Evidence map›Paper›PMID 41790379›Full record

ReviewCurrent hematologic malignancy reports2026

The Intricate Dance Between Inflammation and Myeloproliferative Neoplasms: From Origins to Outcomes.

Angela G Fleischman

Abstract readReview
In one paragraph

Review in Current hematologic malignancy reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. 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

1 author.

Angela G FleischmanDivision of Hematology/Oncology, University of California, Irvine, CA, USA. agf@uci.edu.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purpose of reviewMyeloproliferative neoplasms (MPNs) lie at the intersection of malignancy and chronic inflammatory disease. This review summarizes current understanding of how inflammation drives MPN pathogenesis, from clonal initiation to progression and symptom burden, and explores how emerging therapies modulate the inflammatory microenvironment. RECENT

findingsEvidence from human genetics, epidemiology, and experimental models shows that chronic inflammatory stress promotes the expansion of JAK2- and other MPN-associated clones. Inflammatory cytokine networks sustain myeloproliferation, reshape the bone marrow niche, and contribute to fibrosis. JAK inhibitors remain the cornerstone of therapy and exert much of their clinical benefit through suppression of cytokine signaling. Newer agents also mitigate inflammation through complementary mechanisms. Inflammation is inseparable from MPN biology and represents both a driver and a therapeutic target. Reframing MPN as a disorder of maladaptive immune and stromal interactions highlights opportunities to restore balance within this ecosystem and potentially alter disease course.

Indexed as

InflammationMyeloproliferative DisordersAnimalsCytokinesHumansJanus Kinase 2Signal TransductionTumor MicroenvironmentCytokinesJanus Kinase 2Immune dysregulationInflammationJAK/STAT signalingMyeloproliferative neoplasm

Identifiers

PMID41790379
PMCPMC12965915

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.