Clinical outcome in diagnostically ambiguous foci of ‘gland crowding’ in the endometrium

Division of Women's and Perinatal Pathology, Department of Pathology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA.
Modern Pathology (Impact Factor: 6.19). 11/2010; 23(11):1486-91. DOI: 10.1038/modpathol.2010.140
Source: PubMed


Premalignant endometrial lesions (endometrial intraepithelial neoplasia (EIN)) are clonal neoplasms that arise focally and can be diagnosed using specific criteria: (1) area of glands exceeds that of stroma (glands/stroma >1), (2) nuclear and/or cytoplasmic features of epithelial cells differ between architecturally abnormal glands and normal background glands, and (3) maximum linear dimension exceeds 1 mm. However, localized groups of crowded endometrial glands may be encountered that do not fulfill all of the criteria for EIN, are interpreted as ambiguous, and are reported as 'focal gland crowding'. We conducted a retrospective study of gland crowding using a free-text index search for this term in our pathology files. The age of the patients, number of subsequent specimens, the duration, and the outcome of the follow-ups were recorded. Of the 71,579 consecutive gynecological pathology reports, 206 (0.3%) 'gland crowding' cases were identified, in which 69% (143/206) had follow-up sampling. Of these, 33 (23%) had an outcome diagnosis of EIN (27 cases; 19%) or carcinoma (6 cases; 4%). Included were 18 cases (55%) diagnosed within the first year and presumed concurrent, and an additional 15 (45%) discovered after 1 year and interpreted as a later phase of disease or new events. The term 'crowded glands' is a highly significant finding that carries a substantial risk of an outcome of EIN and occasionally malignancy. It underscores the importance of follow-up when some but not all of the criteria for EIN are encountered in the appropriate clinical setting.

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    ABSTRACT: Endometrial intraepithelial neoplasia (EIN) is a monoclonal premalignant endometrial glandular lesion that precedes the development of endometrioid-type endometrial adenocarcinoma. EIN arises through complex interactions involving the sequential accumulation of genetic damage in endometrial glands and the positive selective pressure of unopposed estrogen. Recent data have revealed a preclinical latent precursor lesion composed of mutated but morphologically nondescript glands that may persist for years in normal-appearing premenopausal cycling endometrium. This latent precursor shares many of the molecular features of EIN and endometrial adenocarcinoma, including frequent inactivation of both the tumor suppressor gene PTEN and the paired box-containing gene PAX2. Upon progression to EIN, the distinctive appearance of crowded and cytologically altered glands heralds a 45-fold increased risk of developing endometrial adenocarcinoma. To preserve the high predictability of EIN for concurrent/ subsequent adenocarcinoma, strict adherence to defined diagnostic criteria is essential. These criteria, as well as potential diagnostic pitfalls and their resolution, are discussed herein.
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