Context
The PTEN gene encodes a phosphatase that is homozygously mutated in a high percentage of human tumours. A major substrate of PTEN is phosphatidylinositol triphosphate (PIP-3), a lipid second messenger produced by phosphatidylinositol-3 kinase (PI-3K). In the absence of PTEN activity, PIP-3 concentrations are increased, resulting in enhanced phosphorylation and activation of the survival-promoting factor Akt/PKB (protein kinase B). Inactivating mutations in the PTEN tumour suppressor gene occur in three related human autosomal dominant disorders characterised by tumour susceptibility. Homozygous deficiency of PTEN in mice results in embryonic death. This paper studies the consequences of haploinsufficiency of PTEN by analysing the phenotype of PTEN heterozygous mice. To characterise the phenotype of mice heterozygous for the tumour suppressor gene PTEN.