Evidence map›Paper›PMID 31741139›Full record

ReviewInternational journal of hematology2020

Progress in elucidation of molecular pathophysiology of myeloproliferative neoplasms and its application to therapeutic decisions.

Ruochen Jia, Robert Kralovics

Abstract readReview
PubMed Publisher
In one paragraph

Review in International journal of hematology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.6field-weighted citation impact, top 16% 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.

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

14 citing papers in PubMed, 20 citations in OpenAlex.

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  14. The Role of Megakaryocytes in Myelofibrosis.Hematology/oncology clinics of North America · 2021
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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

2 authors at 2 institutions in 1 country.

Ruochen JiaDepartment of Laboratory Medicine, Medical University of Vienna, 18-20 Währinger Gürtel, 1090, Vienna, Austria.
Robert KralovicsDepartment of Laboratory Medicine, Medical University of Vienna, 18-20 Währinger Gürtel, 1090, Vienna, Austria. robert.kralovics@meduniwien.ac.at.ORCID http://orcid.org/0000-0002-6997-8539
Austrian Academy of Sciences · ATCeMM Research Center for Molecular Medicine · AT

Funding

Austrian Science Fund FWF P 29018
6 · The paper itself

Abstract

Myeloproliferative neoplasms (MPNs) are hematological diseases that are driven by somatic mutations in hematopoietic stem and progenitor cells. These mutations include JAK2, CALR and MPL mutations as the main disease drivers, mutations driving clonal expansion, and mutations that contribute to progression of chronic MPNs to myelodysplasia and acute leukemia. JAK-STAT pathway has played a central role in the disease pathogenesis of MPNs. Mutant JAK2, CALR or MPL constitutively activates JAK-STAT pathway independent of the cytokine regulation. Symptomatic management is the primary goal of MPN therapy in ET and low-risk PV patients. JAK2 inhibitors and interferon-α are the established therapies in MF and high-risk PV patients.

Indexed as

Decision MakingCalreticulinEnzyme InhibitorsHumansInterferon-alphaJanus Kinase 2MutationMyeloproliferative DisordersReceptors, ThrombopoietinCalreticulinCALR protein, humanEnzyme InhibitorsInterferon-alphaJAK2 protein, humanJanus Kinase 2MPL protein, humanReceptors, ThrombopoietinCalreticulinHematological malignancyJanus kinaseMyeloproliferative neoplasmsThrombopoietin receptor

Identifiers

PMID31741139
OpenAlexW2988301005

What OpenQuestion 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 OpenQuestion graph.