PTEN gene deletions are frequently observed in many tumor types, including renal, melanoma, endometrial, breast, prostate, lung, bladder, and thyroid cancer but also in hematological neoplasms. 

The tumor suppressor gene PTEN (phosphatase and tensin homolog deleted on chromosome ten), often referred to as MMAC1 (mutated in multiple advanced cancers 1), is located on 10q23.31 and encodes a 47 kDa dual-specificity phosphatase that has both lipid and protein phosphatase activity. Its inactivation results in constitutive activation of the PI3K/AKT pathway and in subsequent increase in protein synthesis, cell cycle progression, migration, and survival. Deletions affecting the long arm of chromosome 10 have been detected in 30 to 50% of early and advanced stage sporadic melanomas and about 40 to 70% of prostate cancers. In both tumor entities loss of PTEN has been associated with poor clinical outcome. Currently, several drugs targeting the PI3K/AKT pathway for the therapy of solid tumors have entered clinical trials.