Endometriosis Gene Expression Heterogeneity and Biosignature: A Phylogenetic Analysis

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 micro...

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Published inObstetrics and Gynecology International Vol. 2011; no. 2011; pp. 208 - 219
Main Authors Abu-Asab, Mones S., Zhang, Ming, Amini, Dennis, Abu-Asab, Nihad, Amri, Hakima
Format Journal Article
LanguageEnglish
Published Cairo, Egypt Hindawi Limiteds 01.01.2011
Hindawi Puplishing Corporation
Hindawi Publishing Corporation
Hindawi Limited
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Summary: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.
Bibliography:ObjectType-Article-1
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Academic Editor: Kimberly K. Leslie
ISSN:1687-9589
1687-9597
1687-9589
DOI:10.1155/2011/719059