Evidence map›Paper›PMID 26284582›Full record

ArticleOncotarget2016

Oncogene- and drug resistance-associated alternative exon usage in acute myeloid leukemia (AML).

Aminetou Mint Mohamed, Marie Balsat, Morgan Thenoz, Catherine Koering, Lea Payen-Gay, Meyling Cheok, Hussein Mortada, Didier Auboeuf, Christiane Pinatel, Mohamed El-Hamri and 13 more

Abstract read
In one paragraph

Article in Oncotarget, 2016. 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
–field-weighted citation impact
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.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Review
  9. Review
  10. Review
  11. Article
  12. Review
  13. Aberrant splicing and drug resistance in AML.Journal of hematology & oncology · 2016
    Review
  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

23 authors.

Aminetou Mint MohamedUniversité Lyon 1, CNRS UMR5239, Oncovirologie et Biothérapies, Faculté de Médecine Lyon Sud, ENS - HCL, Pierre Bénite, France.
Marie BalsatUniversité Lyon 1, CNRS UMR5239, Oncovirologie et Biothérapies, Faculté de Médecine Lyon Sud, ENS - HCL, Pierre Bénite, France.
Morgan ThenozUniversité Lyon 1, CNRS UMR5239, Oncovirologie et Biothérapies, Faculté de Médecine Lyon Sud, ENS - HCL, Pierre Bénite, France.
Catherine KoeringUniversité Lyon 1, CNRS UMR5239, Oncovirologie et Biothérapies, Faculté de Médecine Lyon Sud, ENS - HCL, Pierre Bénite, France.
Lea Payen-GayINSERM, UMR-S1052, Centre de Recherche en Cancérologie de Lyon, Lyon, France.
Meyling CheokJean-Pierre Aubert Center, INSERM U837, Facteurs de Persistance des Cellules Leucémiques, Institute for Cancer Research in Lille, Lille Cedex, France.
Hussein MortadaCentre de Recherche sur le Cancer de Lyon, Inserm, Epissage Alternatif et Progression Tumorale, Lyon, France.
Didier AuboeufCentre de Recherche sur le Cancer de Lyon, Inserm, Epissage Alternatif et Progression Tumorale, Lyon, France.
Christiane PinatelCentre de Recherche sur le Cancer de Lyon, Inserm, Echappement aux Systèmes de Sauvegarde et Plasticité Cellulaire, Lyon, France.
Mohamed El-HamriUniversité Lyon I, Service d'Hématologie, Pavillon Marcel Bérard, Centre Hospitalier Lyon-Sud, Pierre Bénite, France.
Charles DumontetCentre de Recherche sur le Cancer de Lyon, Inserm, Anticorps Anticancer, Lyon, France.
Emeline CrosCentre de Recherche sur le Cancer de Lyon, Inserm, Anticorps Anticancer, Lyon, France.
Pascale Flandrin-GrestaUniversité Lyon 1, CNRS UMR5239, Oncovirologie et Biothérapies, Faculté de Médecine Lyon Sud, ENS - HCL, Pierre Bénite, France.
Olivier NibourelCentre de Recherche sur le Cancer de Lyon, Inserm, Epissage Alternatif et Progression Tumorale, Lyon, France.
Claude PreudhommeCentre de Recherche sur le Cancer de Lyon, Inserm, Epissage Alternatif et Progression Tumorale, Lyon, France.
Mauricette MichalletUniversité Lyon 1, CNRS UMR5239, Oncovirologie et Biothérapies, Faculté de Médecine Lyon Sud, ENS - HCL, Pierre Bénite, France.
Xavier ThomasUniversité Lyon I, Service d'Hématologie, Pavillon Marcel Bérard, Centre Hospitalier Lyon-Sud, Pierre Bénite, France.
Franck NicoliniUniversité Lyon I, Service d'Hématologie, Pavillon Marcel Bérard, Centre Hospitalier Lyon-Sud, Pierre Bénite, France.
Françoise SollyUniversité Lyon 1, CNRS UMR5239, Oncovirologie et Biothérapies, Faculté de Médecine Lyon Sud, ENS - HCL, Pierre Bénite, France.
Denis GuyotatUniversité Lyon 1, CNRS UMR5239, Oncovirologie et Biothérapies, Faculté de Médecine Lyon Sud, ENS - HCL, Pierre Bénite, France.
Lydia CamposUniversité Lyon 1, CNRS UMR5239, Oncovirologie et Biothérapies, Faculté de Médecine Lyon Sud, ENS - HCL, Pierre Bénite, France.
Eric WattelUniversité Lyon 1, CNRS UMR5239, Oncovirologie et Biothérapies, Faculté de Médecine Lyon Sud, ENS - HCL, Pierre Bénite, France.
Franck MortreuxUniversité Lyon 1, CNRS UMR5239, Oncovirologie et Biothérapies, Faculté de Médecine Lyon Sud, ENS - HCL, Pierre Bénite, France.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In addition to spliceosome gene mutations, oncogene expression and drug resistance in AML might influence exon expression. We performed exon-array analysis and exon-specific PCR (ESPCR) to identify specific landscapes of exon expression that are associated with DEK and WT1 oncogene expression and the resistance of AML cells to AraC, doxorubicin or azacitidine. Data were obtained for these five conditions through exon-array analysis of 17 cell lines and 24 patient samples and were extended through qESPCR of samples from 152 additional AML cases. More than 70% of AEUs identified by exon-array were technically validated through ESPCR. In vitro, 1,130 to 5,868 exon events distinguished the 5 conditions from their respective controls while in vivo 6,560 and 9,378 events distinguished chemosensitive and chemoresistant AML, respectively, from normal bone marrow. Whatever the cause of this effect, 30 to 80% of mis-spliced mRNAs involved genes unmodified at the whole transcriptional level. These AEUs unmasked new functional pathways that are distinct from those generated by transcriptional deregulation. These results also identified new putative pathways that could help increase the understanding of the effects mediated by DEK or WT1, which may allow the targeting of these pathways to prevent resistance of AML cells to chemotherapeutic agents.

Indexed as

AgedAlternative SplicingAnthracyclinesAntineoplastic AgentsAzacitidineCell Line, TumorChromosomal Proteins, Non-HistoneCytarabineDoxorubicinDrug Resistance, NeoplasmExonsGene Expression ProfilingHEK293 CellsHumansLeukemia, Myeloid, AcuteMaleAnthracyclinesAntineoplastic AgentsAzacitidineChromosomal Proteins, Non-HistoneCytarabineDEK protein, humanDoxorubicinOncogene ProteinsPoly-ADP-Ribose Binding ProteinsRNA, Small InterferingWT1 protein, humanWT1 Proteinsacute myeloid leukemiaalternative splicingDEKmultidrug resistanceWT1

Identifiers

PMID26284582
PMCPMC4823079

What OpenQuestion holds

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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.