Evidence map›Paper›PMID 33914703›Full record

ArticleThe Journal of clinical investigation2021

PPARγ agonists promote the resolution of myelofibrosis in preclinical models.

Juliette Lambert, Joseph Saliba, Carolina Calderon, Karine Sii-Felice, Mohammad Salma, Valérie Edmond, Jean-Claude Alvarez, Marc Delord, Caroline Marty, Isabelle Plo and 6 more

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2021. 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
0.8field-weighted citation impact, top 28% 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, 8 citations in OpenAlex.

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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

16 authors at 5 institutions in 1 country.

Juliette LambertDivision of Innovative Therapies, CEA/DRF/François Jacob Biology Institute, UMR1184 IMVA-HB/IDMIT, Université Paris-Saclay, Fontenay-aux-Roses, France.
Joseph SalibaDivision of Innovative Therapies, CEA/DRF/François Jacob Biology Institute, UMR1184 IMVA-HB/IDMIT, Université Paris-Saclay, Fontenay-aux-Roses, France.
Carolina CalderonDivision of Innovative Therapies, CEA/DRF/François Jacob Biology Institute, UMR1184 IMVA-HB/IDMIT, Université Paris-Saclay, Fontenay-aux-Roses, France.
Karine Sii-FeliceDivision of Innovative Therapies, CEA/DRF/François Jacob Biology Institute, UMR1184 IMVA-HB/IDMIT, Université Paris-Saclay, Fontenay-aux-Roses, France.
Mohammad SalmaInstitut de Génétique Moléculaire de Montpellier, University of Montpellier, CNRS, Montpellier, France.
Valérie EdmondINSERM, UMR1287, Université Paris-Saclay, Gustave Roussy, Villejuif, France.
Jean-Claude AlvarezDépartement de Pharmacologie-Toxicologie, Hôpitaux Universitaires Paris Ile-de-France Ouest, AP-HP, Hôpital Raymond-Poincaré, FHU Sepsis, Garches, France.
Marc DelordRecherche Clinique, Centre Hospitalier de Versailles, Le Chesnay, France.
Caroline MartyINSERM, UMR1287, Université Paris-Saclay, Gustave Roussy, Villejuif, France.
Isabelle PloINSERM, UMR1287, Université Paris-Saclay, Gustave Roussy, Villejuif, France.
Jean-Jacques KiladjianOpale Carnot Institute, Paris, France.
Eric SolerInstitut de Génétique Moléculaire de Montpellier, University of Montpellier, CNRS, Montpellier, France.
William VainchenkerINSERM, UMR1287, Université Paris-Saclay, Gustave Roussy, Villejuif, France.
Jean-Luc VillevalINSERM, UMR1287, Université Paris-Saclay, Gustave Roussy, Villejuif, France.
Philippe RousselotDivision of Innovative Therapies, CEA/DRF/François Jacob Biology Institute, UMR1184 IMVA-HB/IDMIT, Université Paris-Saclay, Fontenay-aux-Roses, France.
Stéphane ProstDivision of Innovative Therapies, CEA/DRF/François Jacob Biology Institute, UMR1184 IMVA-HB/IDMIT, Université Paris-Saclay, Fontenay-aux-Roses, France.
Inserm · FRCommissariat à l'Énergie Atomique et aux Énergies Alternatives · FRCentre National de la Recherche Scientifique · FRCentre Hospitalier de Versailles · FRUniversité de Versailles Saint-Quentin-en-Yvelines · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Myelofibrosis (MF) is a non-BCR-ABL myeloproliferative neoplasm associated with poor outcomes. Current treatment has little effect on the natural history of the disease. MF results from complex interactions between (a) the malignant clone, (b) an inflammatory context, and (c) remodeling of the bone marrow (BM) microenvironment. Each of these points is a potential target of PPARγ activation. Here, we demonstrated the therapeutic potential of PPARγ agonists in resolving MF in 3 mouse models. We showed that PPARγ agonists reduce myeloproliferation, modulate inflammation, and protect the BM stroma in vitro and ex vivo. Activation of PPARγ constitutes a relevant therapeutic target in MF, and our data support the possibility of using PPARγ agonists in clinical practice.

Indexed as

AnimalsAntineoplastic AgentsBone Marrow CellsDisease Models, AnimalHematologic NeoplasmsMiceMice, TransgenicNeoplasm ProteinsNeoplasms, ExperimentalPPAR gammaPrimary MyelofibrosisTumor MicroenvironmentAntineoplastic AgentsNeoplasm ProteinsPPAR gammaPparg protein, mouseFibrosisHematologyLeukemiasStem cells

Identifiers

PMID33914703
PMCPMC8159700
OpenAlexW3158082876

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.