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Artigo Produção Nacional Revisado por pares

BIBTEX RIS

Oxidative stress markers in blood and liver from diabetic dams and their offsprings

2015; Elsevier BV; Volume: 36; Issue: 4 Linguagem: Inglês

10.1016/j.placenta.2015.01.472

1532-3102

Bruna Dallaqua, Yuri Karen Sinzato, Franciane Quintanilha Gallego, Isabela Lovizutto Iessi, Sérgio Luís Felisbino, Jaqueline de Carvalho Rinaldi, Flávia Karina Delella, Iracema Mércia Calderon, Marilza Vieira Cunha Rudge, Tiago Rodrigues, Débora Cristina Damasceno,

Cancer, Lipids, and Metabolism

Chronic inflammation is postulated to influence prostate cancer progression. Preclinical studies have claimed that inflammatory mediators are involved in prostate cancer development and therefore suggested these as attractive targets for intervention. However, among the many pro-inflammatory mediators, there is no consensus regarding the identity of the primary one(s). In clinical studies, chronic inflammation has been found in prostate tumor specimens, and tissues resected for treatment of benign prostatic hyperplasia (BPH). Although collective evidence from molecular, experimental and clinical data suggests that inflammation can contribute or promote prostate carcinogenesis, an etiologic link has not yet been established. Moreover, the role of chronic inflammation in the onset of castration resistant and metastatic disease is unclear. Therefore it is important to open a dialog regarding recent findings on how chronic inflammatory mediators contribute to prostate cancer progression, and their usefulness to prevent disease progression. In this commentary, we assess the current literature with respect to chronic inflammation as a potential initiator and promoter of prostate carcinogenesis and discuss the prospects for its potential clinical applications.