Evidence map›Paper›PMID 39633552›Full record

ReviewHaematologica2025

Pathogenesis and management of high molecular risk myeloproliferative neoplasms.

Victoria Y Ling, Florian H Heidel, Megan J Bywater

Abstract readReview
In one paragraph

Review in Haematologica, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed, 1 pooled it
–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

17 citing papers in PubMed, 1 synthesis or guideline pooled it.

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  15. The deacetylases HDAC1/HDAC2 control JAK2Signal transduction and targeted therapy · 2025
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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.

Victoria Y LingQIMR Berghofer Medical Research Institute, Brisbane, Queensland, Australia; Department of Haematology, Princess Alexandra Hospital, Brisbane, Queensland, Australia; Pathology Queensland, Brisbane, Queensland, Australia; The University of Queensland, Brisbane, QLD.
Florian H HeidelHematology, Hemostasis, Oncology and Stem Cell Transplantation, Hannover Medical School (MHH), Hannover, Germany; Leibniz Institute on Aging, Jena, Germany; Cellular Therapy Center (CTC), Hannover Medical School (MHH), Hannover.
Megan J BywaterQIMR Berghofer Medical Research Institute, Brisbane, Queensland, Australia; The University of Queensland, Brisbane, QLD.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Classical myeloproliferative neoplasms (MPN) are clonal stem cell disorders characterized by driver mutations that affect the constitutive activation of JAK-signaling. Mutations additional to an MPN-driver occur in a large number of patients and have been shown be associated with disease presentation and progression. In this review, we outline the current hypotheses regarding how clonal evolution in MPN is thought to occur and the functional mechanisms as to how concomitant somatic mutations (i.e., mutations in genes other than the 'driver' genes) contribute to disease progression. We discuss the definitions of high molecular risk MPN, provide an overview of how concomitant mutations influence the clinical management of MPN and suggest how the rapidly developing genetic risk stratification can be utilized to improve clinical outcomes.

Indexed as

MutationMyeloproliferative DisordersClonal EvolutionDisease ManagementGenetic Predisposition to DiseaseHumansSignal Transduction

Identifiers

PMID39633552
PMCPMC11959265

What OpenQuestion holds

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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.