Abstract
Endometriosis is a debilitating gynecologic disease affecting up to 1-in-10 reproductive-aged women. Progesterone resistance is the primary cause of endometriosis treatment failure as well as contributes to endometriosis related infertility, however the mechanisms mediating progesterone resistance are not completely known. We have previously categorized human endometriotic lesions as having high, medium, or low PR expression in women undergoing surgery for endometriosis. While those with low PR failed to respond to P, some with moderate PR levels also failed to respond, suggesting that posttranslational modifications may mediate progesterone resistance.
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