Endometrial large cell neuroendocrine carcinoma: A case report and literature review.

Endometrial large cell neuroendocrine carcinoma (LCNEC) is a highly malignant tumor that presents with neuroendocrine function. It is difficult to diagnose at an early stage. Moreover, the diagnosis depends on the pathological and immunohistochemical findings. It is also prone to distant metastasis, but is difficult to treat and shows poor prognosis. Presently, there exists no unified treatment plan, and the prognosis of this disease is also poor. We reported here an analysis and literature review of a case of endometrial LCNEC to facilitate the comprehension of this disease and provide help toward clinical diagnosis and treatment.

Adjuvant Radiotherapy After Minimally Invasive Surgery in Patients With Stage IA1-IIA1 Cervical Cancer.

To estimate whether adjuvant radiotherapy is necessary for patients with stage IA1-IIA1 cervical cancer after laparoscopic hysterectomy, 221 patients were retrospectively analyzed. Sixty-two of them were treated with laparoscopic hysterectomy and adjuvant radiotherapy (group A), 115 underwent open surgery (group B) and 44 received laparoscopic hysterectomy alone (group C). Results showed that the 3-year local recurrence-free survival (LRFS) rates of group A, B and C were 98.4%, 97.4% and 86.4%, respectively. The LRFS rates of group A and B surpassed C (A vs. B, p=0.634; A vs. C, p=0.011; B vs. C, p=0.006). The inter-group differences of 3-year overall survival (OS) and distant metastasis free survival (DMFS) were not statistically significant. In subgroup analysis of stage IB disease, the 3-year LRFS rates of group A, B and C were 100%, 98.8% and 83.1%, the 3-year OS rates of group A, B and C were 100%, 98.9% and 91.5%, respectively. The 3-year LRFS and OS rates of group A and B were significantly superior to group C (p<0.05). Our findings suggest that adjuvant radiotherapy can reduce the risk of recurrence for women with early-stage cervical cancer after laparoscopic hysterectomy and bring survival benefits for patients with stage IB disease.

LINC01541 Functions as a ceRNA to Modulate the Wnt/ß-Catenin Pathway by Decoying miR-506-5p in Endometriosis.

Endometriosis is one of the most common gynecological diseases that adversely effects the lives of women. Our previous studies showed that LINC01541 plays a key role in 17ß-estradiol (17ß-E2)-stimulated endometrial stromal cells (ESCs); however, the mechanism by which LINC01541 exerts if effects requires further elaboration. Here, we report that LINC01541 serves to reduce the bioavailability of miR-506-5p by acting as a molecular sponge. Samples of control endometrial tissue and ectopic endometrial tissue were obtained from 10 healthy volunteers and 18 patients with endometriosis, respectively, and the levels of LINC01541 and miR-506-5p expressions in those tissues were measured. The relationship between LINC01541 and miR-506-5p was verified in 17ß-E2-stimulated ESCs. Overexpression or silencing of miR-506-5p in ESCs was performed explore its role in endometriosis, and we also investigated whether WNT inhibitory factor 1 (WIF1) might be a target gene of miR-506-5p. Our results showed that LINC01541 was expressed at low levels and miR-506-5p was expressed at high levels in ectopic tissues. LINC01541 expression was negatively correlated with miR-506-5p expression. We also found that miR-506-5p activated the Wnt/ß-catenin pathway by inhibiting WIF1 expression, and thereby induced the proliferation, migration, and invasion of ESCs. Furthermore, silencing of miR-506-5p promoted apoptosis and suppressed the proliferation of 17ß-E2-treated ESCs. Overexpression of miR-506-5p could reverse the inhibitory effect of LINC01541 in endometriosis. In summary, this study found that in endometriosis, LINC01541 functions as a ceRNA that modulates the Wnt/ß-catenin pathway by decoying miR-506-5p.

LINC01541 overexpression attenuates the 17ß-Estradiol-induced migration and invasion capabilities of endometrial stromal cells.

