Published in Cancer Weekly, June 1st, 2010
"In AKT1, the E17K substitution leads to a PI3K-independent activation of AKT1. A mutational profiling of AKT1 and of the mutational hotspots in PIK3CA and PIK3R1 was carried out in samples from primary and recurrent prostate tumours. We show that, in prostate cancer, AKT1(E17K) had a prevalence of 1.4%. The...
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