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Blaustein’s Pathology of the Female Genital Tract pp 359–391Cite as

Precursor Lesions of Endometrial Carcinoma

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Abstract

Endometrial hyperplasia often precedes the development of endometrioid carcinoma, the most common type of endometrial carcinoma. More recently, studies have found that the risk of endometrial hyperplasia is associated with increasing body mass index and nulliparity [24]. In addition, obesity, anovulatory cycles, and exogenous hormones are associated with both endometrioid carcinoma and hyperplasia. All of these factors are thought to result in unopposed estrogen stimulation of the endometrium. The role of unopposed estrogen stimulation in the development of endometrial hyperplasia and carcinoma is further supported by studies demonstrating elevated serum estrogen levels in patients with endometrioid carcinoma [14, 72]. However, other histologic types of endometrial carcinoma appear to be unrelated to hormonal factors and hyperplasia [81]. Serous carcinoma is the prototypic endometrial carcinoma that is not related to estrogenic stimulation or hyperplasia. It usually arises in atrophic endometrium through a precursor lesion called endometrial intraepithelial carcinoma (EIC). Over the past 3 decades, clinicopathologic, immunohistochemical, and molecular genetic studies have provided data to support the development of a dualistic model of endometrial carcinogenesis. In this model, two types of precursor lesions precede the two most common types of endometrial carcinoma. Atypical hyperplasia (AH) is recognized as the precursor for endometrioid carcinoma and endometrial intraepithelial carcinoma (EIC) is recognized as the precursor for serous carcinoma. The following discussion summarizes current knowledge about these precursor lesions including their differential diagnosis, treatment, and relationship to endometrial carcinoma.

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Authors and Affiliations

  1. Department of Pathology and Laboratory Medicine, Weill Cornell Medical College and New York Presbyterian Hospital, 525 East 68th Street, Starr 1015, New York, NY, 10065, USA

    Lora Hedrick Ellenson

  2. Department of Pathology, Division of Gynecologic Pathology, Johns Hopkins University School of Medicine, Weinberg Building 2242, 401 N. Broadway, Baltimore, MD, 21231, USA

    Brigitte M. Ronnett

  3. Departments of Gynecology, Obstetrics, Pathology and Oncology, Division of Gynecologic Pathology, Johns Hopkins University School of Medicine, Weinberg Building Room 2242 401 N. Broadway, Baltimore, MD, 21231, USA

    Robert J. Kurman

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  1. Lora Hedrick Ellenson
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  2. Brigitte M. Ronnett
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  3. Robert J. Kurman
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Correspondence to Lora Hedrick Ellenson .

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Editors and Affiliations

  1. Departments of Gynecology, Obstetrics, Pathology and Oncology, The Johns Hopkins University School of Medicine and Director of Gynecologic Pathology, The Johns Hopkins Hospital, 401 N. Broadway, Weinberg Building Room 2242, Baltimore, MD, 21231, USA

    Robert J. Kurman (Richard W. TeLinde Distinguished Professor of Gynecologic Pathology) (Richard W. TeLinde Distinguished Professor of Gynecologic Pathology)

  2. Department of Pathology and Laboratory Medicine, Weill Cornell Medical College and New York Presbyterian Hospital, 525 East 68th Street, Starr 1015, New York, NY, 10065, USA

    Lora Hedrick Ellenson

  3. Department of Pathology, Johns Hopkins University School of Medicine, 401 N. Broadway, Weinberg Building 2242, Baltimore, MD, 21231, USA

    Brigitte M. Ronnett

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Ellenson, L.H., Ronnett, B.M., Kurman, R.J. (2011). Precursor Lesions of Endometrial Carcinoma. In: Kurman, R.J., Ellenson, L.H., Ronnett, B.M. (eds) Blaustein’s Pathology of the Female Genital Tract. Springer, Boston, MA. https://doi.org/10.1007/978-1-4419-0489-8_8

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  • DOI: https://doi.org/10.1007/978-1-4419-0489-8_8

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