Loss of PTEN function by mutational or other mechanisms is an early event in endometrial tumorigenesis that may occur in response to known endocrine risk factors and offers an informative immunohistochemical biomarker for premalignant disease. Individual PTEN-negative glands in estrogen-exposed endometria are the earliest recognizable stage of endometrial carcinogenesis. Proliferation into dense clusters that form discrete premalignant lesions follows.

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A task force of experts in the field of diagnostic DNA image cytometry, invited by the ESACP, and further scientists or physicians revealing experience in that diagnostic procedure (names are given in Addendum A), agreed upon the following 4th updated Consensus Report on Standardised Diagnostic DNA Image Cytometry during the 7th International Congress of that society in Caen, 2001. This report is based on the three preceding ones [6,14,17]. It deals with the following items: – Critical review and update of the definitions given in the 1997 Consensus Update; – Review and detailed description of basic terms, principles and algorithms for diagnostic interpretation; – Recommendations concerning diagnostic or prognostic applications in specific fields of tumour pathology. This update is not aimed to substitute the 1997 consensus, but to make necessary addenda and give more detailed descriptions of those items not unequivocally to interpret by potential users of the methodology.

Objective-To compare the accuracy of cancer progression prediction of the molecular-genetics and morphometry-based Endometrial Intraepithelial Neoplasia (EIN) and the WHO-94 classification schemes in endometrial hyperplasias.Study Design-A multicenter multivariate analysis of 477 endometria, with a required 1 year minimum cancer-free interval from the index biopsy (1-18 years follow-up). Comparison with 197 patients with <1 year follow-up.Results-24/477 (5.0%) hyperplasias progressed to cancer over an average of 4 years (10 yrs maximum). According to WHO94, 16/123 (13%) atypical and 8/354 (2.3%) non-atypical hyperplasias progressed (Hazard ratio=HR=7). 22/118 (19%) of EINs and 2/359 (0.6%) of non-EINs progressed (HR=45). EIN was prognostic within each WHO94 subcategory. Progression rates in simple (SH), complex (CH), simple atypical (SAH), and complex atypical (CAH) hyperplasias with EIN were 3, 22, 17 and 38% respectively, contrasting with 0.0-2.0% if EIN was absent. EIN detected precancer (sensitivity 92%) better than WHO94 atypical hyperplasias collectively (67%) or CAH alone (46%). With Cox regression EIN was the strongest prognostic index of future endometrial cancer. The same holds for patients with <1 year follow-up (HR for EIN, Atypia and CAH 58, 7 and 8 respectively). Conclusions-The