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BRAF inhibitors such as vemurafenib and dabrafenib bind to AhR transcription factor. This activates an off-target transcriptional program regardless of the BRAF mutational status of the cells. This new mechanism may play a role in the generation of melanoma resistance and BRAF inhibitor side effects that are not explained by the MAPK paradoxical effect alone.
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This page is a summary of: Sustained activation of the Aryl hydrocarbon Receptor transcription factor promotes resistance to BRAF-inhibitors in melanoma, Nature Communications, November 2018, Springer Science + Business Media,
DOI: 10.1038/s41467-018-06951-2.
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