Endometriosis Gene Expression Heterogeneity and Biosignature: A Phylogenetic Analysis

Mones Abu-Asab, Mones Abu‐Asab, Ming Zhang, Dennis Amini, Nihad Abu-Asab, N. Abu-Asab, Hakima Amri
Obstetrics and gynecology international · 2011 · vol. 2011 , pp. 1–12 · doi:10.1155/2011/719059 · PMID:22203846 · PMC3238413 · W2157818905
article OA: gold CC0 ⤵ 8 in-corpus citations
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This phylogenetic analysis of endometriosis gene expression data identified heterogeneity among specimens and disruptions in key regulatory pathways, supporting ESR2's central role and distinct molecular biosignatures for eutopic and ectopic lesions.

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Abstract

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.

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endometriosis

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