Published online Dec 10, 2014. doi: 10.5306/wjco.v5.i5.800
Revised: September 18, 2014
Accepted: November 7, 2014
Published online: December 10, 2014
Processing time: 153 Days and 12.7 Hours
Endometriosis is the leading cause of morbidity among premenopausal women and the complex pathogenesis of this disease remains controversial despite extensive research. This disease represents one of the most common gynecological problems. It is generally believed that this disease is due primarily to retrograde menstruation or transplantation of shed endometrium. Based on overwhelming data, ovarian endometrioma is considered a neoplastic process, since most endometriosis-associated ovarian carcinoma occur in the presence of atypical ovarian endometriosis. A study comparing patients with typical epithelial ovarian cancer with endometriosis-associated ovarian cancer demonstrated that the patients with the latter disease strongly differ in both biological and histological characteristics. The prevelance of this disease is not completely established, but approximately 15 percent of women suffer from this disease. In addition, we know about the possible links between endometriosis and cancer for almost 100 years. Despite clear evidence revealing that endometriosis increases ovarian cancer risks, it is possible that it may not affect disease progression after the appearance of ovarian cancer. However, despite clear evidence revealing that endometriosis increases ovarian cancer risk, our knowledge of the risk factors is far from established. In our review, we focused on the most recent approaches including possible biomarkers and genetic approaches.
Core tip: Endometriosis is a multifactorial disease, which, despite intensive research in the last decades, is still not fully explained. In addition, many questions remain to be answered as to the exact events leading from cysts to endometriosis-associated ovarian cancer. Surprisingly, having endometriosis might be less risky than undergoing in vitro fertilization, which can increase the risk of ovarian cancer. Our review summarizes current hypothesis on probable mechanisms and attributing factors such as longstanding estrogen stimulation, repeated heavy menstruation and early events on the molecular level. Thus far, however, no single one can be used for diagnosis or treatment.