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Gueugneau, M

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]

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

Muckenthaler et al., 2017)

Given that the formal FDA reclassification has been announced but not yet officially published, patients and physicians are in a period of transition