Intrauterine adhesions (IUAs) are mainly derived from fibrous tissue formation following endometrial damage. The aim of the present study was to assess whether fibrosis markers, estrogen receptor (ER)α and the stromal derived factor (SDF)-1/C-X-C chemokine receptor type 4 (CXCR-4) axis are abnormally expressed in IUA endometrium. A total of 76 human endometrial biopsy samples (normal, n=20; mild-to-moderate IUAs, n=40; and severe IUAs, n=16) were employed, and Sprague-Dawley rat IUA models at different time points were constructed. Subsequently, the expression of transforming growth factor (TGF)-β1, matrix metalloproteinase (MMP)-9, ERα and the SDF-1/CXCR-4 axis was evaluated in human and rat IUAs using histology, immunohistochemistry, reverse transcription quantitative polymerase chain reaction and western blotting. In patients and rats with IUA formation, the expression of TGF-β1, MMP-9 and ERα was significantly higher compared with the control group at the mRNA and protein levels (P<0.05); in addition, in patients, the TGF-β1, MMP-9 and ERα levels were significantly higher in severe IUAs compared with those in mild-to-moderate IUA endometrium (P<0.05). Although the chemokine SDF-1 level in rats increased significantly during the early postoperative phase (reaching a peak at the second estrus phase) in rat endometrium (P<0.05), its special receptor CXCR-4 expression did not differ significantly compared with the control group in rats or patients (P>0.05). Our findings indicated that aberrant activation of fibrosis and expression of ERα may be involved in the pathology of IUA formation. The role of the SDF-1/CXCR-4 axis in IUAs as inflammatory medium in the short-term or special homing factors for bone marrow mesenchymal stem cells requires further verification in in vivo animal models.

BackgroundLymph node metastasis (LNM) is a critical unfavorable prognostic factor in endometrial cancer (EC). At present, models involving molecular indicators that accurately predict LNM are still uncommon. We addressed this gap by developing nomograms to individualize the risk of LNM in EC and to identify a low-risk group for LNM.MethodsIn all, 776 patients who underwent comprehensive surgical staging with pelvic lymphadenectomy at the First Affiliated Hospital of Chongqing Medical University were divided into a training cohort (used for building the model) and a validation cohort (used for validating the model) according to a predefined ratio of 7:3. Logistics regression analysis was used in the training cohort to screen out predictors related to LNM, after which a nomogram was developed to predict LNM in patients with EC. A calibration curve and consistency index (C-index) were used to estimate the performance of the model. A receiver operating characteristic (ROC) curve and Youden index were used to determine the optimal threshold of the risk probability of LNM predicted by the model proposed in this study. Then, the prediction performance of different models and their discrimination abilities for identifying low-risk patients were compared.ResultLNM occurred in 87 and 42 patients in the training and validation cohorts, respectively. Multivariate logistic regression analysis showed that histological grade (P=0.022), myometrial invasion (P=0.002), lymphovascular space invasion (LVSI) (P=0.001), serum CA125 (P=0.008), Ki67 (P=0.012), estrogen receptor (ER) (0.009), and P53 (P=0.003) were associated with LNM; a nomogram was then successfully established on this basis. The internal and external calibration curves showed that the model fits well, and the C-index showed that the prediction accuracy of the model proposed in this study was better than that of the other models (the C-index of the training and validation cohorts was 0.90 and 0.91, respectively). The optimal threshold of the risk probability of LNM predicted by the model was 0.18. Based on this threshold, the model showed good discrimination for identifying low-risk patients.ConclusionCombining molecular indicators based on classical clinical parameters can predict LNM of patients with EC more accurately. The nomogram proposed in this study showed good discrimination for identifying low-risk patients with LNM.

Endometrium fibrosis may be inhibited and endometrium receptivity may be improved by estrogen with moderate dosage therapy. Compared to the large one, it seems to be advantageous.

VEIL for vulvar cancer treatment is effective, with the advantages of short hospitalization stay, less bleeding, and reduced postoperative complications comparing the OIL.

SummaryBackgroundImportin13 (IPO13) is a novel potential marker of corneal epithelial progenitor cells. We investigated the expression and localization of IPO13 in endometrial, endometriotic and endometrial carcinoma tissue.Material/MethodsIPO13 expression in endometrial, endometriotic and endometrial carcinoma tissue was examined by immunohistochemistry, qPCR and Western blot.ResultsImmunohistochemistry studies showed that IPO13 protein was expressed mainly in cytoplasm of glandular epithelial cell and stromal cells. The rate of importin13-positive cells in proliferative phase endometrium was higher (by about 6-fold) than that in secretory endometrium (P<0.05) and the rate of importin13-positive cells in endometriosis and endometrial carcinoma was higher than that in normal secretory phase endometrial tissues (by about 4- and 9-fold, respectively). Immunofluorescence microscopy revealed co-localization of IPO13 with CD34, CD45, c-kit, telomerase, CD90 and CD146. QPCR revealed significantly increased IPO13 mRNA in endometriosis and endometrial carcinoma versus secretory phase endometrium (by about 2- and 10-fold, respectively). Western blot analysis showed that IPO13 protein is enhanced in endometriosis and endometrial carcinoma versus secretory phase endometrium (p<0.05).ConclusionsThese results demonstrate an increased expression of IPO13 in endometriosis and endometrial carcinoma, which could be involved in the pathogenesis of endometriosis and endometrial carcinoma; IPO13 can serve as an endometrial progenitor/stem cell marker.