CIP2A- and SETBP1-mediated PP2A inhibition reveals AKT S473 phosphorylation to be a new biomarker in AML

•PP2A inhibition occurs in AML by 2 different pathways: CIP2A in normal karyotype patients and SETBP1 in adverse karyotype patients.•AKTS473 phosphorylation is a predictor of survival, and diagnostic levels of AKTS473 could be a novel biomarker in AML. [Display omitted]

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Bibliographic Details
Published inBlood advances Vol. 2; no. 9; pp. 964 - 968
Main Authors Lucas, Claire M., Scott, Laura J., Carmell, Natasha, Holcroft, Alison K., Hills, Robert K., Burnett, Alan K., Clark, Richard E.
Format Journal Article
LanguageEnglish
Published United States Elsevier Inc 08.05.2018
American Society of Hematology
Elsevier
Subjects
Adult
Autoantigens - metabolism
Biomarkers, Tumor - metabolism
Carrier Proteins - metabolism
Female
Humans
Intracellular Signaling Peptides and Proteins
Leukemia, Myeloid, Acute - metabolism
Leukemia, Myeloid, Acute - pathology
Male
Membrane Proteins - metabolism
Middle Aged
Nuclear Proteins - metabolism
Phosphorylation
Protein Phosphatase 2 - metabolism
Proto-Oncogene Proteins c-akt - metabolism
Stimulus Report
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Summary:•PP2A inhibition occurs in AML by 2 different pathways: CIP2A in normal karyotype patients and SETBP1 in adverse karyotype patients.•AKTS473 phosphorylation is a predictor of survival, and diagnostic levels of AKTS473 could be a novel biomarker in AML. [Display omitted]
Bibliography:ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
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ISSN:2473-9529
2473-9537
DOI:10.1182/bloodadvances.2017013615