Somatic mutations are present in all members of the AKT family in endometrial carcinoma

The activating E17K mutations recently discovered in the pleckstrin homology domain of AKT1 in about 2% of endometrial cancer patients ( Shoji et al, 2009 ) suggest a new mechanism for PI3 kinase pathway activation in these patients, as previously described in breast, colorectal and ovarian cancers ( Carpten et al, 2007 ). Additional mechanisms of PI3 kinase pathway activation in endometrial cancer include the somatic mutation of PTEN and PIK3CA ( Kong et al, 1997 ; Oda et al, 2005 ), amplification and overexpression of PIK3CA ( Miyake et al, 2008 ; Salvesen et al, 2009 ), and decreased expression of PTEN ( Kanamori et al, 2001 ; Kappes et al, 2001 ).