Inactivating mutations of the histone methyltransferase gene EZH2 in myeloid disorders
By T. Ernst, A. Chase, J. Score, Claire E Hidalgo-Curtis, C. Bryant, A. Jones, K. Waghorn, K. Zoi, F. Ross, A. Reiter and 8 more. Nature Genetics, 2010
1,197 citations recorded by the source corpus.
Subfields: Genetics, Hematology, Molecular Biology
View Paper: https://www.semanticscholar.org/paper/ee763dbc1c4533bd2539b56249dc62fc79426338
How researchers see this paper
The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.
In Genetics
- S. Baylin
- Peter A. Jones
- Michael R. Stratton
- Chuan He
- Qing Dai
- Chun-Xiao Song
- M. Dawson
- Andrei Krivtsov
In Hematology
- R. Majeti
- M. R. Corces-Zimmerman
- Irving L. Weissman
- Peter A. Jones
- Michael R. Stratton
- M. Dawson
- Andrei Krivtsov
- Tony Kouzarides
In Molecular Biology
- Peter A. Jones
- S. Baylin
- J. Simon
- Chuan He
- Robert E. Kingston
- Tony Kouzarides
- Peter J. Campbell
- M. Dawson
Citations in the corpus
- Clonal evolution and clinical correlates of somatic mutations in myeloproliferative neoplasms. (2014, neutral): “Neutrophils (10(9)/L) average (range) 9 (2-36) 6 (3-16) 8 (3-21)”
- Occupying chromatin: Polycomb mechanisms for getting to genomic targets, stopping transcriptional traffic, and staying put (2013, background): “These critical findings are accompanied by the paradox that PcG mutations found in B cell lymphomas cause gain of function, whereas mutations in T cell and myeloid leukemia subtypes are loss-of-function (Ernst et al., 2010; Ntziachristos et al., 2012).”
- MLL-rearranged Leukemia is Dependent on Aberrant H3K79 Methylation by DOT1L (2011, positive): “Genes encoding histone methyltransferase EZH2 and DNA methyltransferase DNMT3a are frequently mutated in hematopoietic malignancies (Ernst et al., 2010; Ley et al., 2010; Morin et al., 2010; Nikoloski et al., 2010), and recent trials have demonstrated clinical efficacy of epigenetic-directed…”
- Cancer epigenetics: from mechanism to therapy. (2012, background): “In contrast, loss-of-function mutations in EZH2 gene, conferring a poor prognosis, have been described in the myeloid malignancies (Ernst et al., 2010; Nikoloski et al., 2010) and T-ALL (Ntziachristos et al., 2012; Zhang et al., 2012), suggesting a tumor-suppressive role for EZH2 in these cell…”
- Tet2 loss leads to increased hematopoietic stem cell self-renewal and myeloid transformation (2011, positive): “These include somatic mutations in chromatin-modifying enzymes (Ernst et al., 2010; Nikoloski et al., 2010) and in DNAmethyltransferases (Ley et al., 2010; Yamashita et al., 2010).”