Abstract
Endometriosis is characterized by progesterone resistance and hyperactivity of the AKT and MAPK pathways. We previously demonstrated that inhibition of AKT or MEK1/2 increases progesterone receptor levels in endometriotic stromal cells, and that aberrantly active AKT and MAPK may contribute to the pathogenesis of the disease. The objective of this study was to measure the effects of AKT and MEK1/2 inhibition on endometriotic stromal cell viability and proliferation.
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