Although endometriosis frequently involves multiple sites in the pelvis, malignancies associated with this disease are mostly con ned to the ovaries, evolving from an endometrioma. Endometriomas present a 2-3-fold increased risk of transformation in clear-cell, endometrioid, and possibly low-grade serous ovarian cancers, but not in mucinous ovarian cancers. ese last cancers are, in some aspects, di erent from the other epithelial ovarian cancers, as they do not appear to be decreased by the inhibition of ovulation and menstruation. e step by step process of transformation from typical endometrioma, through atypical endometrioma, nally to ovarian cancer seems mainly related to oxidative stress, in ammation, hyperestrogenism, and speci c molecular alterations. Particularly, activation of oncogenic KRAS and PI3K pathways and inactivation of tumor suppressor genes PTEN and ARID1A are suggested as major pathogenic mechanisms for endometriosis associated clear-cell and endometrioid ovarian cancer. Both the risk for endometriomas and their associated ovarian cancers seems to be highly and similarly decreased by the inhibition of ovulation and retrograde menstruation, suggesting a common pathogenetic mechanism and common possible preventive strategies during reproductive life.
Although endometriosis frequently involves multiple sites in the pelvis, malignancies associated with this disease are mostly
confined to the ovaries, evolving from an endometrioma. Endometriomas present a 2-3-fold increased risk of transformation
in clear-cell, endometrioid, and possibly low-grade serous ovarian cancers, but not in mucinous ovarian cancers. These last
cancers are, in some aspects, different from the other epithelial ovarian cancers, as they do not appear to be decreased by the
inhibition of ovulation and menstruation.The step by step process of transformation fromtypical endometrioma, through atypical
endometrioma, finally to ovarian cancer seems mainly related to oxidative stress, inflammation, hyperestrogenism, and specific
molecular alterations. Particularly, activation of oncogenic KRAS and PI3K pathways and inactivation of tumor suppressor genes
PTEN and ARID1A are suggested as major pathogenic mechanisms for endometriosis associated clear-cell and endometrioid
ovarian cancer. Both the risk for endometriomas and their associated ovarian cancers seems to be highly and similarly decreased
by the inhibition of ovulation and retrograde menstruation, suggesting a common pathogenetic mechanism and common possible
preventive strategies during reproductive life.
