Evidence map›Paper›PMID 33182501›Full record

ArticleCells2020

Aberrant Bone Homeostasis in AML Is Associated with Activated Oncogenic FLT3-Dependent Cytokine Networks.

Isabel Bär, Volker Ast, Daria Meyer, Rainer König, Martina Rauner, Lorenz C Hofbauer, Jörg P Müller

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

Article in Cells, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.4field-weighted citation impact, top 35% 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

1 citing paper in PubMed, 4 citations in OpenAlex.

  1. 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

7 authors at 3 institutions in 1 country.

Isabel BärInstitute of Molecular Cell Biology, Center for Molecular Biomedicine (CMB), Jena University Hospital, 07745 Jena, Germany.
Volker AstInstitute for Clinical Chemistry, Medical Faculty Mannheim, Heidelberg University, 69117 Heidelberg, Germany.
Daria MeyerCenter for Infectious Diseases and Infection Control, Jena University Hospital, 07745 Jena, Germany.ORCID 0000-0003-2006-4610
Rainer KönigCenter for Infectious Diseases and Infection Control, Jena University Hospital, 07745 Jena, Germany.
Martina RaunerDepartment of Medicine III & Center for Healthy Aging, Technical University Dresden, 01069 Dresden, Germany.
Lorenz C HofbauerDepartment of Medicine III & Center for Healthy Aging, Technical University Dresden, 01069 Dresden, Germany.
Jörg P MüllerInstitute of Molecular Cell Biology, Center for Molecular Biomedicine (CMB), Jena University Hospital, 07745 Jena, Germany.ORCID 0000-0003-0223-6781
Jena University Hospital · DETechnische Universität Dresden · DEHeidelberg University · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Acute myeloid leukaemia (AML) is a haematopoietic malignancy caused by a combination of genetic and epigenetic lesions. Activation of the oncoprotein FLT3 ITD (Fms-like tyrosine kinase with internal tandem duplications) represents a key driver mutation in 25-30% of AML patients. FLT3 is a class III receptor tyrosine kinase, which plays a role in cell survival, proliferation, and differentiation of haematopoietic progenitors of lymphoid and myeloid lineages. Mutant FLT3 ITD results in an altered signalling quality, which causes cell transformation. Recent evidence indicates an effect of FLT3 ITD on bone homeostasis in addition to haematological aberrations. Using gene expression data repositories of FLT3 ITD-positive AML patients, we identified activated cytokine networks that affect the formation of the haematopoietic niche by controlling osteoclastogenesis and osteoblast functions. In addition, aberrant oncogenic FLT3 signalling of osteogenesis-specific cytokines affects survival of AML patients and may be used for prognosis. Thus, these data highlight the intimate crosstalk between leukaemic and osteogenic cells within the osteohaematopoietic niche.

Indexed as

HomeostasisOncogenesAnimalsBone and BonesCell Line, TumorCytokinesfms-Like Tyrosine Kinase 3Gene DuplicationGene Expression ProfilingGene Expression Regulation, LeukemicHematopoietic Stem CellsHumansLeukemia, Myeloid, AcuteMiceOsteoblastsOsteoclastsCytokinesFLT3 protein, humanfms-Like Tyrosine Kinase 3acute myeloid leukaemia (AML)bone remodellingFMS-like tyrosine kinase 3 (FLT3)haematopoiesishaematopoietic nicheosteoblast (OB)osteoblastogenesisosteoclast (OC)

Identifiers

PMID33182501
PMCPMC7697865
OpenAlexW3098001672

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.