A number of studies exploring this hypothesis further reported allelic chromosomal imbalances26 and clonal abnormalities27,28 in both epithelial and stromal elements of PTs, abnormalities in pathways for stromal proliferation raising from the epithelial component in benign PTs29, as well as correlations of increasing malignancy with a loss of stromal dependency on the epithelium25,29 and of epithelial E-cadherin expression with recurrence and shorter tumor specific survival in non-benign PTs30. This evidence concerns the gene CDH1 and neoplasm.