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Current molecular aspects of the carcinogenesis of the uterine endometrium
  1. M. Inoue
  1. Department of Obstetrics and Gynecology, School of Medicine, Kanazawa University, Kanazawa, Japan
  1. Address correspondence and reprint requests to: Masaki Inoue, MD, PhD, Department of Obstetrics and Gynecology, School of Medicine, Kanazawa University, 13–1, Takaramchi, Kanazawa, Ishikawa, 920–0934 Japan. E-mail: masaki-i{at}


Carcinogenesis in many tissues is a multistep process accompanied by a variety of morphologic, biochemical, and genetic changes in each step. It is well known that endometrial cancers arise through a series of precursor lesions, simple, complex, and atypical hyperplasia, by unopposed and prolonged estrogen stimulation. It is also accepted that there is an estrogen-independent type in which the precursor lesions are not identified. Recent molecular-based evidence has revealed three possible pathways for endometrial carcinogenesis, namely hyperplasia, metaplasia, and de novo pathways. The pathways each have their own features in both histopathology and molecular biology. Such understanding of the molecular profile of endometrial carcinoma prompted us to revise the classic criteria in histopathology regarding endometrial carcinogenesis. The recent molecular-based studies have provided a concept of endometrial intraepithelial lesions: endometrial intraepithelial neoplasia (EIN) as the precursor lesions of endometrial carcinomas. The new terminology might improve cancer screening protocols and treatment modalities.

  • carcinogenesis
  • endometrial cancer
  • endometrial hyperplasia
  • endometrial metaplasia
  • estrogen

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