Evidence map›Paper›PMID 38528080›Full record

ArticleScientific reports2024

Differential prognostic values of the three AKT isoforms in acute myeloid leukemia.

Eulalie Corre, Cécile Soum, Romain Pfeifer, Chloé Bessière, Sandra Dailhau, Catherine Marbœuf, Fabienne Meggetto, Christian Touriol, Christian Récher, Marina Bousquet and 1 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
4.5field-weighted citation impact, top 5% 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

5 citing papers in PubMed, 10 citations in OpenAlex.

  1. Article
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  5. Review
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

11 authors at 5 institutions in 1 country.

Eulalie Corre *Centre de Recherches en Cancérologie de Toulouse (CRCT), INSERM UMR-1037, CNRS UMR-5071, Université de Toulouse, Toulouse, France.
Cécile Soum *Centre de Recherches en Cancérologie de Toulouse (CRCT), INSERM UMR-1037, CNRS UMR-5071, Université de Toulouse, Toulouse, France.
Romain PfeiferCentre de Recherches en Cancérologie de Toulouse (CRCT), INSERM UMR-1037, CNRS UMR-5071, Université de Toulouse, Toulouse, France.
Chloé BessièreCentre de Recherches en Cancérologie de Toulouse (CRCT), INSERM UMR-1037, CNRS UMR-5071, Université de Toulouse, Toulouse, France.
Sandra DailhauCentre de Recherches en Cancérologie de Toulouse (CRCT), INSERM UMR-1037, CNRS UMR-5071, Université de Toulouse, Toulouse, France.
Catherine MarbœufCentre de Recherches en Cancérologie de Toulouse (CRCT), INSERM UMR-1037, CNRS UMR-5071, Université de Toulouse, Toulouse, France.
Fabienne MeggettoCentre de Recherches en Cancérologie de Toulouse (CRCT), INSERM UMR-1037, CNRS UMR-5071, Université de Toulouse, Toulouse, France.
Christian TouriolCentre de Recherches en Cancérologie de Toulouse (CRCT), INSERM UMR-1037, CNRS UMR-5071, Université de Toulouse, Toulouse, France.
Christian RécherService d'Hématologie, Centre Hospitalier Universitaire de Toulouse, Institut Universitaire du Cancer de Toulouse Oncopôle, Toulouse, France.
Marina BousquetCentre de Recherches en Cancérologie de Toulouse (CRCT), INSERM UMR-1037, CNRS UMR-5071, Université de Toulouse, Toulouse, France.
Stéphane PyronnetCentre de Recherches en Cancérologie de Toulouse (CRCT), INSERM UMR-1037, CNRS UMR-5071, Université de Toulouse, Toulouse, France. stephane.pyronnet@inserm.fr.
Centre de Recherche en Cancérologie de Toulouse · FRUniversité de Toulouse · FRCentre National de la Recherche Scientifique · FRInserm · FRCentre Hospitalier Universitaire de Toulouse · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The PI3K-AKT-mTOR pathway lies at the confluence of signaling pathways in which various components are subjected to activating genetic alterations in acute myeloid leukemia (AML), thus contributing to oncogenesis. Three AKT isoforms exist in humans. However, whether one isoform predominates in AML remains unknown. This study reveals that AKT3 behaves very distinctly than AKT1 or AKT2 in both normal myeloid differentiation and AML. During normal differentiation, AKT3 is preferentially expressed in hematopoietic stem cells whilst AKT1 becomes preferentially expressed as cells differentiate into granulocytes or monocytes. AKT2 expression remains unchanged. In AML, AKT3 expression varies widely among patient samples and is counterintuitively high in mature/monocytic leukemia. Furthermore, a low level of AKT3 expression is strongly correlated to genetic alterations associated with a better outcome (NPM1 mutations and RUNX1-RUNX1T1 translocation), while a high level is correlated to alterations associated to a bad outcome (RUNX1 mutations; and SRSF2, U2AF1, SF3B1, ASXL1 and BCOR mutations occurring frequently in MDS and MPN). Consistently, a high AKT3 expression level appears as a very strong predictor of poor survival. Curiously, although modestly varying among AML samples, a high AKT1 expression shows in contrast as a strong predictor of a better patient outcome. These data suggest that AKT3 and AKT1 expressions have strong, yet opposite, prognostic values.

Indexed as

Leukemia, Myeloid, AcuteProto-Oncogene Proteins c-aktCore Binding Factor Alpha 2 SubunitHumansMutationPhosphatidylinositol 3-KinasesPrognosisProtein IsoformsAKT1 protein, humanAKT2 protein, humanAKT3 protein, humanCore Binding Factor Alpha 2 SubunitPhosphatidylinositol 3-KinasesProtein IsoformsProto-Oncogene Proteins c-akt

Identifiers

PMID38528080
PMCPMC10963760
OpenAlexW4393163441

What OpenQuestion holds

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LicenceCC BY
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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.