The objective of this study is to evaluate the clinicopathological features and immunohistochemical characteristics of epithelioid trophoblastic tumor (ETT). Seven cases of epithelioid trophoblastic tumor treated in the Women's Hospital of Zhejiang University from 2004 September to 2008 December were retrospectively analyzed. Immunohistochemical study was performed. The most common presenting symptom was vaginal bleeding. Four patients had prior evidence of molar pregnancy and three patients presented with metastases. Mean age at diagnosis was 34.7 years. Mean pregnancy interval was 3.39 years. Human chorionic gonadotropin levels were 33.25-174315.5 IU/l. One case died from metastasis in lungs. The remaining six patients survived without recurrence. Immunohistochemistry revealed diffusely positive for CK18, and focally positive for β-hCG, HPL, Mel-CAM (CD146) and inhibin-alpha. Nuclear staining of Ki67 and p63 were seen. The confirmation of epithelioid trophoblastic tumor diagnosis is difficult before surgery. Surgical intervention is the recommended primary treatment.

A detailed history and thorough pelvic examination are essential in diagnosing perineal endometriosis. Surgical intervention is the first choice of treatment.

Aim: To investigate the roles of cell migration and invasion mediated by Twist in endometriosis. Methods: The protein levels and locations of Twist, N-cadherin and E-cadherin were measured by Western blot and immunohistochemistry in ectopic endometrium and eutopic endometrium of ovarian endometriosis as well as normal endometrium of nonendometriosis patients. The messenger RNA (mRNA) expressions of Twist, N-cadherin and E-cadherin in these tissues were measured by quantitative reverse transcription polymerase chain reaction. Stable overexpression of Twist in eutopic endometrial stromal cells was transfected with a plasmid-mediated delivery system. The protein and mRNA expressions of N-cadherin and E-cadherin were detected by western blot and reverse transcription polymerase chain reaction. The changes of migration and invasion of endometrial stromal cells were explored by transwell. Results: Levels of protein and mRNA of Twist and N-cadherin showed the highest expression in ectopic endometrium of ovarian endometriosis, while lowest in normal endometrium of nonendometriosis patients. On the contrary, the expression of E-cadherin showed highest in normal endometrium of nonendometriosis patients. The overexpression of Twist after transfection significantly upregulated the protein and mRNA expression of N-cadherin, while downregulated the protein and mRNA expression of E-cadherin. There is significant difference between groups. For transwell, the overexpression of Twist in eutopic endometrial stromal cell significantly promoted cell migration and invasion. Conclusion: Twist might be related with the increase of migration and invasion in endometrial stromal cells, mediated by epithelial-to-mesenchymal transition.

No abstract

The purpose of this study was to investigate the difference of Twist gene promoter methylation among ovarian ectopic endometrium, eutopic endometrium and non-endometriosis (EMs) endometrium . 15 patients with reproductive age hospitalized at Department of obstetrics and gynecology affiliated to Medicine School of Zhejiang University from January 2013 to June 2016 were selected. Among them, 5 patients underwent laparoscopic surgery due to ovarian type EMs, and were selected after histologic confirmation. Ectopic endometrium and eutopic endometrium were obtained simultaneously. Normal endometrium was obtained from 5 cases of tubal infertility confirmed by hysteroscopy. Six pairs of primers for CpG island of Twist gene promoter were designed, and the difference of promoter methylation levels was detected by pyrosequencing method for methylation specific PCR (MSP) in three groups of endometrial tissues. The promoter of Twist gene is hypomethylated in some areas of ovarian ectopic endometrium and eutopic endometrium of ovarian endometriosis. It is speculated that the regional hypomethylation of Twist gene promoter in ovarian ectopic endometrium and eutopic endometrium may cause over-expression of Twist protein, which may directly lead to the pathogenesis of endometriosis.