RT Journal Article
SR Electronic
T1 Mesenchymal–epithelial Transition and Tumor Vascular Remodeling in Eribulin Chemotherapy for Breast Cancer
JF Anticancer Research
JO Anticancer Res
FD International Institute of Anticancer Research
SP 401
OP 410
VO 38
IS 1
A1 SHINICHIRO KASHIWAGI
A1 YUKA ASANO
A1 WATARU GOTO
A1 KOJI TAKADA
A1 KATSUYUKI TAKAHASHI
A1 TAKAHARU HATANO
A1 SAYAKA TANAKA
A1 TSUTOMU TAKASHIMA
A1 SHUHEI TOMITA
A1 HISASHI MOTOMURA
A1 MASAHIKO OHSAWA
A1 KOSEI HIRAKAWA
A1 MASAICHI OHIRA
YR 2018
UL http://ar.iiarjournals.org/content/38/1/401.abstract
AB 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.