Cowden disease (CD) is a genetically heterogeneous inherited cancer syndrome that arises predominantly from germline phosphatase and tensin homologue deleted on chromosome 10 (PTEN) mutation and increased phosphoinositide 3-kinase/mammalian target of rapamycin (PI3K/mTOR) signalling.
Our data suggest that PTEN modulates PLC:PLD activation pathways and indicate that the pathogenesis of CS/BRRS has a more complex biochemical basis beyond simply activating the PI3K pathway.