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氧化应激在卵巢癌发病机制中的作用的最新进展。

Updates of the role of oxidative stress in the pathogenesis of ovarian cancer.

作者信息

Saed Ghassan M, Diamond Michael P, Fletcher Nicole M

机构信息

The Department of Obstetrics and Gynecology, Wayne State University School of Medicine, Detroit, MI, United States.

The Department of Obstetrics and Gynecology, Augusta University, Augusta, GA, United States.

出版信息

Gynecol Oncol. 2017 Jun;145(3):595-602. doi: 10.1016/j.ygyno.2017.02.033. Epub 2017 Feb 23.

DOI:10.1016/j.ygyno.2017.02.033
PMID:28237618
Abstract

Clinical and epidemiological investigations have provided evidence supporting the role of reactive oxygen species (ROS) and reactive nitrogen species (RNS), collectively known as oxidative stress, in the etiology of cancer. Exogenous factors such as chronic inflammation, infection and hypoxia are major sources of cellular oxidative stress. Specifically, oxidative stress plays an important role in the pathogenesis, neoangiogenesis, and dissemination of local or distant ovarian cancer, as it is known to induce phenotypic modifications of tumor cells by cross talk between tumor cells and the surrounding stroma. Subsequently, the biological significance of the relationship between oxidative stress markers and various stages of epithelial ovarian cancer highlights potential therapeutic interventions as well as provides urgently needed early detection biomarkers. In the light of our scientific research and the most recent experimental and clinical observations, this review provides the reader with up to date most relevant findings on the role of oxidative stress in the pathogenesis of ovarian cancer and the possible therapeutic implications.

摘要

临床和流行病学调查已提供证据,支持活性氧(ROS)和活性氮(RNS)(统称为氧化应激)在癌症病因学中的作用。慢性炎症、感染和缺氧等外源性因素是细胞氧化应激的主要来源。具体而言,氧化应激在局部或远处卵巢癌的发病机制、新生血管生成及扩散中起重要作用,因为已知它通过肿瘤细胞与周围基质之间的相互作用诱导肿瘤细胞的表型改变。随后,氧化应激标志物与上皮性卵巢癌各阶段之间关系的生物学意义突出了潜在的治疗干预措施,并提供了急需的早期检测生物标志物。鉴于我们的科学研究以及最新的实验和临床观察结果,本综述为读者提供了关于氧化应激在卵巢癌发病机制中的作用以及可能的治疗意义的最新相关发现。

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