canaani,Tomonori Nakamura,T. Rozovskaia,Sheryl T. Smith,T. Mori,C. M. Croce,A. Mazo
Published 2004 in British Journal of Cancer
ABSTRACT
PUBLICATION RECORD
- Publication year
2004
- Venue
British Journal of Cancer
- Publication date
2004-02-17
- Fields of study
Biology, Medicine
- Identifiers
- External record
- Source metadata
Semantic Scholar, PubMed
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