The aim of this study was to summarize our experience of ovarian cancer diagnosed during pregnancy, to review the literature concerned, and to discuss the rationale for therapy. Twenty-two patients of ovarian malignancies complicating pregnancy were treated at Peking Union Medical College Hospital between 1985 and 2003. Data on treatment and follow-up were reviewed, and their outcomes were analyzed by survival analysis. The incidence of ovarian carcinoma complicating pregnancy in the series was 0.073/1000 pregnancies. Nine (40.9%) were found with ovarian malignant germ cell tumors, six (27.3%) with low malignant potential tumors, five (22.7%) with invasive epithelial tumors, and two (9.1%) with sex cord stromal tumors. Sixteen (72.7%) of the patients were diagnosed in stage I and had achieved complete remission. Four of the five in advanced stage died. Ascites presenting at diagnosis implies advanced disease and gloomy prognosis. The mean follow-up was 47.8 months. The prognosis was significantly related with stage and histologic type (P < 0.05). Thirteen healthy live babies were recorded in this group, and one premature newborn died of respiratory distress syndrome. The clinical characters and prognosis of ovarian cancers complicating pregnancy are similar to those of nonpregnant, reproductive-age women. Management depends on histology of the tumor, stage of the tumor, and the term of the pregnancy. In most of cases, conservative surgical treatment could be performed with adequate staging and debulking equal to the treatment of nonpregnant women. Chemotherapy is not contraindicated during the second or third trimester, but the choice of couple must be considered.
The inactivation of plasminogen activator inhibitor-1 (PAI-1) has been shown to exert beneficial effects in age-related vascular diseases. Limited information is available on the molecular mechanisms regarding the negatively regulated expression of PAI-1 in the vascular system. In this study, we observed an inverse correlation between SIRT1, a class III histone deacetylase, and PAI-1 expression in human atherosclerotic plaques and the aortas of old mice, suggesting that internal negative regulation exists between SIRT1 and PAI-1. SIRT1 overexpression reversed the increased PAI-1 expression in senescent human umbilical vein endothelial cells (HUVECs) and aortas of old mice, accompanied by decreased SA-β-gal activity in vitro and improved endothelial function and reduced arterial stiffness in vivo. Moreover, the SIRT1-mediated inhibition of PAI-1 expression exerted an antisenescence effect in HUVECs. Furthermore, we demonstrated that SIRT1 is able to bind to the PAI-1 promoter, resulting in a decrease in the acetylation of histone H4 lysine 16 (H4K16) on the PAI-1 promoter region. Thus, our findings suggest that the SIRT1-mediated epigenetic inhibition of PAI-1 expression exerts a protective effect in vascular endothelial senescence.
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