Official websites use. Share sensitive information only on official, secure websites. Deep infiltrating endometriosis DIE is a particular clinical and histological entity of endometriosis responsible for chronic pelvic pain and infertility.
Here we characterize the proliferative phenotype of DIE cells, to explore the cellular and molecular mechanisms that could explain their aggressive potential. Included were 22 patients with DIE and 12 control patients without endometriosis. Epithelial and stromal cells were extracted from biopsies of eutopic endometrium and deep infiltrating endometriotic nodules from patients with DIE.
Cell proliferation was determined by thymidine incorporation. Oxidative stress was assayed by spectrofluorometry. The proliferation rate of eutopic endometrial cells and of deep infiltrating endometriotic cells from DIE patients was higher than that of endometrial cells from controls. Little is known about the factors that could explain the clinical and histological heterogeneity of endometriosis and, particularly, the development of deep infiltrating endometriosis DIE.
DIE is an aggressive disease responsible for chronic pelvic pain, 2 in its intensity inducing severe disability 3 and infertility. New drugs have recently been considered for the treatment of endometriosis; the use of antiaromatases, 8,9 antioxidant molecules, 10 or more recently anti-metabolites such as 5-FU 11 has been suggested.
The effectiveness of those treatments in vitro and in animal models relies on the modulation of cellular mechanisms responsible for invasion, unrestrained growth, neoangiogenesis, and distant spreading of endometriotic cells. Little is known about the role of other potentially proproliferative pathways in endometriosis. In the present study, we explored the proliferative phenotype of deep infiltrating endometriotic cells and highlighted the cellular and molecular mechanisms that could explain their aggressive potential.
