List of abbreviations: DDA: dendrogenin A; 5,6-EC: 5,6-epoxycholesterol; 5,6α-EC: 5,6α-epoxycholesterol; 5,6β-EC: 5,6β-epoxycholesterol; CT: Cholestane-3β,5α,6β-triol; OCDO: 6-oxo-cholestan-3β,5α-diol ; AEBS: microsomal antioestrogen binding site; D8D7I: 3β-hydroxyterol-Δ8-Δ7-isomerase; EPB: emopamyl binding protein; DHCR7: 3β-hydroxyterol-Δ7-reductase; ChEH: cholesterol-5,6-epoxide hydrolase; HSD11B1: 11β-hydroxysteroid dehydrogenase type 1; H6PD, HSD11B2: 11β-hydroxysteroid dehydrogenase type 2; ER: estrogen receptor; LXR: liver-X-receptor; GR: glucocorticoid receptor; BC: breact cancer; ER(+)BC: oestrogen receptor positive BC; TNBC, triple negative BC; HER2: Epithelial Growth Factor Receptor of type 2; SERM: selective ER modulators; AI: aromatase inhibitors; 27-HC: 27-hydroxycholesterol; CXCR2: C-X-C Motif Chemokine Receptor 2; SULT2B1b: hydroxysteroid sulfotransferase 2B1b; CYP27A1: Cytochrome P450 Family 27 Subfamily A Member 1; 5,6-ECS: 5,6α-epoxy-cholesterol-3β-sulfate; zymostenol: cholest-8-ene-3β-ol.

Aknowledgement: We thank members of the ENOR consortium for fruitful discussions.

Competing interests: The authors declare no competing financial interests.

Funding: This work was funded by an internal grant from the ‘Institut National de la Santé et de la Recherche Médicale’ and the ‘Université de Toulouse III’, the Fondation de France (R11166BB), the Association pour la Recherche sur le Cancer (PJA 2013 12 00 342), the INCA translational (PRTK-K15-118), the INCA (PLBIO-2018-145), the Fondation Toulouse Cancer Santé (2017CS065); and the associations “Céline”, “Flo” and ”Elles” for their generous support.