Abstract
The orchestration of transcriptional programs depends on proper gene-enhancer pairing. While much remains to be learned about this process in normal development, two recent studies in Cell (Gröschel and colleagues) and this issue of Cancer Cell (Yamazaki and colleagues) highlight how the genomic rearrangement of an enhancer plays a causal role in the onset of a leukemogenic program.
Copyright © 2014 Elsevier Inc. All rights reserved.
Publication types
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Research Support, N.I.H., Extramural
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Research Support, Non-U.S. Gov't
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Comment
MeSH terms
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Animals
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Chromosome Inversion*
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Chromosomes, Human, Pair 3*
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DNA-Binding Proteins / biosynthesis
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DNA-Binding Proteins / genetics*
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Enhancer Elements, Genetic*
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GATA2 Transcription Factor / genetics*
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Gene Expression Regulation, Neoplastic*
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Hematopoiesis / genetics*
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Humans
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Leukemia, Myeloid, Acute / genetics*
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MDS1 and EVI1 Complex Locus Protein
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Myelodysplastic Syndromes / genetics*
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Proto-Oncogenes / genetics*
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Transcription Factors / biosynthesis
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Transcription Factors / genetics*
Substances
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DNA-Binding Proteins
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GATA2 Transcription Factor
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GATA2 protein, human
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MDS1 and EVI1 Complex Locus Protein
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MECOM protein, human
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Transcription Factors