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Cancer Genet. 2015 May;208(5):178-91. doi: 10.1016/j.cancergen.2015.01.005. Epub 2015 Jan 30.

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

Author information

1
Molecular Biology and Biochemistry Graduate Program, Loyola University Chicago, Stritch School of Medicine, Maywood, IL, USA.
2
Molecular Biology and Biochemistry Graduate Program, Loyola University Chicago, Stritch School of Medicine, Maywood, IL, USA; Oncology Research Institute and Department of Pathology, Loyola University Chicago, Stritch School of Medicine, Maywood, IL, USA. Electronic address: adingwall@luc.edu.

Abstract

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.

KEYWORDS:

COMPASS complex; Epigenetics; chromatin; enhancers; lysine methyltransferase

PMID:
25794446
DOI:
10.1016/j.cancergen.2015.01.005
[Indexed for MEDLINE]

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