Anti-Müllerian Hormone Type II Receptor Expression in Endometrial Cancer Tissue.

Aleksandra Piotrowska,Mariusz Krzysztof Majewski,Marta Szadurska-Noga,Marcin Jozwik,Piotr Dzięgiel,Marta Majewska,Marta Wiszpolska,Marek Gowkielewicz,Tomasz Wasniewski,Aleksandra Lipka,Jacek J. Nowakowski

doi:10.3390/cells9102312

Abstract

Anti-Müllerian hormone (AMH) is responsible for the Müllerian ducts’ regression in male fetuses. In cells of cancers with AMH receptors (AMHRII), AMH induces cell cycle arrest or apoptosis. As AMH occurs naturally and does not exhibit significant side effects while reducing neoplastic cell colonies, it can be considered as a potential therapeutic agent for cancer treatment. The purpose of this study was to assess the AMHRII expression in endometrial cancer (EC) in correlation to various demographic data and clinical conditions. Immunohistochemical analysis was used to assess AMHRII expression in EC tissue samples retrieved from 230 women with pre-cancerous state of endometrium (PCS) and EC. AMHRII was detected in 100% of samples. No statistical difference was observed for AMHRII expression depending on the histopathological type of EC, cancer staging, body mass index, and age, as well as the number of years of menstruation, births and miscarriages, and average and total breastfeeding time. Diabetes mellitus type 2 is the only factor that has an impact on AMHRII expression in EC tissue. Thus, this study supports the idea of theoretical use of AMH in EC treatment because all histopathological types of EC at all stages of advancement present receptors for AMH.

Highlights

During embryo development, the Müllerian ducts in females differentiate into the fallopian tubes, uterus, cervix, proximal vagina, and surface epithelium of the ovaries
Therehistopathological is a paucity of data on conditions that presencetoofFIGO, AMHBMI, typeparity, II receptors of miscarriages, total and average time breastfeeding, birth weight of the the following newborn,factors the length (AMHRII) in endometrial cancer (EC)
Among the analyzed patients in those studies, the average body mass index (BMI) was 30 to 45; the BMI value was not reflected in AMH receptor type II (AMHRII) expression

Summary

Introduction

The Müllerian ducts in females differentiate into the fallopian tubes, uterus, cervix, proximal vagina, and surface epithelium of the ovaries. Anti-Müllerian hormone (AMH) induces regression of the precursors to those structures [1]. The AMH gene, located in chromosome 19p13.3, contains five exons and encodes a 140-kDa dimeric glycoprotein, which belongs to the transforming growth factor β (TGF-β) superfamily [2]. As other factors in the TGF-β superfamily, AMH binds to the serine-threonine kinase receptor complex. AMH attaches directly to the unique AMHRII, which binds type I receptor [4]. Such a complex activates the SMAD protein and the other signaling cascades, which triggers transcription factors to induce gene expression, apoptosis, and regression of the Müllerian ducts [5]

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