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When taken together with our earlier study using Klf9 -null mutant lesions under the same dietary regimen (Heard et al., 2016), our findings suggest that dietary influences on endometriosis progression may be dependent in part, on lesion genotype

oestradiol (E2) bind ER or ER in mammary epithelial cells, followed by receptor dimerisation, nuclear translocation and direct transcriptional regulation of EREs in promoter regions on target genes that regulate cell proliferation cyclin D1, c-Myc -, survival Bcl-2 or survivin -, angiogenesis VEGF -, EMT Snail, Twist -, metastasis MMPs (185), as non-genomic oestrogen signalling via membrane-localized ER and G proteincoupled oestrogen receptor (GPER) leads to rapid stimulation of PI3K/Akt, MAPK/ERK and Src pathways interacting further impetus to mitogenic and anti-apoptotic effects