Evidence map›Paper›PMID 29062038›Full record

ArticleScientific reports2017

The Src family kinase LCK cooperates with oncogenic FLT3/ITD in cellular transformation.

Alissa Marhäll, Julhash U Kazi, Lars Rönnstrand

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. 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
1.3field-weighted citation impact, top 22% 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, 24 citations in OpenAlex.

  1. Review
  2. A Novel Peptide that Disrupts the Lck-IPArchives of microbiology & immunology · 2023
    Article
  3. Article
  4. Article
  5. Review
  6. T cell receptor (TCR) signaling in health and disease.Signal transduction and targeted therapy · 2021
    Review
  7. Review
  8. Article
  9. Article
  10. Article
  11. Beyond TCR Signaling: Emerging Functions of Lck in Cancer and Immunotherapy.International journal of molecular sciences · 2019
    Review
  12. Targeting Tyrosine Kinases in Acute Myeloid Leukemia: Why, Who and How?International journal of molecular sciences · 2019
    Review
  13. Article
  14. 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

3 authors at 1 institution in 1 country.

Alissa MarhällDivision of Translational Cancer Research, Department of Laboratory Medicine, Lund University, Medicon Village, Lund, Sweden.
Julhash U KaziDivision of Translational Cancer Research, Department of Laboratory Medicine, Lund University, Medicon Village, Lund, Sweden.ORCID 0000-0002-0719-5336
Lars RönnstrandDivision of Translational Cancer Research, Department of Laboratory Medicine, Lund University, Medicon Village, Lund, Sweden. lars.ronnstrand@med.lu.se.ORCID 0000-0003-1275-5809
Lund University · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The non-receptor tyrosine kinase LCK belongs to the SRC family of kinases. SRC family kinases are proto-oncogenes that have long been known to play key roles in cell proliferation, motility, morphology and survival. Here we show that LCK regulates the function of the type III receptor tyrosine kinase FLT3 in murine pro-B cells. We observed that expression of LCK significantly enhances the colony forming capacity of the constitutively active FLT3 mutant FLT3-ITD (internal tandem duplication). Furthermore, cells expressing LCK developed tumor earlier compared to cells transfected with empty control vector. Staining of the tissues from mouse xenografts showed higher Ki67 staining in cells expressing LCK suggesting that expression of LCK enhances the FLT3-ITD-mediated proliferative capacity. LCK expression did not affect either FLT3-WT or FLT3-ITD -induced AKT, ERK1/2 or p38 phosphorylation. However, LCK expression significantly enhanced FLT3-ITD-mediated STAT5 phosphorylation. Taken together, our data suggest that LCK cooperates with oncogenic FLT3-ITD in cellular transformation.

Indexed as

Cell Transformation, NeoplasticAnimalsCell Line, TumorCell SurvivalFemalefms-Like Tyrosine Kinase 3Gene Expression Regulation, NeoplasticLymphocyte Specific Protein Tyrosine Kinase p56(lck)MicePhosphorylationSignal TransductionSTAT5 Transcription FactorTandem Repeat SequencesFlt3 protein, mousefms-Like Tyrosine Kinase 3Lymphocyte Specific Protein Tyrosine Kinase p56(lck)STAT5 Transcription Factor

Identifiers

PMID29062038
PMCPMC5653865
OpenAlexW2766768871

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.