Patients with endometriosis carry the potential risk for ovarian cancer later in life, but the histogenesis of endometriosis-associated ovarian cancer (EAOC) still remains unclear. This review outlines recent advances in the understanding of the genetic background and histogenesis of EAOC. This article reviews the English-language literature between 2000 and 2017. The oxidative stress, inflammation, immune response and hormone activity are mainly associated with deregulated pathways contributing to the carcinogenesis of EAOC. Ovarian endometrioid carcinoma (EC) and clear cell carcinoma (CCC) respond similarly to inflammatory and oxidative stimuli and share a common genetic abnormality. Several markers of histogenesis have been used to assess whether EC and CCC arise from the same clone or different precursor cells. Expression of various histogenesis markers may be epigenetically regulated in distinct EAOC subtypes. Secretory cells and ciliated cells in endometriosis are candidates for cells of origin of EC and CCC, respectively. In conclusion, EAOC may arise from the different precursor cells that undergo similar genetic changes.