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Investigation of molecular alterations of AKT-3 in triple-negative breast cancer
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Immunology, Genetics and Pathology. Uppsala University, Science for Life Laboratory, SciLifeLab.
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2014 (English)In: Histopathology, ISSN 0309-0167, E-ISSN 1365-2559, Vol. 64, no 5, 660-670 p.Article in journal (Refereed) Published
Abstract [en]

AIMS: Triple-negative breast cancer (TNBC) is responsible for a disproportionate number of breast cancer (BC) deaths, owing to its intrinsic aggressiveness and a lack of treatment options, especially targeted therapies. Thus, there is an urgent need for the development of better targeted treatments for TNBC. Molecular alteration of AKT-3 was previously reported in oestrogen receptor (ER)-positive BC. AKT-3 has also been suggested to play a role in hormone-unresponsive BC. The aim of this study was to investigate molecular alterations of AKT-3 in TNBC, to perform associated survival analysis, and to compare these findings with the incidence of AKT-3 molecular alterations in ER-positive BC.

RESULTS: Our study revealed AKT-3 amplification and deletions in 11% (9/82) and 13% (11/82) of TNBCs, respectively. In contrast, 1% (2/209) of ER-positive BCs were found to have AKT-3 amplifications and deletions. A higher prevalence of AKT-3 copy number gains was observed in TNBC [26% (21/82)] than in ER-positive BC [9% (19/209)]. AKT-3 amplification together with Akt-3 protein expression was negatively associated with recurrence-free survival in TNBC. Furthermore, a negative association between high AKT-3 copy number and recurrence-free survival was observed.

CONCLUSION: AKT-3 amplification could represent a potentially relevant oncogenic event in a subset of TNBCs that may, in turn, select cells sensitive to Akt-3 inhibitors.

Place, publisher, year, edition, pages
2014. Vol. 64, no 5, 660-670 p.
National Category
Medical and Health Sciences
URN: urn:nbn:se:uu:diva-221321DOI: 10.1111/his.12313ISI: 000332788400007PubMedID: 24138071OAI: oai:DiVA.org:uu-221321DiVA: diva2:708557
Available from: 2014-03-28 Created: 2014-03-28 Last updated: 2014-05-15Bibliographically approved

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O'Hurley, GillianPontén, Fredrik
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Department of Immunology, Genetics and PathologyScience for Life Laboratory, SciLifeLab
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