Does 17betaE2 promote cell proliferation in endometriosis by decreasing PTEN via NFkappaB-dependent pathway?
Total/nuclear PTEN-loss and MAPK/ERK, PI3K/AKt, and NFkappaB signal overactivities coexist in endometriosis. In vitro, 17beta-estradiol can promotes cell proliferation in endometriosis by activating PI3K/AKt pathway via an NFkappaB/PTEN-dependent pathway. For the first time we propose the possibility of the presence of a positive feedback-loop: 17beta-estradiol-->high NFkappaB-->low PTEN-->high PI3K-->high NFkappaB, in endometriosis, which may finally promote the proliferation of ectopic endometrial epithelial cells and in turn contributes to the progression of the disease.
Our results indicate that ADRs can be improved considerably through simple educational efforts. Ultimately, a trial involving a larger number of endoscopists is needed to validate the utility of our training methods and determine whether improvements in ADRs lead to reduced colorectal cancer.