Evidence map›Paper›PMID 31865539›Full record

ReviewInternational journal of hematology2020

The role of driver mutations in myeloproliferative neoplasms: insights from mouse models.

Kotaro Shide

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 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
2.1field-weighted citation impact, top 12% 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

4 citing papers in PubMed, 18 citations in OpenAlex.

  1. Effects of calreticulin mutations on cell transformation and immunity.Journal of cellular and molecular medicine · 2023
    Review
  2. Article
  3. Crucial role of hematopoieticHaematologica · 2021
    Article
  4. 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 at 1 institution in 1 country.

Kotaro ShideDepartment of Gastroenterology and Hematology, Faculty of Medicine, University of Miyazaki, 5200 Kihara, Kiyotake, Miyazaki, 889-1692, Japan. koutaro_shide@med.miyazaki-u.ac.jp.ORCID http://orcid.org/0000-0002-0046-3254
University of Miyazaki · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

High frequency of JAK2V617F or CALR exon 9 mutations is a main molecular feature of myeloproliferative neoplasms (MPNs). Analysis of mouse models driven by these mutations suggests that they are a direct cause of MPNs and that the expression levels of the mutated genes define the disease phenotype. The function of MPN-initiating cells has also been elucidated by these mouse models. Such mouse models also play an important role in modeling disease to investigate the effects and action mechanisms of therapeutic drugs, such as JAK2 inhibitors and interferon α, against MPNs. The mutation landscape of hematological tumors has already been clarified by next-generation sequencing technology, and the importance of functional analysis of mutant genes in vivo should increase further in the future.

Indexed as

AnimalsCalreticulinDisease Models, AnimalGene ExpressionJanus Kinase 2MiceMutationMyeloproliferative DisordersCalreticulinCALR protein, humanJAK2 protein, humanJanus Kinase 2CALRJAK2Mouse modelsMyeloproliferative neoplasms

Identifiers

PMID31865539
OpenAlexW2995766639

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.