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Aim: We aimed to estimate the disease burden and risk factors attributable to ovarian cancer, and epidemiological trends at global, regional, and national levels.Methods: We described ovarian cancer data on incidence, mortality, and disability-adjusted life-years as well as age-standardized rates from 1990 to 2017 from the Global Health Data Exchange database. We also estimated the risk factors attributable to ovarian cancer deaths and disability-adjusted life-years. Measures were stratified by region, country, age, and socio-demographic index. The estimated annual percentage changes and age-standardized rates were calculated to evaluate temporal trends.Results: Globally, ovarian cancer incident, death cases, and disability-adjusted life-years increased by 88.01, 84.20, and 78.00%, respectively. However, all the corresponding age-standardized rates showed downward trends with an estimated annual percentage change of −0.10 (−0.03 to 0.16), −0.33 (−0.38 to −0.27), and −0.38 (−0.32 to 0.25), respectively. South and East Asia and Western Europe carried the heaviest disease burden. The highest incidence, deaths, and disability-adjusted life-years were mainly in people aged 50–69 years from 1990 to 2017. High fasting plasma glucose level was the greatest contributor in age-standardized disability-adjusted life-years rate globally as well as in all socio-demographic index quintiles and most Global Disease Burden regions. Other important factors were high body mass index and occupational exposure to asbestos.Conclusion: Our study provides valuable information on patterns and trends of disease burden and risk factors attributable to ovarian cancer across age, socio-demographic index, region, and country, which may help improve the rational allocation of health resources as well as inform health policies.

Background: Oxidative stress is related to oncogenic transformation in kidney renal clear cell carcinoma (KIRC). We intended to identify a prognostic antioxidant gene signature and investigate its relationship with immune infiltration in KIRC.Methods: With the support of The Cancer Genome Atlas (TCGA) database, we researched the gene expression and clinical data of KIRC patients. Antioxidant related genes with significant differences in expression between KIRC and normal samples were then identified. Through univariate and multivariate Cox analysis, a prognostic gene model was established and all patients were divided into high- and low-risk subgroups. Single sample gene set enrichment analysis was adopted to analyze the immune infiltration, HLA expression, and immune checkpoint genes in different risk groups. Finally, the prognostic nomogram model was established and evaluated.Results: We identified six antioxidant genes significantly correlated with the outcome of KIRC patients as independent predictors, namely DPEP1 (HR = 0.97, P < 0.05), GSTM3 (HR = 0.97, P < 0.05), IYD (HR = 0.33, P < 0.05), KDM3B (HR = 0.96, P < 0.05), PRDX2 (HR = 0.99, P < 0.05), and PRXL2A (HR = 0.96, P < 0.05). The high- and low-risk subgroups of KIRC patients were grouped according to the six-gene signature. Patients with higher risk scores had poorer prognosis, more advanced grade and stage, and more abundance of M0 macrophages, regulatory T cells, and follicular helper T cells. There were statistically significant differences in HLA and checkpoint gene expression between the two risk subgroups. The performance of the nomogram was favorable (concordance index = 0.766) and reliably predicted the 3-year (AUC = 0.792) and 5-year (AUC = 0.766) survival of patients with KIRC.Conclusion: The novel six antioxidant related gene signature could effectively forecast the prognosis of patients with KIRC, supply insights into the interaction between cellular antioxidant mechanisms and cancer, and is an innovative tool for selecting potential patients and targets for immunotherapy.

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