2011
DOI: 10.3892/etm.2011.376
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Modulation of estrogenic action in clear cell carcinoma of the ovary (Review)

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Cited by 27 publications
(33 citation statements)
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References 36 publications
(81 reference statements)
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“…In HGSOC, an estrogen receptor pathway may increase the likelihood of LVSI. However, estrogensignaling is less active in OCCC, suggesting alternative mechanisms related to LVSI in OCCC [18]. Clear cell histology is the most common histologic subtype of renal cell carcinoma, and LVSI is suggested to be a prognostic factor for worse survival outcomes in that tumor as well [19,20].…”
Section: Discussionmentioning
confidence: 98%
“…In HGSOC, an estrogen receptor pathway may increase the likelihood of LVSI. However, estrogensignaling is less active in OCCC, suggesting alternative mechanisms related to LVSI in OCCC [18]. Clear cell histology is the most common histologic subtype of renal cell carcinoma, and LVSI is suggested to be a prognostic factor for worse survival outcomes in that tumor as well [19,20].…”
Section: Discussionmentioning
confidence: 98%
“…However, clear cell carcinomas do not express estrogen or progesterone receptors [44] and therefore endometriosis, that can transform into clear-cell ovarian cancer, could became hormone independent during the transformation process [24,45]. Therefore, an interesting dualistic model for the development of endometriosis-associated endometrioid EOC (with E and P receptor positive, and associated with hyperplastic aspects of the ectopic endometrium) and for endometriosis-associated clear cell EOC (E and P receptor negative, and associated with iron-mediated oxidative stress) could be suggested [46,47]. Synchronous endometrial-ovarian carcinomas are expected to be endometrioid hystotype, thus confirming the hormone-dependent pathway.…”
Section: Discussionmentioning
confidence: 99%
“…The previously described events, mediated by oxidative stress and inflammation secondary to the repeated hemorrhage from endometriosis, result in DNA methylation that has been linked to decreased ER expression [83,84]. Some investigators have postulated a dualistic model for the development of EAOC, in which the loss of ER expression marks a pivotal point in the carcinogenic pathway separating the development of estrogen-dependent carcinomas ( i.e ., endometrioid) from estrogen-independent carcinomas ( i.e ., clear cell) [85,86]. While the separation of estrogen-dependent and estrogen-independent EAOC is supported on the basis of morphology and genomics, the details of both pathways remain areas of further investigation [85,86].…”
Section: Pathways Of Carcinogenesismentioning
confidence: 99%