Evidence map›Paper›PMID 26674329›Full record

ArticleBBA clinical2015

Phosphorylation of GSK3α/β correlates with activation of AKT and is prognostic for poor overall survival in acute myeloid leukemia patients.

Peter P Ruvolo, YiHua Qiu, Kevin R Coombes, Nianxiang Zhang, E Shannon Neeley, Vivian R Ruvolo, Numsen Hail, Gautam Borthakur, Marina Konopleva, Michael Andreeff and 1 more

Open access · hybridAbstract read
In one paragraph

Article in BBA clinical, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

27 citing papers in PubMed, 39 citations in OpenAlex.

  1. Article
  2. GSK3βGut · 2026
    Article
  3. Review
  4. Article
  5. Review
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  8. Review
  9. Article
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  13. Article
  14. Screening of autophagy genes as prognostic indicators for glioma patients.American journal of translational research · 2020
    Article
  15. Article
  16. Review
  17. Review
  18. Article
  19. Review
  20. Role of MSC-derived galectin 3 in the AML microenvironment.Biochimica et biophysica acta. Molecular cell research · 2018
    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

11 authors at 2 institutions in 1 country.

Peter P RuvoloDepartment of Leukemia, University of Texas MD Anderson Cancer Center, Houston, TX 77030, United States.
YiHua QiuDepartment of Leukemia, University of Texas MD Anderson Cancer Center, Houston, TX 77030, United States.
Kevin R CoombesBioinformatics and Computational Biology, The University of Texas M.D. Anderson Cancer Center, Houston, Texas, United States ; Department of Biomedical Informatics, Ohio State University Medical Center, Columbus, OH 43210, United States.
Nianxiang ZhangBioinformatics and Computational Biology, The University of Texas M.D. Anderson Cancer Center, Houston, Texas, United States.
E Shannon NeeleyDepartment of Statistics, Brigham Young University, Provo, UT, United States.
Vivian R RuvoloDepartment of Leukemia, University of Texas MD Anderson Cancer Center, Houston, TX 77030, United States.
Numsen HailDepartment of Leukemia, University of Texas MD Anderson Cancer Center, Houston, TX 77030, United States.
Gautam BorthakurDepartment of Leukemia, University of Texas MD Anderson Cancer Center, Houston, TX 77030, United States.
Marina KonoplevaDepartment of Leukemia, University of Texas MD Anderson Cancer Center, Houston, TX 77030, United States.
Michael AndreeffDepartment of Leukemia, University of Texas MD Anderson Cancer Center, Houston, TX 77030, United States.
Steven M KornblauDepartment of Leukemia, University of Texas MD Anderson Cancer Center, Houston, TX 77030, United States.
The University of Texas MD Anderson Cancer Center · USBrigham Young University · US

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Fabien Delerue · 1985 to 2026
$290.8M
THE THERAPY OF AMLP01CA055164 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI BERRY, DONALD A · 1992 to 2011
$25.3M
NCI NIH HHS P01 CA055164
6 · The paper itself

Abstract

backgroundAcute myeloid leukemia (AML) patients with highly active AKT tend to do poorly. Cell cycle arrest and apoptosis are tightly regulated by AKT via phosphorylation of GSK3α and β isoforms which inactivates these kinases. In the current study we examine the prognostic role of AKT mediated GSK3 phosphorylation in AML.

methodsWe analyzed GSK3α/β phosphorylation by reverse phase protein analysis (RPPA) in a cohort of 511 acute myeloid leukemia (AML) patients. Levels of phosphorylated GSK3 were correlated with patient characteristics including survival and with expression of other proteins important in AML cell survival.

resultsHigh levels of p-GSK3α/β correlated with adverse overall survival and a lower incidence of complete remission duration in patients with intermediate cytogenetics, but not in those with unfavorable cytogenetics. Intermediate cytogenetic patients with FLT3 mutation also fared better respectively when p-GSK3α/β levels were lower. Phosphorylated GSK3α/β expression was compared and contrasted with that of 229 related cell cycle arrest and/or apoptosis proteins. Consistent with p-GSK3α/β as an indicator of AKT activation, RPPA revealed that p-GSK3α/β positively correlated with phosphorylation of AKT, BAD, and P70S6K, and negatively correlated with β-catenin and FOXO3A. PKCδ also positively correlated with p-GSK3α/β expression, suggesting crosstalk between the AKT and PKC signaling pathways in AML cells.

conclusionsThese findings suggest that AKT-mediated phosphorylation of GSK3α/β may be beneficial to AML cell survival, and hence detrimental to the overall survival of AML patients. Intrinsically, p-GSK3α/β may serve as an important adverse prognostic factor for a subset of AML patients.

Indexed as

AKTGSK3LeukemiaPKC deltaRPPASignal transduction

Identifiers

PMID26674329
PMCPMC4661707
OpenAlexW2131968750

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.