Evidence map›Paper›PMID 24220273›Full record

ReviewLeukemia2014

The Ten-Eleven Translocation-2 (TET2) gene in hematopoiesis and hematopoietic diseases.

E Solary, O A Bernard, A Tefferi, F Fuks, W Vainchenker

Abstract readReview
PubMed Publisher
In one paragraph

Review in Leukemia, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 164 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
164citing papers in PubMed, 1 pooled it
10.6field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

164 citing papers in PubMed, 1 synthesis or guideline pooled it, 282 citations in OpenAlex.

  1. Association between MTHFR C677T polymorphism and risk of acute lymphoblastic leukemia: a meta-analysis based on 51 case-control studies.Medical science monitor : international medical journal of experimental and clinical research · 2015
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104 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 3 institutions in 3 countries.

E Solary1] Hematology Department, Gustave Roussy, Villejuif, France [2] Inserm UMR1009, Gustave Roussy, Villejuif cedex, France [3] Faculty of Medicine, University Paris-Sud, Le Kremlin-Bicêtre, France.
O A Bernard1] Hematology Department, Gustave Roussy, Villejuif, France [2] Faculty of Medicine, University Paris-Sud, Le Kremlin-Bicêtre, France [3] Inserm UMR985, Gustave Roussy, Villejuif, France.
A TefferiDivision of Hematology, Department of Medicine, Mayo Clinic, Rochester, MN, USA.
F FuksFaculty of Medicine, Laboratory of Cancer Epigenetics, Université Libre de Bruxelles, Brussels, Belgium.
W Vainchenker1] Hematology Department, Gustave Roussy, Villejuif, France [2] Inserm UMR1009, Gustave Roussy, Villejuif cedex, France [3] Faculty of Medicine, University Paris-Sud, Le Kremlin-Bicêtre, France.
Institut Gustave Roussy · FRMayo Clinic in Arizona · USUniversité Libre de Bruxelles · BE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ten-Eleven Translocation-2 (TET2) inactivation through loss-of-function mutation, deletion and IDH1/2 (Isocitrate Dehydrogenase 1 and 2) gene mutation is a common event in myeloid and lymphoid malignancies. TET2 gene mutations similar to those observed in myeloid and lymphoid malignancies also accumulate with age in otherwise healthy subjects with clonal hematopoiesis. TET2 is one of the three proteins of the TET (Ten-Eleven Translocation) family, which are evolutionarily conserved dioxygenases that catalyze the conversion of 5-methyl-cytosine (5-mC) to 5-hydroxymethyl-cytosine (5-hmC) and promote DNA demethylation. TET dioxygenases require 2-oxoglutarate, oxygen and Fe(II) for their activity, which is enhanced in the presence of ascorbic acid. TET2 is the most expressed TET gene in the hematopoietic tissue, especially in hematopoietic stem cells. In addition to their hydroxylase activity, TET proteins recruit the O-linked β-D-N-acetylglucosamine (O-GlcNAc) transferase (OGT) enzyme to chromatin, which promotes post-transcriptional modifications of histones and facilitates gene expression. The TET2 level is regulated by interaction with IDAX, originating from TET2 gene fission during evolution, and by the microRNA miR-22. TET2 has pleiotropic roles during hematopoiesis, including stem-cell self-renewal, lineage commitment and terminal differentiation of monocytes. Analysis of Tet2 knockout mice, which are viable and fertile, demonstrated that Tet2 functions as a tumor suppressor whose haploinsufficiency initiates myeloid and lymphoid transformations. This review summarizes the recently identified TET2 physiological and pathological functions and discusses how this knowledge influences our therapeutic approaches in hematological malignancies and possibly other tumor types.

Indexed as

AgingAscorbic AcidDioxygenasesDNA-Binding ProteinsDNA MethylationEmbryonic Stem CellsEpigenesis, GeneticGenes, Tumor SuppressorHematologic DiseasesHematopoiesisHumansMicroRNAsMutationProto-Oncogene ProteinsAscorbic AcidDioxygenasesDNA-Binding ProteinsMicroRNAsMIRN22 microRNA, humanProto-Oncogene ProteinsTET2 protein, human

Identifiers

PMID24220273
OpenAlexW2015678735

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.