title: Reduction of apoptosis and proliferation in endometriosis.
abstract: OBJECTIVE
  To evaluate whether endometriosis could be related to an impaired balance between apoptosis and proliferation, two processes which could be modulated by hormonal status.
  
  
  METHODS
  Immunohistochemical study.
  
  
  METHODS
  Academic research laboratory.
  
  
  METHODS
  Endometriotic samples obtained from peritoneum of women aged 26-40 years who were undergoing laparoscopy for pain or infertility.
  
  
  METHODS
  Apoptotic cells were detected with the use of the terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL) assay. The production of p53 and bcl-2, estrogen and Progesterone (P) receptors, and cellular proliferation were assessed by immunohistochemistry in eutopic and ectopic endometria from 30 patients with endometriosis throughout the menstrual cycle. Results were compared with those from normal endometria from 15 fertile patients.
  
  
  RESULTS
  Endometriotic lesions were characterized by reduced TUNEL and p53 stainings and by enhanced bcl-2 staining. No correlation between apoptosis and estrogen receptor or P receptor levels was found. A lower amount of steroid receptor was found in endometriotic tissues, without cyclic modulation, compared with the eutopic endometrium.
  
  
  CONCLUSIONS
  Our results suggest that when endometrial tissue is located at ectopic locations, it differs from eutopic endometrium by its proliferation rate, steroid hormone levels, and markers of apoptosis. A reduced sensitivity of endometriotic cells to apoptosis could promote the dissemination and implantation of these cells to ectopic sites.
authors.affiliation: Laboratory of Tumor and Development Biology, University of Liège, Liège, Belgium.
authors.forename: Aude
authors.initials: A
authors.lastname: Béliard
authors.forename: Agnès
authors.initials: A
authors.lastname: Noël
authors.forename: Jean-Michel
authors.initials: JM
authors.lastname: Foidart
mesh_terms: D000328:Adult; D017209:Apoptosis; D016022:Case-Control Studies; D002455:Cell Division; D004715:Endometriosis / Q000378:metabolism / Q000473:pathology* / Q000503:physiopathology*; D005260:Female; D006801:Humans; D007150:Immunohistochemistry; D020287:In Situ Nick-End Labeling; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000378:metabolism; D011960:Receptors, Estrogen / Q000378:metabolism; D011980:Receptors, Progesterone / Q000378:metabolism; D013194:Staining and Labeling; D016159:Tumor Suppressor Protein p53 / Q000378:metabolism
chemical_list: D019253:Proto-Oncogene Proteins c-bcl-2; D011960:Receptors, Estrogen; D011980:Receptors, Progesterone; D016159:Tumor Suppressor Protein p53