Evidence map›Paper›PMID 39470742›Full record

ArticleJCI insight2024

Comprehensive analysis of mesenchymal cells reveals a dysregulated TGF-β/WNT/HOXB7 axis in patients with myelofibrosis.

Saravanan Ganesan, Sarah Awan-Toor, Fabien Guidez, Nabih Maslah, Rifkath Rahimy, Céline Aoun, Panhong Gou, Chloé Guiguen, Juliette Soret, Odonchimeg Ravdan and 9 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in JCI insight, 2024. 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
–field-weighted citation impact
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.

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

19 authors.

Saravanan GanesanINSERM UMRS 1131, Institut de Recherche Saint-Louis, Université Paris Cité, Paris, France.
Sarah Awan-ToorINSERM UMRS 1131, Institut de Recherche Saint-Louis, Université Paris Cité, Paris, France.
Fabien GuidezINSERM UMRS 1131, Institut de Recherche Saint-Louis, Université Paris Cité, Paris, France.
Nabih MaslahINSERM UMRS 1131, Institut de Recherche Saint-Louis, Université Paris Cité, Paris, France.
Rifkath RahimyLaboratoire de recherche en génétique et hématologie translationnelle, Institut Gonçalo Moniz, Salvador, Bahia, Brazil.
Céline AounINSERM UMRS 1131, Institut de Recherche Saint-Louis, Université Paris Cité, Paris, France.
Panhong GouINSERM UMRS 1131, Institut de Recherche Saint-Louis, Université Paris Cité, Paris, France.
Chloé GuiguenINSERM UMRS 1131, Institut de Recherche Saint-Louis, Université Paris Cité, Paris, France.
Juliette SoretINSERM CIC 1427, Université Paris Cité, Centre d'Investigations Cliniques, Hôpital Saint-Louis, AP-HP, Paris, France.
Odonchimeg RavdanService de Biologie Cellulaire, Hôpital Saint-Louis, AP-HP, Paris, France.
Valeria BisioINSERM UMRS 1160, Institut de Recherche Saint-Louis, Université Paris-Cité, Paris, France.
Nicolas DulphyINSERM UMRS 1160, Institut de Recherche Saint-Louis, Université Paris-Cité, Paris, France.
Camille LobryINSERM U944, CNRS UMR7212, Institut de Recherche Saint-Louis, Université Paris-Cité, Paris, France.
Marie-Hélène SchlageterService de Biologie Cellulaire, Hôpital Saint-Louis, AP-HP, Paris, France.
Michèle SouyriINSERM UMRS 1131, Institut de Recherche Saint-Louis, Université Paris Cité, Paris, France.
Stéphane GiraudierINSERM UMRS 1131, Institut de Recherche Saint-Louis, Université Paris Cité, Paris, France.
Jean-Jacques KiladjianINSERM UMRS 1131, Institut de Recherche Saint-Louis, Université Paris Cité, Paris, France.
Christine ChomienneINSERM UMRS 1131, Institut de Recherche Saint-Louis, Université Paris Cité, Paris, France.
Bruno CassinatINSERM UMRS 1131, Institut de Recherche Saint-Louis, Université Paris Cité, Paris, France.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Despite the advances in the understanding and treatment of myeloproliferative neoplasm (MPN), the disease remains incurable with the risk of evolution to acute myeloid leukemia or myelofibrosis (MF). Unfortunately, the evolution of the disease to MF remains poorly understood, impeding preventive and therapeutic options. Recent studies in solid tumor microenvironment and organ fibrosis have shed instrumental insights on their respective pathogenesis and drug resistance, yet such precise data are lacking in MPN. In this study, through a patient sample-driven transcriptomic and epigenetic description of the MF microenvironment landscape and cell-based analyses, we identify homeobox B7 (HOXB7) overexpression and more precisely a potentially novel TGF-β/WNT/HOXB7 pathway as associated to a pro-fibrotic and pro-osteoblastic biased differentiation of mesenchymal stromal cells (MSCs). Using gene-based and chemical inhibition of this pathway, we reversed the abnormal phenotype of MSCs from patients with MF, providing the MPN field a potentially novel target to prevent and manage evolution to MF.

Indexed as

Homeodomain ProteinsMesenchymal Stem CellsPrimary MyelofibrosisTransforming Growth Factor betaCell DifferentiationFemaleHumansMaleTumor MicroenvironmentWnt ProteinsWnt Signaling PathwayHomeodomain ProteinsTransforming Growth Factor betaWnt ProteinsBone marrowFibrosisHematology

Identifiers

PMID39470742
PMCPMC11623938

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.