Gaetje R, Kotzian S, Herrmann G, Baumann R, Starzinski-Powitz A
Zentrum für Frauenheilkunde und Geburtschilfe, Universitätsklinikum, Frankfurt am Main, Germany.
Lancet. 1995 Dec 2;346(8988):1463-4. doi: 10.1016/s0140-6736(95)92474-4.
The pathogenesis of endometriosis is not known. The currently favoured theory is that viable endometrial cells, shed from the endometrium into the pelvic cavity by retrograde menstruation, reattach and invade other tissues. We used a collagen gel invasion assay to assess invasive potential of endometriotic cells. The invasion indices of cells from peritoneal endometriotic lesions and a metastatic bladder carcinoma cell line (EJ28) were similar (2.2-15.6 vs 8.4-11.6) whereas cells from normal endometrium and non-metastatic carcinoma cells (RT112) were non-invasive (indices < 1). Invasiveness of endometriotic cells might contribute to the pathogenesis of endometriosis.
子宫内膜异位症的发病机制尚不清楚。目前最受认可的理论是，存活的子宫内膜细胞经逆行月经从子宫内膜脱落后进入盆腔，重新附着并侵入其他组织。我们使用胶原凝胶侵袭试验来评估子宫内膜异位症细胞的侵袭潜能。来自腹膜子宫内膜异位症病变的细胞和转移性膀胱癌细胞系（EJ28）的侵袭指数相似（2.2 - 15.6对8.4 - 11.6），而来自正常子宫内膜的细胞和非转移性癌细胞（RT112）则无侵袭性（指数<1）。子宫内膜异位症细胞的侵袭性可能与子宫内膜异位症的发病机制有关。
