We therefore developed and characterised genetically modified murine models with prostate tumour-specific alterations: (1) PbCre Ctnnb1(ex3Δ)/+Ptenfl/+, with heterozygous deletion of Ctnnb1 exon 3, leading to constitutive β-catenin activation and heterozygous loss of Pten in the prostatic epithelium; (2) PbCre Spry2fl/+Ptenfl/fl, with heterozygous loss of Spry2 and homozygous loss of Pten.11 Prostate cancer cell lines were generated from the PbCre Ctnnb1(ex3Δ)/+Ptenfl/+ and PbCre Spry2fl/+Ptenfl/fl tumours, hereafter referred to as CP2 and SP1 cells, respectively. The gene discussed is PTEN; the disease is neoplasm.