TY - JOUR T1 - Mesenchymal–epithelial Transition and Tumor Vascular Remodeling in Eribulin Chemotherapy for Breast Cancer JF - Anticancer Research JO - Anticancer Res SP - 401 LP - 410 VL - 38 IS - 1 AU - SHINICHIRO KASHIWAGI AU - YUKA ASANO AU - WATARU GOTO AU - KOJI TAKADA AU - KATSUYUKI TAKAHASHI AU - TAKAHARU HATANO AU - SAYAKA TANAKA AU - TSUTOMU TAKASHIMA AU - SHUHEI TOMITA AU - HISASHI MOTOMURA AU - MASAHIKO OHSAWA AU - KOSEI HIRAKAWA AU - MASAICHI OHIRA Y1 - 2018/01/01 UR - http://ar.iiarjournals.org/content/38/1/401.abstract N2 - Background/Aim: Eribulin mesylate (eribulin) is currently used for the treatment of locally advanced or metastatic breast cancer (MBC). It is a cytotoxic agent with unique mechanisms that suppress the epithelial–mesenchymal transition (EMT) of cancer cells and promote tumor vascular remodeling. In this study, we investigated the expression of markers for EMT and hypoxia in sets of clinical specimens collected before and after eribulin treatment to verify its unique mechanisms. Patients and Methods: The expression of markers for EMT and cellular hypoxia [E-cadherin, N-cadherin, vimentin, and carbonic anhydrase 9 (CA9)] was examined immunohistochemically in MBC tissues collected from 20 patients before and after chemotherapy with either eribulin (n=10) or paclitaxel (n=10). Results: An increase of E-cadherin and decrease of CA9 expression were observed in MBC tissues from patients with objective clinical responses to eribulin treatment. Patients with E-cadherin-positive conversion and CA9-negative conversion had significantly higher response rates (p=0.004 and p=0.024, respectively) and prolonged time to treatment failure (p=0.018 and p=0.038, respectively) than patients without changes in marker expression. Conclusion: Expression of EMT and hypoxia markers in clinical samples from patients with MBC was suppressed by eribulin treatment. The results provide additional clinical data on improved survival of patients treated with eribulin and the mechanism of response. ER -