[Prevention and treatment of endometrial cancer].

Endometrial cancer is rising in incidence, especially in young women. This rise in incidence has implications for both primary prevention and screening in high-risk population. In the past several years, our understanding of the integration of clinically related genomic and pathologic data optimized the management of endometrial cancer. The updated 2023 FIGO staging includes the histological and molecular classification to better reflect the improved understanding of the heterogenous nature of endometrial carcinoma. Standard primary treatment is quite essential, however, selection of patients for adjuvant radiation or chemotherapy remains in controversy. Molecular characterization of endometrial cancer is becoming critical in directing treatment for advanced and recurrent disease, and the addition of immunotherapy to frontline chemotherapy is becoming the standard of care. More attention should be given to increase awareness of survivorship issues and improve patient quality-of-life.

MicroRNA-18a suppresses ovarian carcinoma progression by targeting CBX7 and regulating ERK/MAPK signaling pathway and epithelial-to-mesenchymal transition.

OBJECTIVE: Ovarian carcinoma (OC) is one prevalent fatal malignancy in gynecology. Currently, there is an imperative need to better investigate the pathogenesis of OC. Accumulating evidence has indicated that microRNAs (miRNAs) play pivotal roles in OC occurrence and development. In this study, we mainly investigated the potential roles of miR-18a in OC progression. PATIENTS AND METHODS: We first examined miR-18a expressions in OC tissue samples and cell lines using quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). Moreover, OC patients involved in current study were assigned into two groups based on the mean miR-18a expression level. Kaplan-Meier analysis was carried out to assess the overall survival rate of miR-18a in OC patients. Next, we investigated whether miR-18a could regulate OC cell proliferation abilities by using MTT (3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyl tetrazolium bromide) assays. Next, transwell assay was used to detect the effects of miR-18a on cell invasion and migration. We further performed Luciferase reporter assays by cotransfecting with miR-18a mimics and the Luciferase reporter vector containing CBX7 3'UTR-WT or MUT. We then performed immunohistochemistry (IHC) assays to determine the expression of CBX7 in OC tissues. RESULTS: QRT-PCR results indicated that miR-18a expressions were notably decreased in OC related cell lines and tissues. Moreover, the low miR-18a expression was related to the malignant phenotype and poor prognosis of OC patients. Overexpression of miR-18a in OC cells could prominently suppress the proliferation, migration and invasion abilities via modulating ERK/MAPK pathway and epithelial-to-mesenchymal transition (EMT). Furthermore, CBX7 was confirmed as a functional target of miR-18a, indicating that miR-18a exerted the suppressive functions in OC cells partially via the regulation of CBX7. Additionally, restoration of miR-18a remarkably reduced the OC tumor growth in vivo. CONCLUSIONS: Taken together, our study rationally suggested that miR-18a may serve as an effective diagnostic and therapeutic biomarker for OC.

Morphine pretreatment increases opioid inhibitory effects on maternal behavior.

Ongoing maternal behavior in rats is under the inhibitory influence of opiates. Exposure to drugs of abuse may result in a progressive and enduring enhancement of their reinforcing effects. Little attention has been paid to the possibility that puerperal treatment with morphine may lead to sensitization to this drug, ultimately influencing the effects of opiates on maternal behavior. The aim of the present study was to investigate if the abrupt withdrawal of repeated treatment with morphine chlorhydrate (MC) during late pregnancy and early lactation may influence maternal behavior in lactating rats. The premise that a possible change in sensitivity to the inhibitory effect of MC on maternal behavior would last at least until day 17 of lactation without any reinforcement was tested. In addition, the hypothesis that the MC-induced inhibition would be reversed by the opioid antagonist naloxone was also tested. In all experiments female Wistar rats were treated with MC (5.0 mg/kg/day, subcutaneous [s.c.]) or saline for 7 days starting on the 17th day of pregnancy. After the abrupt discontinuation of long-term treatment, animals were acutely challenged with MC (5.0 mg/kg, s.c.) or saline and tested for maternal behavior in three different experimental situations: first, on days 5, 10, and 17 postpartum (Experiment 1); second, on day 17 postpartum (Experiment 2); third, on day 6 postpartum following naloxone pretreatment (1.0 mg/kg; Experiment 3). In Experiment 1, animals were treated for 7 days with morphine and acutely challenged with MC (group MM). Experimental MM animals showed significantly longer latencies for all maternal behavior parameters than all other groups during all observation days. The other groups (treated with MC for 7 days and acutely challenged with saline, group MS; treated with saline for 7 days and acutely challenged with MC, group SM; and treated with saline for 7 days and acutely challenged with saline, group SS) did not differ significantly from one another. In Experiment 2, in which rats were submitted to a single test on day 17 of lactation, the MM group showed significantly longer latencies for all behavioral parameters as compared to group SM. Previous acute naloxone treatment (Experiment 3) reversed the inhibitory effects of MC on maternal behavior in lactating rats. These data suggest that repeated administration of MC to female rats during late pregnancy sensitizes the animals to the inhibitory effects of opioids on rat ongoing maternal behavior.