Endometriosis-associated ovarian carcinogenesis induced by iron-dependent oxidative stress

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The aim of the present study is to describe genomic instability, genetic polymorphisms and their haplotype, epigenetic alterations associated with endometriosis predisposition, and the key factors that have been linked to endometriosis-related ovarian neoplasms. Retrograde menstruation leads to iron overload, which facilitates the accumulation of somatic mutations through a Fenton reaction-mediated oxidative stress. There seems to be at least three spatiotemporally distinct phases of endometriosis development: The initial phase of genetic background inherited from parents would be followed by the second big wave of epigenetic modifications in the female offspring and the final phase of the iron overload that is subject to dynamic modulation later in life. The dramatic regulation of endometriosis susceptibility genes may come from a mechanism responsible for epigenetic and genetic mutations based on the microenvironmental changes.