Table of Contents Author Guidelines Submit a Manuscript
Obstetrics and Gynecology International
Volume 2011 (2011), Article ID 719059, 12 pages
Clinical Study

Endometriosis Gene Expression Heterogeneity and Biosignature: A Phylogenetic Analysis

1Laboratory of Immunology, Section of Immunopathology, National Eye Institute, National Institutes of Health, Bethesda, MD 20892, USA
2Department of Biochemistry and Cellular & Molecular Biology, Georgetown University Medical Center, Washington, DC 20007, USA
3Department of Obstetrics and Gynecology, Georgetown University Hospital, Washington, DC 20007, USA
4Armidale Rural Referral Hospital, University of New England and The University of Newcastle, Armidale, NSW 2351, Australia

Received 13 July 2011; Accepted 13 September 2011

Academic Editor: Kimberly K. Leslie

Copyright © 2011 Mones Abu-Asab et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Endometriosis is a multifactorial disease with poorly understood etiology, and reflecting an evolutionary nature where genetic alterations accumulate throughout pathogenesis. Our objective was to characterize the heterogeneous pathological process using parsimony phylogenetics. Gene expression microarray data of ovarian endometriosis obtained from NCBI database were polarized and coded into derived (abnormal) and ancestral (normal) states. Such alterations are referred to as synapomorphies in a phylogenetic sense (or biomarkers). Subsequent gene linkage was modeled by Genomatix BiblioSphere Pathway software. A list of clonally shared derived (abnormal) expressions revealed the pattern of heterogeneity among specimens. In addition, it has identified disruptions within the major regulatory pathways including those involved in cell proliferation, steroidogenesis, angiogenesis, cytoskeletal organization and integrity, and tumorigenesis, as well as cell adhesion and migration. Furthermore, the analysis supported the potential central involvement of ESR2 in the initiation of endometriosis. The pathogenesis mapping showed that eutopic and ectopic lesions have different molecular biosignatures.