AKT hyperactivation is a common event in human cancers, and inhibition
of oncogenic AKT activation is a major goal of drug discovery programs.
Mouse tumor models that replicate AKT activation typical of human
cancers provide a powerful means by which to investigate mechanisms
of oncogenic signaling, identify potential therapeutic targets and
determine treatment regimes with maximal therapeutic efficacy. This
Perspective highlights recent advances using in vivo studies that
reveal how AKT signaling supports tumor formation, cooperates with
other mutations to promote tumor progression and facilitates tumor-cell
dissemination, focusing on well-characterized prostate carcinoma
mouse models that are highly sensitive to AKT activation. The implications
of these findings on the therapeutic targeting of AKT and potential
new drug targets are also explored.
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