| Autor: |
Blontzos N; Endoscopic Surgery Unit, 1st Department of Obstetrics Gynecology, Medical School, National and Kapodistrian University of Athens, 11528 Athens, Greece.; Experimental Laboratory, 1st Department of Obstetrics Gynecology, Medical School, National and Kapodistrian University of Athens, 11528 Athens, Greece., Mavrogianni D; Experimental Laboratory, 1st Department of Obstetrics Gynecology, Medical School, National and Kapodistrian University of Athens, 11528 Athens, Greece., Ntzeros K; Experimental Laboratory, 1st Department of Obstetrics Gynecology, Medical School, National and Kapodistrian University of Athens, 11528 Athens, Greece., Kathopoulis N; Endoscopic Surgery Unit, 1st Department of Obstetrics Gynecology, Medical School, National and Kapodistrian University of Athens, 11528 Athens, Greece., Moustogiannis A; Department of Physiology, Medical School, National and Kapodistrian University of Athens, 11528 Athens, Greece., Philippou A; Department of Physiology, Medical School, National and Kapodistrian University of Athens, 11528 Athens, Greece., Koutsilieris M; Department of Physiology, Medical School, National and Kapodistrian University of Athens, 11528 Athens, Greece., Protopapas A; Endoscopic Surgery Unit, 1st Department of Obstetrics Gynecology, Medical School, National and Kapodistrian University of Athens, 11528 Athens, Greece. |
| Abstrakt: |
Endometriosis is a benign, estrogen-dependent gynecological condition with an uncertain exact pathogenetic mechanism. The aim of this study was to evaluate the potential differential expression of Insulin Growth Factor 1 (IGF-1) isoforms in deeply infiltrating endometriotic (DIE) lesions, in ovarian endometriomas, and in the eutopic endometrium of the same endometriosis patients and to compare their expression with that in the eutopic endometrium of women without endometriosis. A total of 39 patients were included: 28 with endometriosis, of whom 15 had endometriomas only, 7 had DIE nodules only, and 6 had both DIE and endometriomas, and 11 without endometriosis served as controls. We noticed a similar pattern of expression between IGF-1Ea and IGF-1Ec, which differed from that of the IGF-1Eb isoform, possibly implying differential biological actions of different isoforms in DIE subtypes. We observed a tendency of lower expression of IGF-1Ea and IGF-1Ec in endometriomas without DIE compared to endometriomas with concurrent DIE or in DIE nodules. In conclusion, differential expression of IGF-1 isoforms may indicate that DIE with its associated ovarian lesions and simple ovarian endometriosis should be considered as two forms of the disease developing under different molecular pathways. |
