In studies on skin and breast cancer in mouse models and in patient-derived xenograft (PDX) tissues, cancer cells undergoing EMT were subdivided into six phenotypically and functionally distinct states on the basis of the extent of loss of the epithelial marker EpCAM (epithelial cell adhesion molecule) and gain of the cell–ECM adhesion receptor integrin α5 (CD51), integrin β3 (CD61), and vascular cell adhesion molecule 1 (VCAM1) (CD106)25. This evidence concerns the gene VCAM1 and breast carcinoma.