| First Author | Canaani E | Year | 2004 |
| Journal | Br J Cancer | Volume | 90 |
| Issue | 4 | Pages | 756-60 |
| PubMed ID | 14970849 | Mgi Jnum | J:88995 |
| Mgi Id | MGI:3037583 | Doi | 10.1038/sj.bjc.6601639 |
| Citation | Canaani E, et al. (2004) ALL-1/MLL1, a homologue of Drosophila TRITHORAX, modifies chromatin and is directly involved in infant acute leukaemia. Br J Cancer 90(4):756-60 |
| abstractText | 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. |
