Evidence map›Paper›PMID 26538820›Full record

ReviewMediators of inflammation2015

Pathogenesis of Myeloproliferative Neoplasms: Role and Mechanisms of Chronic Inflammation.

Sylvie Hermouet, Edith Bigot-Corbel, Betty Gardie

Registry-linked trialOpen access · goldAbstract readReview
In one paragraph

Review in Mediators of inflammation, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT05923372 (Evaluation of the Disability-Adjusted Life Year), which is not on this map. Cited by 71 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
71citing papers in PubMed, 1 pooled it
4.5field-weighted citation impact, top 5% 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.

NCT05923372 unknown statusnot on this mapstarted 2023, after this paper: background citation

Evaluation of the Disability-Adjusted Life Year (DALY) on a Cohort of Patients With Indolent Systemic Mastocytosis (ISM)

TypeobservationalSponsorUniversity Hospital, ToulouseRan2023 to 2024Enrolled160ConditionsMastocytosis, Indolent Systemic
3 · Its place in the literature

Who cites it

71 citing papers in PubMed, 1 synthesis or guideline pooled it, 108 citations in OpenAlex.

  1. Pooled it
  2. Mechanisms of damage and therapies for cardiac amyloidosis: a role for inflammation?Clinical research in cardiology : official journal of the German Cardiac Society · 2026
    Review
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  9. Association of High-Altitude Polycythemia with JAK2V617F Mutation in Pakistani Population.Indian journal of hematology & blood transfusion : an official journal of Indian Society of Hematology and Blood Transfusion · 2025
    Article
  10. Review
  11. Article
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11 more citing papers are in PubMed but not listed here.

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

3 authors at 1 institution in 1 country.

Sylvie HermouetInserm UMR 892, CNRS UMR 6299, Centre de Recherche en Cancérologie Nantes-Angers, Institut de Recherche en Santé, Université de Nantes, 44007 Nantes, France ; Laboratoire d'Hématologie, Centre Hospitalier Universitaire de Nantes, 44093 Nantes Cedex, France.
Edith Bigot-CorbelInserm UMR 892, CNRS UMR 6299, Centre de Recherche en Cancérologie Nantes-Angers, Institut de Recherche en Santé, Université de Nantes, 44007 Nantes, France ; Laboratoire de Biochimie, Centre Hospitalier Universitaire de Nantes, 44093 Nantes Cedex, France.
Betty GardieInserm UMR 892, CNRS UMR 6299, Centre de Recherche en Cancérologie Nantes-Angers, Institut de Recherche en Santé, Université de Nantes, 44007 Nantes, France ; Ecole Pratique des Hautes Etudes, Laboratoire de Génétique Oncologique, 44007 Nantes, France.
Centre National de la Recherche Scientifique · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Myeloproliferative neoplasms (MPNs) are a heterogeneous group of clonal diseases characterized by the excessive and chronic production of mature cells from one or several of the myeloid lineages. Recent advances in the biology of MPNs have greatly facilitated their molecular diagnosis since most patients present with mutation(s) in the JAK2, MPL, or CALR genes. Yet the roles played by these mutations in the pathogenesis and main complications of the different subtypes of MPNs are not fully elucidated. Importantly, chronic inflammation has long been associated with MPN disease and some of the symptoms and complications can be linked to inflammation. Moreover, the JAK inhibitor clinical trials showed that the reduction of symptoms linked to inflammation was beneficial to patients even in the absence of significant decrease in the JAK2-V617F mutant load. These observations suggested that part of the inflammation observed in patients with JAK2-mutated MPNs may not be the consequence of JAK2 mutation. The aim of this paper is to review the different aspects of inflammation in MPNs, the molecular mechanisms involved, the role of specific genetic defects, and the evidence that increased production of certain cytokines depends or not on MPN-associated mutations, and to discuss possible nongenetic causes of inflammation.

Indexed as

CalreticulinCytokinesGenetic Predisposition to DiseaseHumansHypereosinophilic SyndromeInflammationJanus Kinase 2LeukemiaLeukemia, Myelogenous, Chronic, BCR-ABL PositiveMastocytosisMutationMyeloproliferative DisordersNeoplasmsPhenotypePolycythemia VeraPrimary MyelofibrosisCalreticulinCALR protein, humanCytokinesJAK2 protein, humanJanus Kinase 2MPL protein, humanReceptors, Thrombopoietin

Identifiers

PMID26538820
PMCPMC4619950
OpenAlexW2165040076

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Registered trials

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.