Evidence map›Paper›PMID 20111072›Full record

ArticleLeukemia2010

FES kinases are required for oncogenic FLT3 signaling.

E Voisset, S Lopez, A Chaix, C Georges, K Hanssens, T Prébet, P Dubreuil, P De Sepulveda

Abstract read
PubMed Publisher
In one paragraph

Article in Leukemia, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.1field-weighted citation impact, top 23% 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

17 citing papers in PubMed, 33 citations in OpenAlex.

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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

8 authors at 4 institutions in 1 country.

E VoissetINSERM, UMR 891, Centre de Recherche en Cancérologie de Marseille, Laboratoire de Signalisation, Hématopoïèse et Mécanismes de l'Oncogenèse, Marseille, France.
S Lopez
A Chaix
C Georges
K Hanssens
T Prébet
P Dubreuil
P De Sepulveda
Centre de Recherche en Cancérologie de Marseille · FRInstitut Paoli-Calmettes · FRInserm · FRInstitut de Neurobiologie de la Méditerranée · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The closely related non-receptor tyrosine kinases FEline Sarcoma (FES) and FEs Related (FER) are activated by cell surface receptors in hematopoietic cells. Despite the early description of oncogenic viral forms of fes, v-fes, and v-fps, the implication of FES and FER in human pathology is not known. We have recently shown that FES but not FER is necessary for oncogenic KIT receptor signaling. Here, we report that both FES and FER kinases are activated in primary acute myeloid leukemia (AML) blasts and in AML cell lines. FES and FER activation is dependent on FLT3 in cell lines harboring constitutively active FLT3 mutants. Moreover, both FES and FER proteins are critical for FLT3-internal tandem duplication (ITD) signaling and for cell proliferation in relevant AML cell lines. FER is required for cell cycle transitions, whereas FES seems necessary for cell survival. We concluded that FES and FER kinases mediate essential non-redundant functions downstream of FLT3-ITD.

Indexed as

Signal TransductionBlotting, WesternCell CycleCell ProliferationFluorescent Antibody Techniquefms-Like Tyrosine Kinase 3HumansImmunoenzyme TechniquesImmunoprecipitationInverted Repeat SequencesLeukemia, Myeloid, AcuteMutationPhosphorylationProtein-Tyrosine KinasesProto-Oncogene Proteins c-fesReverse Transcriptase Polymerase Chain ReactionFES protein, humanFLT3 protein, humanfms-Like Tyrosine Kinase 3Protein-Tyrosine Kinasesproto-oncogene protein c-fes-fpsProto-Oncogene Proteins c-fesRNA, MessengerRNA, Small Interfering

Identifiers

PMID20111072
OpenAlexW1992419413

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.