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

被引：34

作者：

Canaani, E ^{[1
]}

Nakamura, T

Rozovskaia, T

Smith, ST

Mori, T

Croce, CM

Mazo, A

机构：

[1] Weizmann Inst Sci, Dept Mol Cell Biol, IL-76100 Rehovot, Israel

[2] Thomas Jefferson Univ, Kimmel Canc Ctr, Philadelphia, PA 19107 USA

来源：

BRITISH JOURNAL OF CANCER | 2004年 / 90卷 / 04期

关键词：

acute lymphoblastic and myelogeneous leukaemia; mouse models; chromatin; epigenetic marking;

D O I：

10.1038/sj.bjc.6601639

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

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.

引用

页码：756 / 760

页数：5

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