Evidence map›Paper›PMID 32821971›Full record

ArticleAnnals of hematology2020

Cooperating, congenital neutropenia-associated Csf3r and Runx1 mutations activate pro-inflammatory signaling and inhibit myeloid differentiation of mouse HSPCs.

Malte Ritter, Maksim Klimiankou, Olga Klimenkova, Axel Schambach, Dirk Hoffmann, Amy Schmidt, Lothar Kanz, Daniel C Link, Karl Welte, Julia Skokowa

Open access · hybridAbstract read
In one paragraph

Article in Annals of hematology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
1.8field-weighted citation impact, top 14% 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

5 citing papers in PubMed, 12 citations in OpenAlex.

  1. Review
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  3. Review
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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

10 authors at 5 institutions in 2 countries.

Malte RitterDivision of Translational Oncology, Department of Hematology, Oncology, Clinical Immunology and Rheumatology, University Hospital Tübingen, Otfried-Müller-Straße 10, 72076, Tübingen, Germany.
Maksim KlimiankouDivision of Translational Oncology, Department of Hematology, Oncology, Clinical Immunology and Rheumatology, University Hospital Tübingen, Otfried-Müller-Straße 10, 72076, Tübingen, Germany.
Olga KlimenkovaDivision of Translational Oncology, Department of Hematology, Oncology, Clinical Immunology and Rheumatology, University Hospital Tübingen, Otfried-Müller-Straße 10, 72076, Tübingen, Germany.
Axel SchambachInstitute of Experimental Hematology, Hannover Medical School, Hannover, Germany.
Dirk HoffmannInstitute of Experimental Hematology, Hannover Medical School, Hannover, Germany.
Amy SchmidtDivision of Oncology, Section of Stem Cell Biology, Washington University Medical School, St. Louis, MO, USA.
Lothar KanzDivision of Translational Oncology, Department of Hematology, Oncology, Clinical Immunology and Rheumatology, University Hospital Tübingen, Otfried-Müller-Straße 10, 72076, Tübingen, Germany.
Daniel C LinkDivision of Oncology, Section of Stem Cell Biology, Washington University Medical School, St. Louis, MO, USA.
Karl WelteThe University Children's Hospital Tübingen, Tübingen, Germany.
Julia SkokowaDivision of Translational Oncology, Department of Hematology, Oncology, Clinical Immunology and Rheumatology, University Hospital Tübingen, Otfried-Müller-Straße 10, 72076, Tübingen, Germany. Julia.Skokowa@med.uni-tuebingen.de.ORCID http://orcid.org/0000-0002-4399-2324
Washington University in St. Louis · USBoston Children's Hospital · USMedizinische Hochschule Hannover · DEUniversity Children's Hospital Tübingen · DEUniversity of Tübingen · DE

Funding

Specimen Acquistition and Expression ProfilingP01CA101937 · NCI · WASHINGTON UNIVERSITY · PI PAYTON, JACQUELINE E. · 2003 to 2023
$58.8M
6 · The paper itself

Abstract

Patients with the pre-leukemia bone marrow failure syndrome called severe congenital neutropenia (CN) have an approximately 15% risk of developing acute myeloid leukemia (AML; called here CN/AML). Most CN/AML patients co-acquire CSF3R and RUNX1 mutations, which play cooperative roles in the development of AML. To establish an in vitro model of leukemogenesis, we utilized bone marrow lin

Indexed as

AnimalsCell DivisionColony-Forming Units AssayCongenital Bone Marrow Failure SyndromesCore Binding Factor Alpha 2 SubunitGene Expression ProfilingHematopoietic Stem CellsImmunity, InnateInflammationMaleMiceMice, Inbred C57BLMice, TransgenicMyeloid CellsMyelopoiesisNeutropeniaCore Binding Factor Alpha 2 SubunitCSF3R protein, humanReceptors, Colony-Stimulating FactorRecombinant ProteinsRNA, MessengerRUNX1 protein, humanG-CSFR mutationsPre-leukemia bone marrow failure syndromeRUNX1 mutationsSevere congenital neutropenia

Identifiers

PMID32821971
PMCPMC7481169
OpenAlexW3081126632

What Socratic 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 Socratic graph.