Evidence map›Paper›PMID 28819278›Full record

ArticleLeukemia2018

Interleukin 4 induces apoptosis of acute myeloid leukemia cells in a Stat6-dependent manner.

P Peña-Martínez, M Eriksson, R Ramakrishnan, M Chapellier, C Högberg, C Orsmark-Pietras, J Richter, A Andersson, T Fioretos, M Järås

Open access · hybridAbstract read
In one paragraph

Article in Leukemia, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed, 1 pooled it
2.0field-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

35 citing papers in PubMed, 1 synthesis or guideline pooled it, 50 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. H2-K1 protects murineHaematologica · 2025
    Article
  8. Article
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  14. Article
  15. Article
  16. International journal of molecular sciences · 2023
    Article
  17. Article
  18. Article
  19. Review
  20. Interleukin-4 treatment reduces leukemia burden in acute myeloid leukemia.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2022
    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

10 authors at 1 institution in 1 country.

P Peña-MartínezDepartment of Clinical Genetics, Lund University, Lund, Sweden.
M ErikssonDepartment of Clinical Genetics, Lund University, Lund, Sweden.
R RamakrishnanDepartment of Clinical Genetics, Lund University, Lund, Sweden.
M ChapellierDepartment of Clinical Genetics, Lund University, Lund, Sweden.
C HögbergDepartment of Clinical Genetics, Lund University, Lund, Sweden.
C Orsmark-PietrasDepartment of Clinical Genetics, Lund University, Lund, Sweden.
J RichterDepartment of Molecular Medicine and Gene Therapy, Lund University, Lund, Sweden.
A AnderssonDepartment of Clinical Genetics, Lund University, Lund, Sweden.ORCID 0000-0002-2904-1311
T FioretosDepartment of Clinical Genetics, Lund University, Lund, Sweden.
M JäråsDepartment of Clinical Genetics, Lund University, Lund, Sweden.
Lund University · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cytokines provide signals that regulate immature normal and acute myeloid leukemia (AML) cells in the bone marrow microenvironment. We here identify interleukin 4 (IL4) as a selective inhibitor of AML cell growth and survival in a cytokine screen using fluorescently labeled AML cells. RNA-sequencing of the AML cells revealed an IL4-induced upregulation of Stat6 target genes and enrichment of apoptosis-related gene expression signatures. Consistent with these findings, we found that IL4 stimulation of AML cells induced Stat6 phosphorylation and that disruption of Stat6 using CRISPR/Cas9-genetic engineering rendered cells partially resistant to IL4-induced apoptosis. To evaluate whether IL4 inhibits AML cells in vivo, we expressed IL4 ectopically in AML cells transplanted into mice and also injected IL4 into leukemic mice; both strategies resulted in the suppression of the leukemia cell burden and increased survival. Notably, IL4 exposure caused reduced growth and survival of primary AML CD34

Indexed as

ApoptosisAnimalsBiomarkersCell Line, TumorCytokinesFlow CytometryGene ExpressionHematopoietic Stem CellsHumansInterleukin-4Leukemia, Myeloid, AcuteMiceSTAT6 Transcription FactorTumor Suppressor Protein p53BiomarkersCytokinesIL4 protein, humanInterleukin-4STAT6 protein, humanSTAT6 Transcription FactorTumor Suppressor Protein p53

Identifiers

PMID28819278
PMCPMC5843897
OpenAlexW2746022227

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.