RESUMEN
Purpose: To construct a new clinical staging system including the number of lymph node metastases to supplement the International Federation of Gynecology and Obstetrics (FIGO) staging for the prognosis of endometrial carcinoma patients. Methods: This cohort study retrieved the data of 28,824 patients confirmed as endometrial carcinoma between 2010 and 2015 in the surveillance, epidemiology, and end results (SEER) database. COX risk proportional model was established to evaluate the association between FIGO staging with the all-cause mortality of endometrial carcinoma. The diagnostic value of FIGO staging and the new staging for the mortality of patients were evaluated by receiver operator characteristic curve (ROC). Hazard ratio (HR) and 95% confidence interval (CI) were effect size. Results: The 5-year survival rate of all participants was 77.21%. The median follow-up time was 60.00 (60.00,60.00) months. Patients at FIGO staging IB (HR=1.75, 95% CI: 1.62-1.90), FIGO staging II (HR=2.22, 95% CI: 2.00-2.47), FIGO staging IIIA (HR=2.74, 95% CI: 2.43-3.09), FIGO staging IIIB (HR=4.07, 95% CI: 3.48-4.76), FIGO staging IIIC1 (HR=3.84, 95% CI: 3.52-4.20), FIGO staging IIIC2 (HR=4.52, 95% CI: 4.09-4.99), FIGO staging IVA (HR=5.56, 95% CI: 4.58-6.74), and FIGO staging IVB (HR=7.62, 95% CI: 6.94-8.36) were associated with increased risk of all-cause mortality of endometrial carcinoma patients. After adding positive lymph nodes as another covariate in Model 3, the effect on of FIGO staging survival was reduced when the FIGO staging was higher than stage III/IV. The C-index of the new staging 0.781 (95% CI: 0.774-0.787) was higher than FIGO staging 0.776 (95% CI: 0.770-0.783). Conclusion: Our new staging using the number of positive lymph nodes supplement to the FIGO staging was superior than the FIGO staging for predicting the prognosis of endometrial cancer patients, which might help more accurately identify endometrial carcinoma patients who were at high risk of mortality and offer timely treatments in these patients.
RESUMEN
Ellagic acid has been reported to possess various activities, including anti-inflammatory, anti-oxidative, antiviral and anticancer abilities. However, the effect and underlying molecular mechanism of ellagic acid on cervical carcinoma remain unclear. Therefore, the present study aimed to investigate the effects of ellagic acid on human cervical carcinoma cells and the molecular mechanism involved. The present study assessed the survival of HeLa cells cultured in vitro using an MTT assay. Apoptosis rate and cell cycle of HaLa cells were measured using an Annexin V-Fluorescein isothiocyanate/propidium iodide Apoptosis Detection and Cell Cycle Analysis kits, respectively, following treatment with varying concentrations of ellagic acid. Further effects of ellagic acid on HeLa cells was assessed using flow cytometry and western blotting. Ellagic acid treatment significantly inhibited cell proliferation of the human cervical carcinoma HeLa, SiHa and C33A cells. In HeLa cells, it was observed that ellagic acid arrested the cell cycle at G1 phase, induced cell apoptosis, suppressed the phosphorylation of Janus kinase 2 and signal transducer and activator of transcription 3 (STAT3), as well as modulated the expression of associated proteins. Collectively, the results of the present study provide evidence that ellagic acid inhibits cervical carcinoma cell proliferation, and induces apoptosis and cell cycle arrest at G1 phase possibly via the regulation of STAT3 signaling.