Genetic characterization of TET1, TET2, and TET3 alterations in myeloid malignancies.
By O. Abdel-Wahab, A. Mullally, C. Hedvat, G. Garcia-Manero, Jay P. Patel, M. Wadleigh, Sébastien Malinge, J. Yao, O. Kilpivaara, R. Bhat and 14 more. Blood, 2009
741 citations recorded by the source corpus.
Subfields: Genetics, Hematology
View Paper: https://www.semanticscholar.org/paper/2e7b6314502ecc0dc128d29e3b525a576543d1cc
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In Genetics
- Craig B. Thompson
- Chuan He
- Qing Dai
- Chun-Xiao Song
- Irving L. Weissman
- Patrick S. Ward
- W. Kaelin
- Stephen R. Quake
In Hematology
Citations in the corpus
- Clonal Evolution of Pre-Leukemic Hematopoietic Stem Cells Precedes Human Acute Myeloid Leukemia (2012, background): “In cases SU048 and SU070, preleukemic mutations were identified in a number of genes including TET2, a known recurrently mutated gene (31, 32), and SMC1A, which has recently been reported to be recurrently mutated in humanAML (24).”
- Tet2 loss leads to increased hematopoietic stem cell self-renewal and myeloid transformation (2011, positive): “TET2mutations are most commonly observed in human CMML, with somatic loss-of-function mutations in more than 40% of well-annotated CMML patient cohorts (Abdel-Wahab et al., 2009; Jankowska et al., 2009).”
- Preleukemic mutations in human acute myeloid leukemia affect epigenetic regulators and persist in remission (2014, neutral): “Proc Natl Acad Sci USA 106(10):3925–3929.”
- TET2 inactivation results in pleiotropic hematopoietic abnormalities in mouse and is a recurrent event during human lymphomagenesis. (2011, neutral): “Viable bone marrow cells were available only at the AML phase.”
- 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).”
- Impaired hydroxylation of 5-methylcytosine in myeloid cancers with mutant TET2 (2010, neutral): “myeloid leukemias (AML) and secondary AML (sAML)4–12.”
- Influence of Metabolism on Epigenetics and Disease (2013, positive): “A number of 2-oxoglutarate-dependent enzymes that act on chromatin are themselves targets of inactivating mutations in cancer, including the UTX H3K27 demethylase (also called KDM6A), JARID1C H3K4 demethylase (KDM5C), and TET2, making them attractive candidates for pathogenically relevant inhibition”