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The proto-oncogene protein c-Akt (AKT1) E17K mutant is a specific, recurrent somatic mutation in the AKT1 gene, resulting in constitutive activation of the PI3K/AKT/mTOR signaling pathway. This gain-of-function mutation promotes cell survival, proliferation, and migration, and is implicated in various cancers. While it can be an oncogenic driver, it is also associated with improved prognosis in some contexts, particularly in certain breast cancer subtypes. Tumors harboring this mutation are considered rational targets for AKT inhibitors, although combination therapies may be necessary to overcome resistance or address co-occurring mutations.
Inhibition of AKT kinase activity, blocking downstream signaling in the PI3K/AKT/mTOR pathway
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