Fragmentary progress in endometriosis

A team from the Baylor College of Medicine has treated endometriosis in mice by blocking a pathway that produces a fragment of nuclear receptor coactivator 1 in endometrial tissue.1 Now, small molecule inhibitors are needed to elucidate the fragment's precise role in endometriosis and determine whether other pathway components are potential disease targets as well.

Endometriosis affects about 10% of women of reproductive age and involves the ectopic growth of tissue from the uterine lining (endometrium) in the peritoneal cavity, resulting in pelvic pain, infertility and other symptoms. The underlying pathogenesis of the disease is not well understood. What is known is that endometriotic lesions produce high levels of estrogen that enable growth of the lesion.

As a result most therapies reduce levels of estradiol and other estrogens. Treatments include GnRH/LHRH receptor-targeting compounds, aromatase inhibitors or contraceptives that can only halt-not reverse-lesion growth and may not completely control pain. Additionally, these therapies can have side effects such as cognitive deficits, hirsutism (excessive hairiness), the inability to conceive and an increased risk of osteoporosis.

Previous studies have shown that levels of nuclear receptor coactivator

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