For instance, blocking N-cadherin ligation can prevent its association with the receptor tyrosine kinase fibroblast growth factor receptor (FGFR), resulting in the inhibition of extracellular signal-regulated kinase (ERK)-dependent activation of matrix metalloproteinase 9 transcription, thus inhibiting invasion of breast cancer epithelial cells.3, 37 The potential of N-cadherin as a therapeutic target has also been explored in xenograft models of melanoma, prostate and pancreatic cancers by inhibiting N-cadherin ligation with peptide antagonists and blocking antibodies.38, 39, 40. This evidence concerns the gene CDH2 and familial pancreatic carcinoma.