ECE-1 expression is significantly increased in well-differentiated endometrial adenocarcinomas, suggesting it may play a role in tumor angiogenesis and could be a potential therapeutic target.
Should not yet alter endometrial cancer management; hypothesis-generating for ECE-1 as angiogenesis target.
Endothelin-1 (ET-1) is a potent mitogen in various precursor tumor cells, including endometrial adenocarcinoma. It is proposed that ET-1 produced by endometrial adenocarcinoma may participate in the angiogenesis of this carcinoma in vivo. Endothelin converting enzyme-1 (ECE-1) is the key enzyme that synthesizes ET-1. In this study, we tried to demonstrate the expression of ECE-1 in endometrial carcinomas. Deparaffinized tissue sections from patients with endometrial adenocarcinoma were analyzed by immunohistochemistry for the presence of ECE-1. Our study showed that the expression of ECE-1 was markedly increased in 9 of 15 (60%) well-differentiated endometrial adenocarcinomas; in contrast, only 2 out of 10 (20%) control specimens showed a mild labeling. With new selective inhibitory molecules emerging, research is currently evaluating the possible inhibition of ECE-1 as an alternative approach for the treatment of endometrial as well as other carcinomas.
No takes yet. Share an insight, caveat, or question.
Arun et al. (2001) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: