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Complex mechanisms are proposed to explain the anti-estrogenic nature of AhR in breast and other cancers [132, 133] that are associated with the direct interaction with ER, resulting in the inhibition of DNA binding and disruption of coactivator/repressor recruitment [134, 135], that are associated with the anti-proliferative and pro-apoptotic effects of AhR agonist [136]

As of yet, there also exist three clinical trials whose status remains unknown

This adaptive mechanism enables the cell to utilize carbohydrates for energy production at the expense of fatty acids when there is an excess of acetyl-CoA

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