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Updated: Aug 22, 2025

Generation of Multicellular Human Primary Endometrial Organoids
Published on: October 4, 2019
Endometrial Hyperplasia
Kari L Ring1, Anne M Mills, Susan C Modesitt
1Gynecologic Oncology Division, Department of Obstetrics and Gynecology, and the Department of Pathology, University of Virginia Health System, Charlottesville, Virginia; and the Gynecologic Oncology Division, Gynecology and Obstetrics Department, Emory University, Atlanta, Georgia.
Abstract:
The objectives of this Clinical Expert Series on endometrial hyperplasia are to review the etiology and risk factors, histologic classification and subtypes, malignant progression risks, prevention options, and to outline both surgical and nonsurgical treatment options. Abnormal uterine and postmenopausal bleeding remain the hallmark of endometrial pathology, and up to 10-20% of postmenopausal bleeding will be either hyperplasia or cancer; thus, immediate evaluation of any abnormal bleeding with either tissue procurement for pathology or imaging should be undertaken. Although anyone with a uterus may develop atypical hyperplasia, also known as endometrial intraepithelial neoplasia (EIN), genetic predispositions (eg, Lynch syndrome), obesity, chronic anovulation, and polycystic ovarian syndrome all markedly increase these risks, whereas use of oral contraceptive pills or progesterone-containing intrauterine devices will decrease the risk. An EIN diagnosis carries a high risk of concomitant endometrial cancer or eventual progression to cancer in the absence of treatment. The definitive and curative treatment for EIN remains hysterectomy; however, the obesity epidemic, the potential desire for fertility-sparing treatments, the recognition of varying rates of malignant transformation, medical comorbidities, and an aging population all may factor into decisions to employ nonsurgical treatment modalities.
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