THE CLINICOMORPHOLOGICAL AND MOLECULAR BIOLOGICAL CHARACTERISTICS OF ADENOMYOSIS CONCURRENT WITH ENDOMETRIAL ADENOCARCINOMA


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Objective. To study the clinicomorphological and molecular biological characteristics of adenomyosis concurrent with endometrial adenocarcinoma. Material and methods. The study material was uteri removed from 70 patients, including 37 with adenomyosis (AM) concurrent with endometrioid adenocarcinoma (EAC) of the corpus uteri (Group 1) and 33 with AM without EAC (Group 2). Monoclonal and polyclonal antibodies against ApoCas, Ki-67, COX-2, EGFR, VEGF, MMP-2, MMP-9, and TIMP-1 were used as primary antibodies. Results. The clinical features of AM concurrent with EAC were found, which were characterized by a predominance of the symptoms of endometrial carcinoma and the presence of active AM with atypical epithelial hyperplasia. Examination of AM foci revealed the following 4 types of epithelial changes: proliferation-phase type; hyperplasias with and without atypia, and those with atrophy. Immunohistochemical study showed a considerable increase in Ki-67 expression with a less marked rise in ApoCas, as well as COX-2. The activity of VEGF and EGFR enhanced with epithelial changes in the foci of proliferation-phase AM to hyperplasia with atypia. The concomitance of AM and EAC is not incidental, noted for the clinical symptoms and morphological and molecular biological characteristics of AM. This fact is confirmed by not on1y the high rate of EAC concurrent with AM, the probable common source of origin - basal endometrial cells, and the presence of epithelial hyperplasia with atypia in the foci of AM in patients with cancer of the corpus uteri. Adenomyosis differs from EAC not only morphologically, but also in the expression of molecular markers in the epithelial cells: it shows the high activity of E-cadherin, preserved close contacts with membrane claudin 3 and 5 staining; significant TIMP-1 expression with the high activity of metalloproteinases (MMP). This all determines differences in the mechanisms of invasion: unlike adenocarcinoma, AM spreads by invasion of stromal cells.

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作者简介

E. KOGAN

Academician V.I. Kulakov Research Center of Obstetrics, Gynecology, and Perinatology, Ministry of Health and Social Development of Russia

I. SIDOROVA

I.M. Sechenov First Moscow State Medical University

Department of Obstetrics and Gynecology, Therapy Faculty One

N. NIZYAEVA

I.M. Sechenov First Moscow State Medical University

Email: niziaeva@gmail.com
Department of Morbid Anatomy, Therapy Faculty

T. DEMURA

Academician V.I. Kulakov Research Center of Obstetrics, Gynecology, and Perinatology, Ministry of Health and Social Development of Russia

L. EZHOVA

Academician V.I. Kulakov Research Center of Obstetrics, Gynecology, and Perinatology, Ministry of Health and Social Development of Russia

A. UNANYAN

I.M. Sechenov First Moscow State Medical University

Department of Obstetrics and Gynecology, Therapy Faculty One

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