Re: Possible Role of Ovarian Epithelial Inflammation in Ovarian Cancer.

In the September 1, 1999, issue of the Journal, Ness and Cottreau (1) discuss the role of inflammation in the pathogenesis of ovarian cancer. In reviewing the current literature, they conclude that neither incessant ovulation nor gonadotropin stimulation provides a completely satisfactory explanation for the genesis of ovarian cancer. They suggest that ovarian inflammation, with rapid DNA turnover, oxidative stress, and increased cytokine production, may be an important contributor to the development of ovarian malignancies. For the past 10 years, we have been studying the role of cytokines in human ovarian cancer biology. We have found that the cytokine network in this tumor is rich in proinflammatory cytokines, growth factors, and chemokines (2–4). Our experiments to date suggest that the proinflammatory cytokine tumour necrosis factora (TNF-a) is central to this ovarian cancer microenvironment. TNF-a is expressed in the epithelial tumor islands of ovarian cancer biopsy specimens (the level of expression increasing with tumor grade) and is implicated in the process of ovarian cancer