Editorial: Molecular physiopathology of epithelial ovarian cancer: role of inflammation

Inflammation emerges as an important risk factor associated with epithelial ovarian cancer (EOC), the most common type of ovarian cancer. Increased inflammation and inflammatory mediators are also associated with poor prognosis and shorter survival in EOC patients. Inflammation can be caused by several factors such as repeated ovulation, peritoneal infection, endometriosis, obesity, or exposure to foreign particles (e.g., pollutants). A chronic inflammatory microenvironment is established by increased levels of reactive oxygen species (ROS), cytokines, chemokines, and growth factors produced by the ovaries, immune cells, tumor cells, and tumor stroma. This inflammatory microenvironment can cause DNA damage, activation of signaling pathways, epigenetic alterations, chromosomal aberrations, and the impaired innate and adaptive immune response to promote tumor cell initiation, progression, metastasis, and drug resistance (reviewed in Savant SS et al., Cancers (Basel). 2018 Jul 30;10(8):251). This Research Topic was proposed to collect new studies that address how chronic inflammation, caused by individual characteristics (e.g., genetics and hormone levels) and environmental factors (e.g., infections and pollutants), can promote EOC initiation, progression, immunosuppression, and therapy resistance. Five articles in this Research Topic provide some insights on how inflammation could affect EOC progression.