Absence of AKT1 mutations in glioblastoma.
<h4>Background</h4>Oncogenic activation of the PI3K signalling pathway plays a pivotal role in the development of glioblastoma multiforme (GBM). A central node in PI3K downstream signalling is controlled by the serine-threonine kinase AKT1. A somatic mutation affecting residue E17 of the...
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2009
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oai:doaj.org-article:9852c5c98a3b47aa91e3f8d3b920641e2021-11-25T06:22:35ZAbsence of AKT1 mutations in glioblastoma.1932-620310.1371/journal.pone.0005638https://doaj.org/article/9852c5c98a3b47aa91e3f8d3b920641e2009-05-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/19461960/pdf/?tool=EBIhttps://doaj.org/toc/1932-6203<h4>Background</h4>Oncogenic activation of the PI3K signalling pathway plays a pivotal role in the development of glioblastoma multiforme (GBM). A central node in PI3K downstream signalling is controlled by the serine-threonine kinase AKT1. A somatic mutation affecting residue E17 of the AKT1 gene has recently been identified in breast and colon cancer. The E17K change results in constitutive AKT1 activation, induces leukaemia in mice, and accordingly, may be therapeutically exploited to target the PI3K pathway. Assessing whether AKT1 is activated by somatic mutations in GBM is relevant to establish its role in this aggressive disease.<h4>Methodology/principal findings</h4>We performed a systematic mutational analysis of the complete coding sequence of the AKT1 gene in a panel of 109 tumor GBM samples and nine high grade astrocytoma cell lines. However, no somatic mutations were detected in the coding region of AKT1.<h4>Conclusions/significance</h4>Our data indicate that in GBM oncogenic deregulation of the PI3K pathway does not involve somatic mutations in the coding region of AKT1.Fonnet E BleekerSimona LambaCarlo ZanonAngela A van TilborgSieger LeenstraDirk TroostTheo HulsebosW Peter VandertopAlberto BardelliPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 4, Iss 5, p e5638 (2009) |
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Medicine R Science Q Fonnet E Bleeker Simona Lamba Carlo Zanon Angela A van Tilborg Sieger Leenstra Dirk Troost Theo Hulsebos W Peter Vandertop Alberto Bardelli Absence of AKT1 mutations in glioblastoma. |
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<h4>Background</h4>Oncogenic activation of the PI3K signalling pathway plays a pivotal role in the development of glioblastoma multiforme (GBM). A central node in PI3K downstream signalling is controlled by the serine-threonine kinase AKT1. A somatic mutation affecting residue E17 of the AKT1 gene has recently been identified in breast and colon cancer. The E17K change results in constitutive AKT1 activation, induces leukaemia in mice, and accordingly, may be therapeutically exploited to target the PI3K pathway. Assessing whether AKT1 is activated by somatic mutations in GBM is relevant to establish its role in this aggressive disease.<h4>Methodology/principal findings</h4>We performed a systematic mutational analysis of the complete coding sequence of the AKT1 gene in a panel of 109 tumor GBM samples and nine high grade astrocytoma cell lines. However, no somatic mutations were detected in the coding region of AKT1.<h4>Conclusions/significance</h4>Our data indicate that in GBM oncogenic deregulation of the PI3K pathway does not involve somatic mutations in the coding region of AKT1. |
format |
article |
author |
Fonnet E Bleeker Simona Lamba Carlo Zanon Angela A van Tilborg Sieger Leenstra Dirk Troost Theo Hulsebos W Peter Vandertop Alberto Bardelli |
author_facet |
Fonnet E Bleeker Simona Lamba Carlo Zanon Angela A van Tilborg Sieger Leenstra Dirk Troost Theo Hulsebos W Peter Vandertop Alberto Bardelli |
author_sort |
Fonnet E Bleeker |
title |
Absence of AKT1 mutations in glioblastoma. |
title_short |
Absence of AKT1 mutations in glioblastoma. |
title_full |
Absence of AKT1 mutations in glioblastoma. |
title_fullStr |
Absence of AKT1 mutations in glioblastoma. |
title_full_unstemmed |
Absence of AKT1 mutations in glioblastoma. |
title_sort |
absence of akt1 mutations in glioblastoma. |
publisher |
Public Library of Science (PLoS) |
publishDate |
2009 |
url |
https://doaj.org/article/9852c5c98a3b47aa91e3f8d3b920641e |
work_keys_str_mv |
AT fonnetebleeker absenceofakt1mutationsinglioblastoma AT simonalamba absenceofakt1mutationsinglioblastoma AT carlozanon absenceofakt1mutationsinglioblastoma AT angelaavantilborg absenceofakt1mutationsinglioblastoma AT siegerleenstra absenceofakt1mutationsinglioblastoma AT dirktroost absenceofakt1mutationsinglioblastoma AT theohulsebos absenceofakt1mutationsinglioblastoma AT wpetervandertop absenceofakt1mutationsinglioblastoma AT albertobardelli absenceofakt1mutationsinglioblastoma |
_version_ |
1718413815066918912 |