[Expression of oncogenes (c-myc-neu) and prolactin receptor (PRLr) in tissues of women with endometriosis].
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This study evaluated oncogenes (c-myc, neu) and the prolactin receptor (PRLr) in women with endometriosis, finding differential expression of myc and PRLr between eutopic and ectopic tissues, while neu expression was similar.
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Abstract
Endometriosis is a disease of unknown ethology; there are several theories that are unproven. It is known that women with such disease present with infertility, and that recurrence is very high, and apparently not depending of estrogenic stimulus. This phenomenon has been contributed to other growth factors and some oncogens. There are few studies about oncogens or other hormonal receptors; so, this study tries to evaluate them in eutopic tissue and in ectopic one of women with previous diagnosis of endometriosis. Our results show that myc as PRLr are expressed differently in the different tissues; and neu is expressed in the same way in both tissues. So, it was concluded that the cells of the endometriosis focus, have a differential status relating to expression of some of their genes, which target on their development and maintenance in a hormonal environment which differs from the uterine cavity.
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Cited by (3)
- Enhanced epithelial to mesenchymal transition (EMT) and upregulated MYC in ectopic lesions contribute independently to endometriosis 2015
- The expression of estrogen receptors as well as GREB1, c-MYC, and cyclin D1, estrogen-regulated genes implicated in proliferation, is increased in peritoneal endometriosis 2012
- 60S acidic ribosomal protein P1 (RPLP1) is elevated in human endometriotic tissue and in a murine model of endometriosis and is essential for endometriotic epithelial cell survival <i>in vitro</i> 2019
Cited by (3)
- 60S acidic ribosomal protein P1 (RPLP1) is elevated in human endometriotic tissue and in a murine model of endometriosis and is essential for endometriotic epithelial cell survival <i>in vitro</i> 2019
- Enhanced epithelial to mesenchymal transition (EMT) and upregulated MYC in ectopic lesions contribute independently to endometriosis 2015
- The expression of estrogen receptors as well as GREB1, c-MYC, and cyclin D1, estrogen-regulated genes implicated in proliferation, is increased in peritoneal endometriosis 2012
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