Published online Apr 24, 2024. doi: 10.5306/wjco.v15.i4.496
Peer-review started: December 15, 2023
First decision: January 15, 2024
Revised: January 29, 2024
Accepted: March 18, 2024
Article in press: March 18, 2024
Published online: April 24, 2024
Processing time: 128 Days and 10.1 Hours
Endometriosis is an estrogen-dependent inflammatory disease, defined by the presence of functional endometrial tissue outside of the uterine cavity. This disease is one of the main gynecological diseases, affecting around 10%-15% women and girls of reproductive age, being a common gynecologic disorder. Although endometriosis is a benign disease, it shares several characteristics with invasive cancer. Studies support that it has been linked with an increased chance of developing endometrial ovarian cancer, representing an earlier stage of neoplastic processes. This is particularly true for women with clear cell carcinoma, low-grade serous carcinoma and endometrioid. However, the carcinogenic pathways between both pathologies remain poorly understood. Current studies suggest a connection between endometriosis and endometriosis-associated ovarian cancers (EAOCs) via pathways associated with oxidative stress, inflammation, and hyperestrogenism. This article aims to review current data on the molecular events linked to the development of EAOCs from endometriosis, specifically focusing on the complex relationship between the immune response to endometriosis and cancer, including the molecular mechanisms and their ramifications. Examining recent developments in immunotherapy and their potential to boost the effectiveness of future treatments.
Core Tip: Current investigations imply a relationship between endometriosis and endometriosis-associated ovarian cancers (EAOCs) through pathways involving oxidative stress, inflammation, and hyperestrogenism. This article endeavors to examine the current data on the molecular events associated with the development of EAOCs from endometriosis, with a particular emphasis on the intricate relationship between the immune response to endometriosis and cancer, including the molecular mechanisms and their implications.