Evidence mapPaperPMID 41537939Full record

ReviewCurrent hematologic malignancy reports2026

Understanding Triple Negative Myeloproliferative Neoplasms and Identifying Molecular Drivers.

Valentina Boldrini, Giuseppe G Loscocco, Paola Guglielmelli, Naseema Gangat, Alessandro M Vannucchi, Ayalew Tefferi

Abstract readReview
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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. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

6 authors.

Valentina BoldriniDepartment of Experimental and Clinical Medicine, Center for Research and Innovation of Myeloproliferative Neoplasms, Azienda Ospedaliera Universitaria Careggi, CRIMM, University of Florence, Florence, Italy.
Giuseppe G LoscoccoDepartment of Experimental and Clinical Medicine, Center for Research and Innovation of Myeloproliferative Neoplasms, Azienda Ospedaliera Universitaria Careggi, CRIMM, University of Florence, Florence, Italy. gloscocco@unifi.it.ORCID http://orcid.org/0000-0002-6241-1206
Paola GuglielmelliDepartment of Experimental and Clinical Medicine, Center for Research and Innovation of Myeloproliferative Neoplasms, Azienda Ospedaliera Universitaria Careggi, CRIMM, University of Florence, Florence, Italy.
Naseema GangatDivision of Hematology, Mayo Clinic, Rochester, MN, USA.
Alessandro M VannucchiDepartment of Experimental and Clinical Medicine, Center for Research and Innovation of Myeloproliferative Neoplasms, Azienda Ospedaliera Universitaria Careggi, CRIMM, University of Florence, Florence, Italy.
Ayalew TefferiDivision of Hematology, Mayo Clinic, Rochester, MN, USA.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purpose of reviewTriple-negative (TN) myeloproliferative neoplasms (MPNs), defined by the absence of canonical driver JAK2, CALR and MPL mutations, represent a heterogeneous and still poorly understood subgroup of chronic myeloid neoplasms. This review summarizes current knowledge on characteristics and molecular landscape of TN MPNs. RECENT

findingsAlthough TN MPNs share clinical and morphological features with classic forms of primary myelofibrosis and essential thrombocythemia, their clinical behavior varies widely, from indolent in TN essential thrombocythemia to aggressive in TN myelofibrosis. Recent next-generation sequencing analyses have identified mutations affecting epigenetic regulation, RNA splicing, and various signaling pathways (e.g., TET2, ASXL1, SRSF2, EZH2, SETBP1), thereby underscoring the substantial biological complexity within these subgroups. This review provides an updated overview of the molecular landscape, clinicopathological features, and prognostic implications of TN MPNs, with a focus on the molecular mechanisms that have been uncovered through recent advances in diagnostic and genomic profiling techniques. Understanding the underlying disease mechanisms may lead to personalized treatments and better risk assessment for these patients.

Indexed as

Myeloproliferative DisordersCalreticulinEpigenesis, GeneticHumansJanus Kinase 2MutationPrognosisReceptors, ThrombopoietinSignal TransductionCalreticulinJAK2 protein, humanJanus Kinase 2Receptors, Thrombopoietin

Identifiers

PMID41537939

What Socratic 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 Socratic graph.