Abstract
is causative for familial diseases including Cowden syndrome, which is characterized by multiple hamartomas, developmental defects, and increased cancer susceptibility.The major tumor-suppressive activity of PTEN is attributed to its ability to hydrolyze the 3′ phosphate of phosphoinositides at the plasma membrane and thereby negatively regulate phosphoinositide 3-kinase (PI3K) signaling, a promoter of cell growth and survival. In mouse models, Pten is haploinsufficient for tumor suppression. Progressive reduction of Pten dose is also associated with more aggressive cancers in the mouse, leading to the notion that subtle variations in Pten levels could have critical conse-quences for tumor progression. Indeed, in addition to the loss of
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