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Immunohistochemical expression of hormone receptors, Ki-67, endoglin (CD105), claudins 3 and 4, MMP -2 and -9 in endometrial polyps and endometrial cancer type I

Authors Peres GF, Spadoto-Dias D, Bueloni-Dias FN, Leite NJ, Elias LV, Domingues MA, Padovani CR, Dias R

Received 22 December 2017

Accepted for publication 27 March 2018

Published 9 July 2018 Volume 2018:11 Pages 3949—3958


Checked for plagiarism Yes

Review by Single-blind

Peer reviewer comments 4

Editor who approved publication: Dr Yao Dai

Gustavo Filipov Peres,1 Daniel Spadoto-Dias,1 Flávia Neves Bueloni-Dias,1 Nilton José Leite,1 Leonardo Vieira Elias,1 Maria Aparecida Custódio Domingues,2 Carlos Roberto Padovani,3 Rogério Dias1

1Department of Gynecology and Obstetrics, 2Department of Clinical Pathology, 3Department of Biostatistics, Institute of Biosciences, Botucatu Medical School, São Paulo State University, Botucatu, São Paulo, Brazil

Objective: The aim of this study was to investigate the malignant potential of endometrial polyps (EP) by assessing the immunoexpressions of both estrogen receptor (ER) and progesterone receptor (PR), Ki-67 cell proliferation index, neovascularization network (endoglin – CD105), cellular adhesion molecules (claudins 3 and 4), and extracellular matrix proteins (MMP-2 and -9) in both EP and endometrioid adenocarcinoma (type I) in comparison with the normal endometrium.
Study design: This is a cross-sectional comparative study. Patients were identified from the database of Botucatu Medical School, São Paulo State University (BMS-UNESP) Clinical Pathology Laboratory.
Setting: The study was conducted using a convenience sample of patients attending the Sectors of Gynecologic Endoscopy and Family Planning and Gynecologic Oncology of the Department of Gynecology and Obstetrics of BMS-UNESP, Brazil.
Patients: A total of 90 women were allocated into the following three groups: EP without atypia (EP, n=30), endometrioid endometrial cancer (EC, n=30), and normal endometrium (control, n=30).
Methods: Epidemiological and clinical data were obtained by reviewing medical records. Adenocarcinoma and control cases were assessed using the tissue microarray technique. The immunoexpressions of ER, PR, Ki-67, CD105, claudins 3 and 4, and MMP-2 and -9 were assessed in paraffin blocks containing sections of the largest polyploid lesion fragment and tissue microarray recipient blocks.
Major results: Compared to the control group, significant differences in the expression of ER (P<0.001), PR (P<0.05), Ki-67 (P<0.001), CD105 (P<0.001), and claudin 3 (P<0.001) were observed in EP and EC. No significant differences were found between EP and EC (P≥0.05). MMP-2 and -9 expression were nearly absent in all groups.
Conclusion: The malignant potential of EP could not be determined through the immunohistochemical parameters used in this study. No MMP-2 or -9 expression was observed in any endometrial tissue sample. Further studies are necessary for a better understanding of the biomolecular mechanisms underlying endometrial carcinogenesis.

Keywords: endometrium/pathology, immunohistochemistry, endometrial neoplasia, polyps/epidemiology

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