SULT1E1 inhibition |
KER1: from SULT1E1 inhibition to increased E2 availability in the uterus |
0.61 |
0.06 |
KER2: from increased E2 availability in the uterus to ER activation |
0.75 |
0.06 |
Reduced availability of GnRH leading to uterine adenocarcinoma via increased estrogen availability at the target organ level |
KER1: reduced GnRH availability pulsatory release leads to decrease/delayed LH surge |
0.82 |
0.04 |
KER2: reduced LH surge leads to delayed ovulation |
0.82 |
0.05 |
KER3: delayed ovulation leads to estrogen dominance |
0.68 |
0.04 |
ER activation led to uterine adenocarcinoma via epigenetic modulation |
KER1: era activation leading to epigenetic modulation |
0.4 |
0.11 |
KER2: epigenetic modulation leading to altered expression of factors ruling proliferation |
0.62 |
0.1 |
KER3: expression of factors ruling proliferation leading to an increased proliferation (hyperplasia) |
0.84 |
0.05 |
KER4: increased proliferation leads to genetic instability (accumulation of mutations) |
0.54 |
0.06 |
KER5: genetic instability (accumulation of mutations) leads to uterine adenocarcinoma |
0.4 |
0.08 |