Endometriosis-associated
ovarian cancers (EAOCs) including endometrioid and clear cell ovarian
carcinoma are subgroups of
epithelial ovarian carcinomas (EOCs), which is generally acknowledged as the most lethal gynecological
malignancy.
Endometriosis (ES), a common clinical disease among women, presents with clinical symptoms of
pelvic pain,
infertility, or adnexal masses with the formation of
endometrioma. It has long been considered to be a potential risk factor for developing EOCs, mainly of endometrioid and clear cell subtypes. Here, we compiled data from previous researches on deregulated molecular functions among ES and EOCs using gene set-based integrative analysis to decipher molecular and genetic relationships between ovarian ES and EOCs, especially EAOCs. We conclude that
epidermal growth factor receptor (ERBB) and
Phosphoinositide 3-kinases (PI3K)-related pathways are important in the
carcinogenesis of type I EOCs, including clear cell, endometrioid, and mucinous ovarian
carcinoma. Dysfunctional molecular pathways, such as deregulated
oxidoreductase activity, metabolism,
hormone activity,
inflammatory response, innate immune response, and cell-cell signaling, played key roles in the malignant transformation of EAOCs. Nine genes related to
inflammasome complex and
inflammasome-related pathway were identified, indicating the importance of
inflammation/immunity in EAOC transformation. We also collect progressive treatments of EAOC focused on targeted
therapies and
immunotherapy so far. This summarized information can contribute toward effective detection and treatment of EAOCs in the future.