Investigation of molecular alterations of AKT-3 in triple-negative breast cancer.

Histopathology (2013-10-22)
Gillian O'Hurley, Etáin Daly, Anthony O'Grady, Robert Cummins, Cecily Quinn, Louise Flanagan, Aisling Pierce, Yue Fan, Miriam A Lynn, Máirín Rafferty, Dara Fitzgerald, Fredrik Pontén, Michael J Duffy, Karin Jirström, Elaine W Kay, William M Gallagher
要旨

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. 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. 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.

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製品内容

Sigma-Aldrich
モノクローナル抗AKT3抗体 マウス宿主抗体, clone 6E11, purified immunoglobulin, buffered aqueous solution
Sigma-Aldrich
抗AKT3 ウサギ宿主抗体, Prestige Antibodies® Powered by Atlas Antibodies, affinity isolated antibody, buffered aqueous glycerol solution

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