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Receptor (nuc nuclear staining); ER estrogen receptor; PR progesterone receptor. No
Receptor (nuc nuclear staining); ER estrogen receptor; PR progesterone receptor. No cytoplasmic GPER expression was detected in the stroma of endometrium and endometriosis. P-Values were calculated by an exact 2-sided Pearson chi-square test; p 0.05 was considered as statistically significant and is reported in bold type.Samartzis et al. Reproductive Biology and Endocrinology 2012, 10:30 http://www.rbej.com/content/10/1/Page 9 ofwithin the various types of endometriosis, i.e., the more frequent high cytoplasmic expression levels in epithelial ovarian endometriotic cells, as well as the differences in epithelial and stromal expression patterns, appear to contradict the classification of endometriosis as a homogenous disease. Finally, the detection of specific GPER receptor antagonists may provide novel therapeutic treatment options for endometriosis.Competing interests The authors declare that they have no competing interests. Acknowledgments This project was supported by a grant of the Center for Clinical Research, University and University Hospital Zurich as well as by grants from the EMDO and the Hartmann-Mueller Foundations. We wish to thank Mrs. M. Storz and Mrs. S. Behnke for their excellent technical support. We are also grateful to Prof. B. Seifert of the Institute for Biostatistics at the University of Zurich, Switzerland for performing the statistical support in this study. The entire manuscript was edited by a professional language editing service (Nature Publishing Group Language Editing). Author details 1 Department of Gynecology, University Hospital Zurich, Zurich, Switzerland. 2 Department of Pathology, University Hospital Zurich, Zurich, Switzerland. Authors’ contributions NS and EPS constructed the tissue microarray (TMA), scored the immunohistochemical (IHC) staining, performed statistical analyses and drafted the manuscript. AN and RC revised diagnosis of the paraffin embedded tissue samples and analyzed the IHC-staining of the TMA. AF contributed to the interpretation of data. KJD and DF assisted with the interpretation of data and contributed to the draft of the manuscript. PI conceived the study, collected data and coordinated the procedures during this study. All authors read and approved the final manuscript. MGCD516 solubility 28549975″ title=View Abstract(s)”>PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/28549975 Received: 4 November 2011 Accepted: 20 April 2012 Published: 20 April 2012 References 1. Giudice LC, Kao LC: Endometriosis. Lancet 2004, 364:1789?799. 2. Bulun SE: Endometriosis. N Engl J Med 2009, 360:268?79. 3. Eskenazi B, Warner ML: Epidemiology of endometriosis. Obstet Gynecol Clin North Am 1997, 24:235?58. 4. Giudice LC: Clinical practice. Endometriosis. N Engl J Med 2010, 362:2389?398. 5. Prossnitz ER, Maggiolini M: Mechanisms of estrogen signaling and gene expression via GPR30. Mol Cell Endocrinol 2009, 308:32?8. 6. Maggiolini M, Picard D: The unfolding stories of GPR30, a new membrane-bound estrogen receptor. J Endocrinol 2010, 204:105?14. 7. Lin BC, Suzawa M, Blind RD, Tobias SC, Bulun SE, Scanlan TS, Ingraham HA: Stimulating the GPR30 estrogen PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/26024392 receptor with a novel tamoxifen analogue activates SF-1 and promotes endometrial cell proliferation. Cancer Res 2009, 69:5415?423. 8. Revankar CM, Cimino DF, Sklar LA, Arterburn JB, Prossnitz ER: A transmembrane intracellular estrogen receptor mediates rapid cell signaling. Science 2005, 307:1625?630. 9. Prossnitz ER, Oprea TI, Sklar LA, Arterburn JB: The ins and outs of GPR30: a transmembrane estrogen receptor. J Steroid Biochem Mol Biol 2008, 109:350?53. 1.

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