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In general, increased methylation results in lower gene expression

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Epigenetic modifications, including hypomethylation of ER and aromatase promoters, further sustain this estrogen-driven phenotype, with endocrine-disrupting chemicals (EDCs) such as dioxins and phthalates potentially exacerbating these epigenetic alterations ( Progesterone resistance, characterized by impaired progesterone receptor (PR) signaling despite bioavailable progesterone, perpetuates ectopic lesion survival and contributes to infertility ( The interplay of estrogen dominance and progesterone resistance disrupts endometrial homeostasis, directly impacting fertility

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In a clinical environment, safety protocols are non-negotiable