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summary
Many oncogenes and tumor suppressors mutated during cancer development act as enzymatic switches that phosphorylate (kinases) or dephosphorylate (phosphatases). Much attention has been paid to the therapeutic inhibition of mutation-activated oncogenic kinases. However, there has been less focus on targeting phosphatases, despite their importance in cancer development. Tumor suppressor PTEN (homolog of phosphatase and tensin on chromosome 10) is the most frequently inactivated phosphatase in human cancer (1, 2). The loss of PTEN phosphatase activity increases the downstream activity of the phosphatidylinositol 3-kinase (PI3K) -AKT signaling pathway (3, 4). Preclinical studies have shown that targeting the PI3K-AKT pathway reduces tumor growth when PTEN is inactivated (5). However, many mutant PTEN tumors are resistant to these therapies. On page 651 of this issue, Lee et al. (6) activate PTEN-phosphatase by inhibiting a recently described inhibitory system and thereby reduce PI3K-AKT signaling and tumor growth in mice.
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