Acquired mutations in TET2 are common in myelodysplastic syndromes

By S. Langemeijer, R. Kuiper, M. Berends, Ruth Knops, M. Aslanyan, Marion Massop, E. Stevens-Linders, P. Hoogen, A. G. Kessel, R. Raymakers and 8 more. Nature Genetics, 2009

787 citations recorded by the source corpus.

Subfields: Genetics, Hematology, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/aec95ec685b7aa0215c3cca08c0bc8fd41c4d900

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Genetics

1. Yi Zhang
2. Hao Wu
3. Craig B. Thompson
4. K. Guan
5. Anjana Rao
6. Chuan He
7. Qing Dai
8. Chun-Xiao Song

In Hematology

1. Yi Zhang
2. Hao Wu
3. M. Dawson
4. Tony Kouzarides
5. Leonard I. Zon
6. Margaret A. Goodell
7. David R. Liu

In Molecular Biology

1. Hao Wu
2. Yi Zhang
3. Craig B. Thompson
4. Chuan He
5. Tony Kouzarides
6. Christoph Bock
7. Chao Lu
8. Patrick S. Ward

Citations in the corpus

• Tet2 loss leads to increased hematopoietic stem cell self-renewal and myeloid transformation (2011, positive): “Specifically, somatic deletions and loss-of-function mutations in the ten-eleven translocation 2 (TET2) gene were identified in 10%–20% of patients with MDS and MPN (Delhommeau et al., 2009; Langemeijer et al., 2009); subsequent studies identified recurrent TET2 mutations in patients with chronic my”
• 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).”
• 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.”
• Mechanisms and functions of Tet protein-mediated 5-methylcytosine oxidation. (2011, background): “…of myeloid malignancies, including MDS (19%–26%), MPN (12%–37%), chronic myelomonocytic leukemia (CMML; 20%–50%), de novo AML (7%–23%), and secondary AML (sAML) (Abdel-Wahab et al. 2009; Delhommeau et al. 2009; Langemeijer et al. 2009; Tefferi et al. 2009a,b; Abdel-Wahab 2011; Pronier et al. 2011).”
• Somatic SF3B1 Mutation in Myelodysplasia with Ring Sideroblasts (2011, background): “Several other amino acid residues in this region were also hot spots for mutation, including E622 (5 mutations), R625 (7), H662 (7), K666 (13), and I704 (3) (Fig.”
• 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).”
• Oncometabolite 2-Hydroxyglutarate Is a Competitive Inhibitor of α-Ketoglutarate-Dependent Dioxygenases (2011, positive): “, 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).”
• 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).”
• The Behaviour of 5-Hydroxymethylcytosine in Bisulfite Sequencing (2010, background): “Conversely, a tumour suppressor function seems likely for TET2, based on many reports of homozygous null mutations and chromosomal deletions involving the TET2 locus in myelodysplastic syndromes (MDS), myeloproliferative disorders (MPD) and frank myeloid malignancies ([22–27] ; reviewed in [28,29]).”