Evidence map›Paper›PMID 28386106›Full record

ArticleLeukemia2017

Myeloproliferative leukemia protein activation directly induces fibrocyte differentiation to cause myelofibrosis.

T Maekawa, Y Osawa, T Izumi, S Nagao, K Takano, Y Okada, N Tachi, M Teramoto, T Kawamura, T Horiuchi and 10 more

Erratum issuedAbstract read
PubMed Publisher
In one paragraph

Article in Leukemia, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.5field-weighted citation impact, top 17% 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

19 citing papers in PubMed, 23 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Investigational drugs in early phase trials for myelofibrosis.Expert opinion on investigational drugs · 2024
    Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Immunoproteasome Genes Are Modulated in CD34International journal of molecular sciences · 2020
    Article
  16. Review
  17. New Concepts of Treatment for Patients with Myelofibrosis.Current treatment options in oncology · 2019
    Review
  18. Article
  19. Management of Myelofibrosis-Related Cytopenias.Current hematologic malignancy reports · 2018
    Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

20 authors at 2 institutions in 1 country.

T MaekawaDivision of Hematology, Department of Internal Medicine, National Defense Medical College, Tokorozawa, Japan.
Y OsawaDivision of Hematology, Department of Internal Medicine, National Defense Medical College, Tokorozawa, Japan.
T IzumiDivision of Hematology, Department of Internal Medicine, National Defense Medical College, Tokorozawa, Japan.
S NagaoDivision of Hematology, Department of Internal Medicine, National Defense Medical College, Tokorozawa, Japan.
K TakanoDivision of Hematology, Department of Internal Medicine, National Defense Medical College, Tokorozawa, Japan.
Y OkadaDivision of Hematology, Department of Internal Medicine, National Defense Medical College, Tokorozawa, Japan.
N TachiDivision of Hematology, Department of Internal Medicine, National Defense Medical College, Tokorozawa, Japan.
M TeramotoDivision of Hematology, Department of Internal Medicine, National Defense Medical College, Tokorozawa, Japan.
T KawamuraDivision of Hematology, Department of Internal Medicine, National Defense Medical College, Tokorozawa, Japan.
T HoriuchiDivision of Hematology, Department of Internal Medicine, National Defense Medical College, Tokorozawa, Japan.
R SagaDivision of Hematology, Department of Internal Medicine, National Defense Medical College, Tokorozawa, Japan.
S KatoDivision of Hematology, Department of Internal Medicine, National Defense Medical College, Tokorozawa, Japan.
T YamamuraDivision of Hematology, Department of Internal Medicine, National Defense Medical College, Tokorozawa, Japan.
J WatanabeDivision of Hematology, Department of Internal Medicine, National Defense Medical College, Tokorozawa, Japan.
A KobayashiDivision of Hematology, Department of Internal Medicine, National Defense Medical College, Tokorozawa, Japan.
S KobayashiDivision of Hematology, Department of Internal Medicine, National Defense Medical College, Tokorozawa, Japan.
K SatoDivision of Hematology, Department of Internal Medicine, National Defense Medical College, Tokorozawa, Japan.
M HashimotoSuzu Project Laboratory, Center for AIDS Research, Kumamoto University, Kumamoto, Japan.
S SuzuSuzu Project Laboratory, Center for AIDS Research, Kumamoto University, Kumamoto, Japan.
F KimuraDivision of Hematology, Department of Internal Medicine, National Defense Medical College, Tokorozawa, Japan.
National Defense Medical College · JPKumamoto University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Myelofibrosis (MF) may be caused by various pathogenic mechanisms such as elevation in circulating cytokine levels, cellular interactions and genetic mutations. However, the underlying mechanism of MF still remains unknown. Recent studies have revealed that fibrocytes, the spindle-shaped fibroblast-like hematopoietic cells, and the thrombopoietin (TPO)/myeloproliferative leukemia protein (MPL; TPO receptor) signaling pathway play a certain role in the development of MF. In the present study, we aimed to investigate the relationship between fibrocytes and MPL activation. We showed that TPO or a TPO receptor agonist directly induces fibrocyte differentiation using murine fibrocyte cell lines and a murine MF model. Conversely, elimination of macrophages expressing MPL by clodronate liposomes reversed the MF phenotype of the murine model, suggesting that fibrocyte differentiation induced by MPL activation contributes to the progression of MF. Furthermore, we revealed that SLAMF7

Indexed as

AnimalsBone MarrowCell DifferentiationCell LineClodronic AcidFibroblastsHematopoietic Stem CellsHumansImmunohistochemistryJanus Kinase 2MacrophagesMiceMonocytesPhenotypePrimary MyelofibrosisReceptors, ThrombopoietinClodronic AcidJanus Kinase 2MPL protein, humanReceptors, ThrombopoietinSTAT Transcription FactorsThrombopoietin

Identifiers

PMID28386106
OpenAlexW2605217861

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.