PI3K/AKT pathway activation in acute myeloid leukaemias is not associated with AKT1 pleckstrin homology domain mutation.

Abstract:

:Despite its' central role, the precise mechanisms of the phosphoinositide 3-kinase/Akt (PI3K)/Akt pathway activation in acute myeloid leukaemia (AML) have not been elucidated. Recently, a recurrent novel AKT1 pleckstrin homology domain (PHD) mutation leading to membrane translocation, constitutive AKT activation and leukaemia development in mice was described. To assess AKT1 PHD mutations in AML, we sequenced 57 specimens from 49 AML patients, all of whom showed PI3K/AKT pathway activation by analysis of total and phospho-protein expression for AKT, mTor, p70S6Kinase, S6ribosomal protein and PTEN. No mutations in AKT1 PHD were identified, making this mutation an unlikely cause of PI3K/AKT pathway activation in AML.

journal_name

Br J Haematol

authors

Tibes R,Kornblau SM,Qiu Y,Mousses SM,Robbins C,Moses T,Carpten JD

doi

10.1111/j.1365-2141.2007.06920.x

subject

Has Abstract

pub_date

2008-02-01 00:00:00

pages

344-7

issue

3

eissn

0007-1048

issn

1365-2141

pii

BJH6920

journal_volume

140

pub_type

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