The tumor suppressor PTEN interacts with p53 in hereditary cancer (Review).

[cowden syndrome]

Numerous hereditary syndromes caused by mutations in multiple tumor suppressor genes can cause cancers . Germline mutations in PTEN and p 53 tumor suppressor cause Cowden syndrome and Li-Fraumeni syndrome , respectively . There exists some phenotypic overlap in these syndromes , and they are associated with high risks of breast cancer . The tumor suppressor protein PTEN is a dual-specificity phosphatase which has protein phosphatase activity and lipid phosphatase activity that antagonizes PI 3 K activity . Cells that lack PTEN have constitutively higher levels of PIP 3 and activated downstream targets . PTEN gene is recognized as one of the most frequently mutated or mutated in many human cancers . Li-Fraumeni syndrome results from germline mutations of the tumor suppressor p 53 gene encoding a transcriptional factor able to regulate cell cycle and apoptosis when DNA damage occurs . The p 53 protein cooperates with PTEN and might be an essential blockage in development of mammary tumors . Many findings have demonstrated that PTEN as well as p 53 plays a critical role in DNA damage response . This review summarizes the function of PTEN and p 53 in carcinogenic cell signaling . In addition , we will discuss the role of PTEN signaling through its interaction with p 53 and MDM 2 pathways for the potential implications in hereditary cancer prevention and therapeutic intervention .