Evidence map›Paper›PMID 30859397›Full record

Trial reportInternational journal of hematology2019

STAT3 mutations in natural killer cells are associated with cytopenia in patients with chronic lymphoproliferative disorder of natural killer cells.

Toru Kawakami, Nodoka Sekiguchi, Jun Kobayashi, Taku Yamane, Sayaka Nishina, Hitoshi Sakai, Yukio Hirabayashi, Hideyuki Nakazawa, Fumihiro Ishida

Abstract readClinical TrialMulticenter Study
PubMed Publisher
In one paragraph

Trial report in International journal of hematology, 2019. 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
1.5field-weighted citation impact, top 18% 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, 25 citations in OpenAlex.

  1. Article
  2. Article
  3. Haematologica · 2024
    Article
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  6. Article
  7. Review
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  13. Review
  14. T-cell large granular lymphocytic (LGL) leukemia consists of CD4Journal of clinical and experimental hematopathology : JCEH · 2019
    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

9 authors at 2 institutions in 1 country.

Toru KawakamiDivision of Hematology, Department of Internal Medicine, Shinshu University School of Medicine, Matsumoto, Japan.
Nodoka SekiguchiDivision of Hematology, Department of Internal Medicine, Shinshu University School of Medicine, Matsumoto, Japan.
Jun KobayashiDepartment of Health and Medical Sciences, Graduate School of Medicine, Shinshu University, Matsumoto, Japan.
Taku YamaneDepartment of Biomedical Laboratory Sciences, Shinshu University School of Medicine, Matsumoto, Japan.
Sayaka NishinaDivision of Hematology, Department of Internal Medicine, Shinshu University School of Medicine, Matsumoto, Japan.
Hitoshi SakaiDivision of Hematology, Department of Internal Medicine, Shinshu University School of Medicine, Matsumoto, Japan.
Yukio HirabayashiDivision of Hematology, Matsumoto Medical Center Masumoto Hospital, Matsumoto, Japan.
Hideyuki NakazawaDivision of Hematology, Department of Internal Medicine, Shinshu University School of Medicine, Matsumoto, Japan.
Fumihiro IshidaDivision of Hematology, Department of Internal Medicine, Shinshu University School of Medicine, Matsumoto, Japan. fumishi@shinshu-u.ac.jp.
Shinshu University · JPMatsumoto City Hospital · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chronic lymphoproliferative disorder of natural killer (NK) cells (CLPD-NK) is a rare disease with an indolent clinical course, which is characterized by persistent increase in large granular lymphocytes of NK-cell type. A somatic mutation in signal transducer and activator transcription 3 (STAT3) has been reported in patients with CLPD-NK; however, the details of the mutational profiles and their clinical significance remain unclear. We performed mutation analyses of the STAT3, STAT5B, and TNF-alpha-induced protein 3 (TNFAIP3) genes for mononuclear cell-derived DNA in 17 CLPD-NK patients using allele-specific polymerase chain reaction and amplicon sequencing. Mutations in STAT3 and TNFAIP3 were found in 29% (5/17) and 6% (1/17) of cases, respectively. All patients were negative for STAT5B mutations. In all three STAT3-mutation (+) patients studied, STAT3 mutations were restricted to sorted NK cells. STAT3 mutation (+) patients had a lower hemoglobin level (6.6 g/dL vs. 13.9 g/dL, P = 0.0044) and showed a trend toward reduced neutrophil counts (1.22 × 10

Indexed as

Killer Cells, NaturalAgedAged, 80 and overAnemiaChronic DiseaseFemaleHumansLymphoproliferative DisordersMaleMiddle AgedNeutropeniaSTAT3 Transcription FactorSTAT3 protein, humanSTAT3 Transcription FactorCLPD-NKCytopeniaSTAT3TNFAIP3

Identifiers

PMID30859397
OpenAlexW2921340109

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.