Evidence map›Paper›PMID 26604428›Full record

ReviewMediators of inflammation2015

MPNs as Inflammatory Diseases: The Evidence, Consequences, and Perspectives.

Hans Carl Hasselbalch, Mads Emil Bjørn

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 NCT07319026 (Myeloid-derived Suppressor Cells), which is not on this map. Cited by 133 papers.

0numbers the graph read from it
0cells of the map it votes in
133citing papers in PubMed
7.4field-weighted citation impact, top 2% 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.

NCT07319026 completednot on this mapstarted 2023, after this paper: background citation

Myeloid-derived Suppressor Cells: Characterization Of Their Role In Primary Myelofibrosis Pathogenesis For The Identification Of A New Therapeutic Target

Typeobservational_patient_registrySponsorFondazione IRCCS Policlinico San Matteo di PaviaRan2023 to 2025Enrolled70ConditionsPrimary Myelofibrosis (PMF), Healthy Subjects
3 · Its place in the literature

Who cites it

133 citing papers in PubMed, 195 citations in OpenAlex.

  1. Article
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  3. Review
  4. Acquired Hemophilia A Associated with Post-Essential Thrombocythemia Myelofibrosis: A Rare Autoimmune Bleeding ComplicationTurkish journal of haematology : official journal of Turkish Society of Haematology · 2026
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  19. bioRxiv : the preprint server for biology · 2025
    Article
  20. Article

73 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

2 authors at 1 institution in 1 country.

Hans Carl HasselbalchDepartment of Hematology, Roskilde Hospital, University of Copenhagen, Køgevej 7-13, 4000 Roskilde, Denmark.
Mads Emil BjørnDepartment of Hematology, Roskilde Hospital, University of Copenhagen, Køgevej 7-13, 4000 Roskilde, Denmark ; Institute for Inflammation Research, Department of Rheumatology, Rigshospitalet, University of Copenhagen, Blegdamsvej 9, 2100 Copenhagen, Denmark.
Roskilde Sygehus · DK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In recent years the evidence is increasing that chronic inflammation may be an important driving force for clonal evolution and disease progression in the Philadelphia-negative myeloproliferative neoplasms (MPNs), essential thrombocythemia (ET), polycythemia vera (PV), and myelofibrosis (MF). Abnormal expression and activity of a number of proinflammatory cytokines are associated with MPNs, in particular MF, in which immune dysregulation is pronounced as evidenced by dysregulation of several immune and inflammation genes. In addition, chronic inflammation has been suggested to contribute to the development of premature atherosclerosis and may drive the development of other cancers in MPNs, both nonhematologic and hematologic. The MPN population has a substantial inflammation-mediated comorbidity burden. This review describes the evidence for considering the MPNs as inflammatory diseases, A Human Inflammation Model of Cancer Development, and the role of cytokines in disease initiation and progression. The consequences of this model are discussed, including the increased risk of second cancers and other inflammation-mediated diseases, emphasizing the urgent need for rethinking our therapeutic approach. Early intervention with interferon-alpha2, which as monotherapy has been shown to be able to induce minimal residual disease, in combination with potent anti-inflammatory agents such as JAK-inhibitors is foreseen as the most promising new treatment modality in the years to come.

Indexed as

Bone Diseases, MetabolicHumansInflammationNeoplasmsPolycythemia VeraPrimary MyelofibrosisRenal Insufficiency, ChronicThrombocythemia, Essential

Identifiers

PMID26604428
PMCPMC4641200
OpenAlexW1884746267

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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.