The cancer COMPASS: navigating the functions of MLL complexes in cancer

被引：115

作者：

Ford, David J. ^{[1
]}

Dingwall, Andrew K. ^{[1
,2
,3
]}

机构：

[1] Loyola Univ Chicago, Stritch Sch Med, Mol Biol & Biochem Grad Program, Maywood, IL 60153 USA

[2] Loyola Univ Chicago, Stritch Sch Med, Oncol Res Inst, Maywood, IL USA

[3] Loyola Univ Chicago, Stritch Sch Med, Dept Pathol, Maywood, IL USA

来源：

CANCER GENETICS | 2015年 / 208卷 / 05期

基金：

美国国家科学基金会;

关键词：

Epigenetics; enhancers; chromatin; lysine methyltransferase; COMPASS complex; B-VIRUS DNA; MUTATIONAL LANDSCAPE; HISTONE METHYLTRANSFERASE; SOMATIC MUTATIONS; BREAST-CANCER; WHOLE-GENOME; GENE-EXPRESSION; COACTIVATOR COMPLEX; RECURRENT MUTATIONS; FREQUENT MUTATIONS;

D O I：

10.1016/j.cancergen.2015.01.005

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

The mixed-lineage leukemia family of histone methyltransferases (MLL1-4, or KMT2A-D) were previously linked to cancer through the founding member, MLL1/KMT2A, which is often involved in translocation-associated gene fusion events in childhood leukemias. However, in recent years, a multitude of tumor exome sequencing studies have revealed that orthologues MLL3/KMT2C and MLL2/KMT2D are mutated in a significant percentage of a large variety of malignancies, particularly solid tumors. These unexpected findings necessitate a deeper inspection into the activities and functional differences between the MLL/KMT2 family members. This review provides an overview of this protein family and its relation to cancers, focusing on the recent links between MLL3/KMT2C and MLL2/4/KMT2D and their potential roles as tumor suppressors in an assortment of cell types.

引用

页码：178 / 191

页数：14

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