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Absence of E17K mutation in the pleckstrin homology domain of AKT1 in gastrointestinal and liver cancers in the Korean population  

AKT/PKB (protein kinase B) kinases regulate diverse cellular processes, including cell proliferation and survival, tumor cell invasion and angiogenesis (1). Growth-factor-induced AKT/ PKB activation is mediated by phosphatidylinositol-3 kinase (PI3K), which in turn activates phosphoinositide-dependent kinase (PDK)1 and PDK2 by the production of phosphatidylinositol-3,4,5-trisphosphate (PtdIns(3, 4,5)P3) or phosphatidylinositol-3,4-bisphosphate (PtdIns(3,4)P2) lipids (2, 3). The lipids also recruit AKT to the plasma membrane by means of its pleckstrin homology (PH) domain, and AKT is subsequently phosphorylated, resulting in full activation (3, 4). Several lines of evidence suggest that components of the AKT pathway are involved in the oncogenic transformation of normal cells. First, amplification and frequent somatic mutations of the PI3K catalytic subunit have been identified in ovarian, breast and colon cancers (5–7). In addition, PI3K is a potent transforming gene in cultured chicken embryo fibroblasts and induces activation of AKT activity (8). Second, AKT fused to the membrane-targeting gag sequence is able to transform fibroblasts (9) and activated AKT is a well-established survival factor, exerting anti-apoptotic activity by preventing release of cytochrome c from mitochondria (10). AKT1 kinase activity is often increased in prostate and breast cancers, and is associated with a poor prognosis (11). Furthermore, an activating somatic mutation (E17K) in the PH domain of the PKB/AKT gene, which results in an increased level of AKT phosphorylation, has also been identified in breast, colorectal and ovarian cancers (12). Third, a negative regu-