Endometriosis affects 6-10% of healthy women of reproductive age. Therefore, it is important to study the molecular mechanism by which endometriosis develops. This study examined whether aberrant expression of LINC01541 contributes to the pathogenesis of endometriosis. Human endometrial stromal cells (ESCs) were stimulated with 10 nmol/L of 17ß-Estradiol (17ß-E2) to simulate ectopic cells found in endometriosis. Next, the levels of proteins related to the epithelial-mesenchymal transition (EMT), cell invasion, and metastasis were investigated. The effects of LINCO1541 silencing and overexpression were also examined in ESCs. Cell proliferation and apoptosis were detected by cell counting kit-8 and flow cytometry assays, respectively. ESCs stimulated with 17ß-E2 displayed increased levels of N-Cadherin and vimentin expression, but decreased levels of E-Cadherin expression. 17ß-E2 promoted the migration and invasion of ESCs, and those affects were partially reversed by overexpression of LINC01541. Furthermore, silencing of LINC01541 attenuated apoptosis and promoted the EMT of ESCs, while overexpression of LINC01541 stimulated cell apoptosis, increased the levels of caspase 3 protein, and decreased the levels of B cell leukemia/lymphoma 2 protein. Overexpression of LINC01541 also decreased the expression of vascular endothelial growth factor A (VEGFA) by repressing the Wnt/ß-catenin pathway. Our, results suggest that LINC01541 can inhibit the EMT process, metastasis of ESCs, and VEGFA expression by regulating the Wnt/ß-catenin pathway, which may play an important role in the pathogenesis of endometriosis. Abbreviations: ESCs: endometrial stromal cells; 17ß-E2: 17ß-Estradiol; EMT: epithelial-mesenchymal transition; CASP3: caspase 3; BCL2: B cell leukemia/lymphoma 2; VEGFA: vascular endothelial growth factor A; lncRNA: long non-coding RNA; GAPDH: glyceraldehyde-3-phosphate dehydrogenase; RT-qPCR: reverse transcription-quantitative polymerase chain reaction.

A systematic review and meta-analysis of the association of transforming growth factor ß receptor I 6A/9A gene polymorphism with ovarian cancer risk.

Ovarian cancer is the leading cause of cancer-related death in women. This meta-analysis was conducted to evaluate the association of transforming growth factor ß receptor I (TßR-I) 6A/9A gene polymorphism with ovarian cancer risk. The association literatures were identified from PubMed and Cochrane Library on 1 October 2013, and eligible reports were recruited and synthesized. Four reports were recruited into this meta-analysis for the association of TßR-I 6A/9A gene polymorphism with ovarian cancer risk. 6A allele and 6A/6A genotype of TßR-I were associated with the ovarian cancer risk (6A: OR = 1.24, 95% CI: 1.02-1.51, p = 0.03; 6A/6A: OR = 2.30, 95% CI: 1.01-5.22, p = 0.05). However, TßR-I 9A/9A genotype was not associated with the risk of ovarian cancer (OR = 0.82, 95% CI: 0.66-1.02, p = 0.08). In conclusion, TßR-I 6A allele and 6A/6A genotype are associated with the ovarian cancer risk. However, more studies should be performed to confirm this relationship in the future.

Characterization and anti-allergic effect of a polysaccharide from the flower buds of Lonicera japonica.

A water-soluble polysaccharide (LJP-1), with a molecular weight of 1.8×10(5) Da, was isolated from the flower buds of Lonicera japonica. Gas chromatography (GC) analysis showed that the LJP-1 was mainly composed of d-glucose and a small amount of d-arabinose. On the basis of methylation analysis, LJP-1 had the backbone chain mainly consisting of 1,6-linked Glc and 1,3,6-linked Glc, which was terminated with 1-linked Ara residues at the O-3 position of 1,3,6-linked Glc in a relative molar ratio of 2.9:1:0.9. The anti-allergic effect of LJP-1 was evaluated on allergic contact dermatitis (ACD) induced by picryl chloride (PC) in mouse ear. Similar to prednisolone, orally administrated LJP-1 (20, 40 and 80 mg/kg) potently inhibited the PC-induced ACD, leading to substantial reductions in ear thickness, serum level of IgE and histamine, as well as tissue TNF-α. These results demonstrate that treatment with LJP-1 may be effective for preventing the development of PC-induced ACD.