It has been more than fifty years since Hertig first reported that women with endome-trial cancer may have diagnosable precursor lesions that antedate cancer occurrence by several years (14). A clinical concept of premalignant disease based on heightened risk of cancer outcomes in women with endometrial "hyperplasias" quickly emerged as a diagnostic entity and therapeutic target (15,16). Statistical association of cancer outcome with presence or absence of atypical endometrial hyperplasia, as observed in study populations, became the basis for a cancer prevention strategy incorporating timely precancer diagnosis and ablation (16). In practice, classification into pure premalignant and benign categories using hyperplasia criteria was at best fuzzy, because of the subjective nature of the histological criteria discovery process, limited access to patients of defined clinical outcomes, and poor diagnostic reproducibility during implementation. This is a particular problem in the case of precursors to type I cancers, which are admixed in most study populations with "hyperplasias" caused by the systemic effects of prolonged estrogen exposure.
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