Mutation in TET2 in myeloid cancers.

By F. Delhommeau, S. Dupont, V. Della Valle, C. James, Severine Trannoy, A. Massé, O. Kosmider, J. L. Le Couédic, F. Robert, A. Alberdi and 13 more. New England Journal of Medicine, 2009

1,719 citations recorded by the source corpus.

Subfields: Genetics, Hematology, Public Health, Environmental and Occupational Health

View Paper: https://www.semanticscholar.org/paper/28242057fb8b27b9acd18ff54f8aa224339a4f72

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Citations in the corpus

Oncometabolite 2-Hydroxyglutarate Is a Competitive Inhibitor of α-Ketoglutarate-Dependent Dioxygenases (2011, neutral): “, 2002), it was recently discovered that TET2 is mutationally inactivated in 15% of myeloid cancers, including 22% of AML (Delhommeau et al., 2009; Langemeijer et al., 2009).”
Inactivating mutations of the histone methyltransferase gene EZH2 in myeloid disorders (2010, background): “We identified another individual that tested positive for both EZH2 and TET2 (refs”
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)”
Leukemic IDH1 and IDH2 mutations result in a hypermethylation phenotype, disrupt TET2 function, and impair hematopoietic differentiation (2010, background): “TET2 is an Fe(II)- and aKG-dependent enzyme known to display loss-of-functionmutations in AML and other myeloid malignancies (Abdel-Wahab et al., 2009; 558 Cancer Cell 18, 553–567, December 14, 2010 ª2010 Elsevier Inc Delhommeau et al., 2009; Langemeijer et al., 2009).”
LOSS OF 5-HYDROXYMETHYLCYTOSINE IS AN EPIGENETIC HALLMARK OF MELANOMA (2012, background): “Frequent TET2 mutational inactivation has been reported to associate with decreased 5-hmC levels in various myeloid leukemias (Delhommeau et al., 2009; Langemeijer et al., 2009).”
Lessons from the cancer genome. (2013, neutral): “Soon thereafter, genomic surveys found that a family member TET2 shows recurrent inactivating mutations in AML, MDS, and other myeloproliferative disorders (Delhommeau et al., 2009; Langemeijer et al., 2009).”
Epigenomic profiling of young and aged HSCs reveals concerted changes during aging that reinforce self-renewal (2014, background): “, 2011), and TET2 is recurrently mutated in myelodysplastic syndrome (MDS) and acute myeloid lymphoma (AML) patients (Delhommeau et al., 2009; Langemeijer et al., 2009).”
Diagnosis and treatment of primary myelodysplastic syndromes in adults: recommendations from the European LeukemiaNet. (2013, methodology): “These include flow cytometry immunophenotyping, 29 and screening for recurrent molecular defects using genome-wide and massive parallel genotyping technology.(30-38) Investigations of value in the diagnostic approach to MDS and their grade of recommendation are reported in Table 2.”
Signal transduction in cancer. (2015, neutral): “…with cancer affect epigenetic regulators that influence multiple cellular programs—for example, DNMT1 and TET1, which control DNA methylation, and the histone-modifying enzymes EZH2, SETD2, and KDM6A are deleted or mutated in cancer (Delhommeau et al. 2009; Ley et al. 2010; Wu et al. 2012).”
The role of mutations in epigenetic regulators in myeloid malignancies (2012, background): “TET2 mutations were first identified in MPN and MDS cases based on mapping of loss-of-heterozygosity and microdeletions within a minimal region of chromosome 4q24 (40, 41).”