A single oncogenic enhancer rearrangement causes concomitant EVI1 and GATA2 deregulation in leukemia.
By Stefan Gröschel, M. Sanders, R. Hoogenboezem, E. D. Wit, Britta A. M. Bouwman, Claudia A J Erpelinck, V. Velden, M. Havermans, Roberto Avellino, K. Lom and 11 more. Cell, 2014
635 citations recorded by the source corpus.
Subfields: Hematology, Molecular Biology
View Paper: https://www.semanticscholar.org/paper/d75fbefd66c8fd3ef9c691c3dbb13ba0ca10af85
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Citations in the corpus
- Control of cell identity genes occurs in insulated neighborhoods in mammalian chromosomes (2014, neutral): “The proper association of super-enhancers and their target genes in such “insulated neighborhoods” is of considerable importance since the mis-targeting of a single super-enhancer is sufficient to cause leukemia (Groschel et al., 2014).”
- Regulation of disease-associated gene expression in the 3D genome (2016, neutral): “4Cseq redirect an enhancer from the GATA2 tumour suppres sor gene to the EVI1 oncogene, with both the enhancer loss and gain independently being oncogenic events 146 (FIG.”
- dbSUPER: a database of super-enhancers in mouse and human genome (2015, background): “In chronic myeloid leukemia, a super-enhancer associated with GATA2 gene is responsible for 80% of GATA2 expression (19).”
- Diagnosis and management of AML in adults: 2017 ELN recommendations from an international expert panel. (2017, background): “2) was revisited showing that repositioning of a GATA2 enhancer element leads to overexpression of theMECOM (EVI1) gene and to haploinsufficiency of GATA2.(7,8) A new provisional entity “AML with BCR-ABL1” was introduced to recognize that patients with this abnormality should receive therapy with a ”
- Transcriptional Addiction in Cancer (2017, neutral): “Moreover, chromosomal rearrangements that disrupt insulated neighborhoods can activate oncogenes without altering the sequences of the oncogenes themselves (Groschel et al., 2014; Hnisz et al., 2016b).”
- The 2016 revision to the World Health Organization classification of myeloid neoplasms and acute leukemia. (2016, neutral): “2) does not represent a fusion gene, but repositions a distal GATA2 enhancer to activate MECOM expression and simultaneously confer GATA2 haploinsufficiency.(76,77) In order to stress the significance of the PML-RARA fusion, which may be cryptic or result Table 9.”