Evidence map›Paper›PMID 32572036›Full record

ArticleScientific reports2020

Evidence for a role of RUNX1 as recombinase cofactor for TCRβ rearrangements and pathological deletions in ETV6-RUNX1 ALL.

V Seitz, K Kleo, A Dröge, S Schaper, S Elezkurtaj, N Bedjaoui, L Dimitrova, A Sommerfeld, E Berg, E von der Wall and 11 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.5field-weighted citation impact, top 29% 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

4 citing papers in PubMed, 6 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
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

21 authors at 6 institutions in 2 countries.

V Seitz *Charité University Medicine Berlin, Institute of Pathology, Berlin, Germany.
K Kleo *Charité University Medicine Berlin, Institute of Pathology, Berlin, Germany.
A DrögeHS Diagnomics GmbH, Berlin, Germany.
S SchaperHS Diagnomics GmbH, Berlin, Germany.
S ElezkurtajCharité University Medicine Berlin, Institute of Pathology, Berlin, Germany.
N BedjaouiUniversity of Paris, Institute Necker-Enfants Malades (INEM), INSERM U1151, Laboratoire d'Onco-Hematology, Assistance Publique-Hôpitaux de Paris (AP-HP), Hôpital Necker Enfants-Malades, Paris, France.
L DimitrovaCharité University Medicine Berlin, Institute of Pathology, Berlin, Germany.
A SommerfeldCharité University Medicine Berlin, Institute of Pathology, Berlin, Germany.
E BergCharité University Medicine Berlin, Institute of Pathology, Berlin, Germany.
E von der WallCharité University Medicine Berlin, Institute of Pathology, Berlin, Germany.
U MüllerHeinrich-Pette-Institute, Leibniz-Institute for Experimental Virology, Hamburg, Germany.
M JoostenCharité University Medicine Berlin, Institute of Pathology, Berlin, Germany.
D LenzeCharité University Medicine Berlin, Institute of Pathology, Berlin, Germany.
M M HeimesaatCharité University Medicine Berlin, Institute of Microbiology, Infectious Diseases and Immunology, Berlin, Germany.
C BaldusUniversity Medical Center Schleswig-Holstein, Department of Internal Medicine II, Kiel, Germany.
C ZinserPrecigen Bioinformatics Germany GmbH, Munich, Germany.
A CieslakUniversity of Paris, Institute Necker-Enfants Malades (INEM), INSERM U1151, Laboratoire d'Onco-Hematology, Assistance Publique-Hôpitaux de Paris (AP-HP), Hôpital Necker Enfants-Malades, Paris, France.ORCID http://orcid.org/0000-0003-1015-9448
E MacintyreUniversity of Paris, Institute Necker-Enfants Malades (INEM), INSERM U1151, Laboratoire d'Onco-Hematology, Assistance Publique-Hôpitaux de Paris (AP-HP), Hôpital Necker Enfants-Malades, Paris, France.
C StockingUniversity Medical Center Eppendorf, Department of Stem Cell Transplantation, Hamburg, Germany.
S HennigHS Diagnomics GmbH, Berlin, Germany.
M HummelCharité University Medicine Berlin, Institute of Pathology, Berlin, Germany. michael.hummel@charite.de.
Charité - Universitätsmedizin Berlin · DEHôpital Necker-Enfants Malades · FRBerlin Institute of Health at Charité - Universitätsmedizin Berlin · DELeibniz Institute of Virology (LIV) · DEUniversität Hamburg · DEUniversity Hospital Schleswig-Holstein · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

T-cell receptor gene beta (TCRβ) gene rearrangement represents a complex, tightly regulated molecular mechanism involving excision, deletion and recombination of DNA during T-cell development. RUNX1, a well-known transcription factor for T-cell differentiation, has recently been described to act in addition as a recombinase cofactor for TCRδ gene rearrangements. In this work we employed a RUNX1 knock-out mouse model and demonstrate by deep TCRβ sequencing, immunostaining and chromatin immunoprecipitation that RUNX1 binds to the initiation site of TCRβ rearrangement and its homozygous inactivation induces severe structural changes of the rearranged TCRβ gene, whereas heterozygous inactivation has almost no impact. To compare the mouse model results to the situation in Acute Lymphoblastic Leukemia (ALL) we analyzed TCRβ gene rearrangements in T-ALL samples harboring heterozygous Runx1 mutations. Comparable to the Runx1

Indexed as

Gene DeletionAnimalsB-LymphocytesCore Binding Factor Alpha 2 SubunitETS Translocation Variant 6 ProteinGene Rearrangement, beta-Chain T-Cell Antigen ReceptorLymphocyte CountMice, KnockoutPrecursor Cell Lymphoblastic Leukemia-LymphomaProto-Oncogene Proteins c-etsReceptors, Antigen, T-Cell, alpha-betaRepressor ProteinsThymus GlandT-LymphocytesCore Binding Factor Alpha 2 SubunitETS Translocation Variant 6 ProteinProto-Oncogene Proteins c-etsReceptors, Antigen, T-Cell, alpha-betaRepressor ProteinsRunx1 protein, mouse

Identifiers

PMID32572036
PMCPMC7308335
OpenAlexW3036419463

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.