This Article Full Text (PDF) References Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Add to Saved Citations Download to citation manager Request Permissions Request Reprints Add to My Marked Citations Citing Articles Citing Articles via Google Scholar Citing Articles via Scopus Google Scholar Articles by Gogusev, J. Articles by Levradon, M. Search for Related Content PubMed PubMed Citation Articles by Gogusev, J. Articles by de Jolinière, J. B. Articles by Telvi, L. Articles by Doussau, M. Articles by Stojkoski, A. Articles by Levradon, M. Social Bookmarking                         What's this?

Cellular and Genetic Constitution of Human Endometriosis Tissues

INSERM U507, Hôpital Necker, Paris; Service de Gynécologie Obstétrique, Hôpital Beaujon, Clichy; Service de Cytogénétique, Hôpital St. Vincent de Paul, Paris, France; INSERM U507, Hôpital Necker, 161, Rue de Sevres, 75743-Paris Cedex 15, France gogusev{at}necker.fr

Jean Bouquet de Jolinière, MD, PhD

Louise Telvi, MD, PhD

Mireille Doussau, BS

Alexandre Stojkoski, MS

Michel Levradon, MD

INSERM U507, Hôpital Necker, Paris; Service de Gynécologie Obstétrique, Hôpital Beaujon, Clichy; and Service de Cytogénétique, Hôpital St. Vincent de Paul, Paris, France

For many years, endometriosis has been an enigmatic and confusing disorder, but there have been recent contributions to the subject, provided by modern techniques in cellular and molecular biology, regarding the cell lineage involved, the stage of differentiation, and genomic features. This review deals mainly with the cellular, cytochemical, cytogenetic, and molecular cytogenetic features of primary endometriotic lesions and cultured endometriotic cells. The FbEM-1 cell line, taken as an in vitro model, showed cell proliferation and differentiation features suggesting an immature endometriosis-related cell lineage. Chromosomal analysis of these cells demonstrate a complex karyotype including a rearrangement interpreted as der(5) t(5q34;6p11) indicating a clonal cell proliferation. Data of recurrent DNA sequence copy number alterations detected by the comparative genomic hybridization in a series of primary endometriotic lesions also are described. Predominant recurrent anomalies were found on chromosome 1p and 22q in 50% of the studied samples. Additional losses were seen on chromosomes 5p(33%), 6q(27%), 9q(22%), and 1q(22%), as well as on 17q segments in one case. Gain of DNA sequences was seen on chromosomes 6q, 7q, and 17q. The potential role of the genetic changes identified are discussed in relation to the putative oncogenes and/or tumor suppressor genes possibly involved in development of endometriosis.

Key Words: Endometriosis • permanent cell line • chromosome • comparative genomic hybridization • fluorescence in situ hybridization

Journal of the Society for Gynecologic Investigation, Vol. 7, No. 2, 79-87 (2000)
DOI: 10.1177/107155760000700201


CiteULike    Complore    Connotea    Del.icio.us    Digg    Reddit    Technorati    Twitter    What's this?