Current Updates on Salpingectomy for the Prevention of Ovarian Cancer and Its Practice Patterns Worldwide.

A paradigm shift of the origin of ovarian cancer to fallopian tube has brought more focus on bilateral salpingectomy as a preventive method for ovarian cancer. Bilateral salpingectomy has shown a dramatic reduction in the risk of ovarian cancer. Bilateral salpingo-oophorectomy has been a long-used practice to prevent ovarian cancer, but it brings surgical menopause and an increased mortality rate to women undergoing such a surgery at the age of <47.5. With the prophylactic bilateral salpingectomy, however, the ovarian function remains unaltered. Recent studies have shown that prophylactic salpingectomy was helpful not only in preventing high-grade serous type ovarian cancer, but also in decreasing adnexal pathologies. With the publication of committee opinion, more practitioners have accepted this proposal, but some are more concerned about its disadvantages. This review illustrates the latest updates on salpingectomy as a preventive method for ovarian cancer, including its advantages and disadvantages, clinicians' opinions, public opinions, so as to find out Obstetricians' and Gynecologists' practice pattern related to opportunistic salpingectomy worldwide.

Nrf2 induces cisplatin resistance through activation of autophagy in ovarian carcinoma.

UNLABELLED: Cisplatin resistance is a major problem affecting ovarian carcinoma treatment. NF-E2-related factor 2 (Nrf2), a nuclear transcription factor, plays an important role in chemotherapy resistance. However, the underlying mechanism by which Nrf2 mediates cisplatin chemoresistance is unclear. METHODS: The human ovarian carcinoma cell line, A2780, and its cisplatin-resistant variant, A2780cp were cultivated. Cell viability was determined with WST-8 assay. Western blot was applied to detect the expression of Nrf2, Nrf2 target genes, and autophagy-related proteins. RNA interference was used to knock down target genes. Annexin V and propidium iodide (PI) staining was utilized to quantify apoptosis. The ultrastructural analysis of autophagosomes was performed by transmission electron microscopy (TEM). RESULTS: Nrf2 and its targeting genes, NQO1 and HO-1, are overexpressed in A2780cp cells compared with A2780 cells. Knocking down Nrf2 sensitized A2780cp cells to cisplatin treatment and decreased autophagy-related genes, Atg3, Atg6, Atg12 and p62 in both mRNA and protein levels. Furthermore, we demonstrated that in both cell lines cisplatin could induce the formation of autophagosomes and upregulate the expression of autophagy-related genes Atg3, Atg6 and Atg12. Treatment with an autophagy inhibitor, 3-Methyladenine (3-MA), or beclin 1 siRNA enhanced cisplatin-induced cell death in A2780cp cells, suggesting that inhibition of autophagy renders resistant cells to be more sensitive to cisplatin. Taken together, Nrf2 signaling may regulate cisplatin resistance by activating autophagy. CONCLUSIONS: Nrf2-activated autophagy may function as a novel mechanism causing cisplatin-resistance.