Evidence map›Paper›PMID 25515960›Full record

ArticleBlood2015

The role of the Janus-faced transcription factor PAX5-JAK2 in acute lymphoblastic leukemia.

Dagmar Schinnerl, Klaus Fortschegger, Maximilian Kauer, João R M Marchante, Reinhard Kofler, Monique L Den Boer, Sabine Strehl

Open access · bronzeAbstract read
In one paragraph

Article in Blood, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
3.6field-weighted citation impact, top 7% 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

39 citing papers in PubMed, 56 citations in OpenAlex.

  1. Trial
  2. Trial
  3. Epigenetic, Genetic, and Functional Germline Alterations ofCurrent issues in molecular biology · 2026
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  6. PAX Family, Master Regulator in Cancer.Diagnostics (Basel, Switzerland) · 2025
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  7. Review
  8. Article
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  10. Mycovirus-ContainingInternational journal of molecular sciences · 2024
    Article
  11. Review
  12. Cancers · 2024
    Article
  13. Article
  14. Review
  15. Article
  16. Frontiers in oncology · 2022
    Review
  17. Frontiers in cell and developmental biology · 2022
    Review
  18. Article
  19. Article
  20. 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

7 authors at 4 institutions in 2 countries.

Dagmar SchinnerlCCRI, Children's Cancer Research Institute, St. Anna Kinderkrebsforschung e.V., Vienna, Austria;
Klaus FortscheggerCCRI, Children's Cancer Research Institute, St. Anna Kinderkrebsforschung e.V., Vienna, Austria;
Maximilian KauerCCRI, Children's Cancer Research Institute, St. Anna Kinderkrebsforschung e.V., Vienna, Austria;
João R M MarchanteDepartment of Pediatric Oncology and Hematology, Erasmus MC/Sophia Children's Hospital, University Medical Center Rotterdam, Rotterdam, The Netherlands; and.
Reinhard KoflerDivision of Molecular Pathophysiology, Tyrolean Cancer Research Institute and Biocenter, Innsbruck Medical University, Innsbruck, Austria.
Monique L Den BoerDepartment of Pediatric Oncology and Hematology, Erasmus MC/Sophia Children's Hospital, University Medical Center Rotterdam, Rotterdam, The Netherlands; and.
Sabine StrehlCCRI, Children's Cancer Research Institute, St. Anna Kinderkrebsforschung e.V., Vienna, Austria;
St. Anna Children's Cancer Research InstituteErasmus MC - Sophia Children’s Hospital · NLSt Anna Children's Hospital · ATTyrolean Cancer Research Institute · AT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

PAX5-JAK2 has recently been identified as a novel recurrent fusion gene in B-cell precursor acute lymphoblastic leukemia, but the function of the encoded chimeric protein has not yet been characterized in detail. Herein we show that the PAX5-JAK2 chimera, which consists of the DNA-binding paired domain of PAX5 and the active kinase domain of JAK2, is a nuclear protein that has the ability to bind to wild-type PAX5 target loci. Moreover, our data provide compelling evidence that PAX5-JAK2 functions as a nuclear catalytically active kinase that autophosphorylates and in turn phosphorylates and activates downstream signal transducers and activators of transcription (STATs) in an apparently noncanonical mode. The chimeric protein also enables cytokine-independent growth of Ba/F3 cells and therefore possesses transforming potential. Importantly, the kinase activity of PAX5-JAK2 can be efficiently blocked by JAK2 inhibitors, rendering it a potential target for therapeutic intervention. Together, our data show that PAX5-JAK2 simultaneously deregulates the PAX5 downstream transcriptional program and activates the Janus kinase-STAT signaling cascade and thus, by interfering with these two important pathways, may promote leukemogenesis.

Indexed as

Cell DeathCell Transformation, NeoplasticGene Expression Regulation, LeukemicHEK293 CellsHeLa CellsHumansJanus Kinase 2Oncogene Proteins, FusionPAX5 Transcription FactorPhosphorylationPrecursor Cell Lymphoblastic Leukemia-LymphomaProtein Kinase InhibitorsSTAT Transcription FactorsTranscriptomeTumor Cells, CulturedJAK2 protein, humanJanus Kinase 2Oncogene Proteins, FusionPAX5 protein, humanPAX5 Transcription FactorProtein Kinase InhibitorsSTAT Transcription Factors

Identifiers

PMID25515960
PMCPMC4375719
OpenAlexW2041003921

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.