ALL-1/MLL1, a homologue of Drosophila TRITHORAX, modifies chromatin and is directly involved in infant acute leukaemia.

Authors

E Canaani, Weizmann Institute of Science, Rehovot, Israel
T Nakamura, Thomas Jefferson University
T Rozovskaia, Thomas Jefferson University
S T Smith, Thomas Jefferson UniversityFollow
T Mori, Thomas Jefferson University
C M Croce, Thomas Jefferson University
Alexander Mazo, Thomas Jefferson UniversityFollow

Document Type

Article

Publication Date

2-23-2004

Comments

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

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.

Recommended Citation

Canaani, E; Nakamura, T; Rozovskaia, T; Smith, S T; Mori, T; Croce, C M; and Mazo, Alexander, "ALL-1/MLL1, a homologue of Drosophila TRITHORAX, modifies chromatin and is directly involved in infant acute leukaemia." (2004). Kimmel Cancer Center Faculty Papers. Paper 33.
https://jdc.jefferson.edu/kimmelccfp/33

PubMed ID

14970849