Evidence map›Paper›PMID 33592069›Full record

ArticlePloS one2021

Gene expression profiling identifies FLT3 mutation-like cases in wild-type FLT3 acute myeloid leukemia.

Adrián Mosquera Orgueira, Andrés Peleteiro Raíndo, Miguel Cid López, Beatriz Antelo Rodríguez, José Ángel Díaz Arias, Roi Ferreiro Ferro, Natalia Alonso Vence, Ángeles Bendaña López, Aitor Abuín Blanco, Laura Bao Pérez and 7 more

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in PloS one, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.3field-weighted citation impact, top 20% 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

13 citing papers in PubMed, 15 citations in OpenAlex.

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  7. Leukemia research reports · 2025
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

17 authors at 6 institutions in 2 countries.

Adrián Mosquera OrgueiraHealth Research Institute of Santiago de Compostela (IDIS), Santiago, Spain.ORCID 0000-0003-4838-6750
Andrés Peleteiro RaíndoHealth Research Institute of Santiago de Compostela (IDIS), Santiago, Spain.
Miguel Cid LópezHealth Research Institute of Santiago de Compostela (IDIS), Santiago, Spain.ORCID 0000-0002-7074-2363
Beatriz Antelo RodríguezHealth Research Institute of Santiago de Compostela (IDIS), Santiago, Spain.
José Ángel Díaz AriasHealth Research Institute of Santiago de Compostela (IDIS), Santiago, Spain.
Roi Ferreiro FerroHealth Research Institute of Santiago de Compostela (IDIS), Santiago, Spain.
Natalia Alonso VenceHealth Research Institute of Santiago de Compostela (IDIS), Santiago, Spain.
Ángeles Bendaña LópezHealth Research Institute of Santiago de Compostela (IDIS), Santiago, Spain.
Aitor Abuín BlancoHealth Research Institute of Santiago de Compostela (IDIS), Santiago, Spain.
Laura Bao PérezHealth Research Institute of Santiago de Compostela (IDIS), Santiago, Spain.
Paula Melero ValentínHealth Research Institute of Santiago de Compostela (IDIS), Santiago, Spain.
Marta Sonia González PérezHealth Research Institute of Santiago de Compostela (IDIS), Santiago, Spain.
Claudio CerchioneUniversity of Bologna, Bologna, Italy.
Giovanni MartinelliIstituto Scientifico Romagnolo per lo Studio e la Cura dei Tumori, Meldola, Italy.
Pau Montesinos FernándezUniversity Hospital of La Fe in Valencia, Valencia, Spain.
Manuel Mateo Pérez EncinasHealth Research Institute of Santiago de Compostela (IDIS), Santiago, Spain.
José Luis Bello LópezHealth Research Institute of Santiago de Compostela (IDIS), Santiago, Spain.
Complejo Hospitalario Universitario de Santiago · ESUniversidade de Santiago de Compostela · ESHospital Universitari i Politècnic La Fe · ESInstituto de Investigación Sanitaria de Santiago · ESIstituto Scientifico Romagnolo per lo Studio e la Cura dei Tumori · ITUniversity of Bologna · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundFLT3 mutation is present in 25-30% of all acute myeloid leukemias (AML), and it is associated with adverse outcome. FLT3 inhibitors have shown improved survival results in AML both as upfront treatment and in relapsed/refractory disease. Curiously, a variable proportion of wild-type FLT3 patients also responded to these drugs.

methodsWe analyzed 6 different transcriptomic datasets of AML cases. Differential expression between mutated and wild-type FLT3 AMLs was performed with the Wilcoxon-rank sum test. Hierarchical clustering was used to identify FLT3-mutation like AMLs. Finally, enrichment in recurrent mutations was performed with the Fisher's test.

resultsA FLT3 mutation-like gene expression pattern was identified among wild-type FLT3 AMLs. This pattern was highly enriched in NPM1 and DNMT3A mutants, and particularly in combined NPM1/DNMT3A mutants.

conclusionsWe identified a FLT3 mutation-like gene expression pattern in AML which was highly enriched in NPM1 and DNMT3A mutations. Future analysis about the predictive role of this biomarker among wild-type FLT3 patients treated with FLT3 inhibitors is envisaged.

Indexed as

BiomarkersDNA (Cytosine-5-)-MethyltransferasesDNA Methyltransferase 3Afms-Like Tyrosine Kinase 3Gene Expression ProfilingHumansLeukemiaLeukemia, Myeloid, AcuteMutationNuclear ProteinsNucleophosminStaurosporineBiomarkersDNA (Cytosine-5-)-MethyltransferasesDNA Methyltransferase 3ADNMT3A protein, humanFLT3 protein, humanfms-Like Tyrosine Kinase 3midostaurinNPM1 protein, humanNuclear ProteinsNucleophosminStaurosporine

Identifiers

PMID33592069
PMCPMC7886212
OpenAlexW3130161455

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Registered trials

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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.