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

被引:111
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
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
收藏
页码:178 / 191
页数:14
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