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and Ottaviano et al. in breast cancer cell lines. Essentially, these authors de scribed that the promoter located in JNJ-7706621 exon 1 of the ESR1 gene is observed to be highly methylated in the cell lines that do not express ER protein and, conversely, is not methylated in normal breast tissue as well as in the cell lines of breast cancer that express functioning estrogen receptors. With respect to the luminal phenotype and ESR1 methylation status, we observed that, in those cases with the better prognosis phenotypes the predominant result of the evaluation of ESR1 fcDNA methylation was negative there was a correl ation between ER expression and better prognosis while, in the phenotype with poor prognosis, the evaluation was predominantly posi tive, Further analysis of each luminal pheno type with respect to methylated ESR1 0.<br><br> 02 relative units versus methylated ESR1 0. 02 relative units, showed that, within each subgroup, those that presented methylated ESR1 had a tendency LDN193189 towards shorter overall survival than those with a methylated ESR level 0. 02 relative units. Hence, it appears that the molecular variant of the methylated promoter region of the ESR1 gene carries prognostic information that is additional to the prognos tic factors that are currently used in the breast cancer clinic. From the above observations, the most relevant of the results obtained is that methylation, as an epigenetic event, can be one of the mechanisms implicated in the non expression of ER in the tumor. We observed signifi cant correlation between ESR1 DNA methylation in peripheral blood and silencing of ER expression in the tumor, and vice versa.<br><br> This finding is of consider LY2157299 溶解度 able interest especially since we observed, as well, the correlation between ESR1 fcDNA methylation and the ER expression in relation to tumor phenotype. The greater expression of the estrogen receptors in the phe notypes that are known to have a better prognosis while showing significantly lower levels of ESR1 in peripheral blood. This contrasts with those pheno types in which the ER expression is low or not present which, in turn is associated with poorer prognosis, The mechanisms involved in the ab sence of ER expression are not known, and neither are the reasons for non response to hormonal treatment. Of note, as well, is that tumors that express ER at the time of diagnosis can cease expressing ER over the time course of the disease.<br><br> Perhaps one of the causal events in the absence of ER expression is that tumors expressing ER at the time of diagnosis are methylated. In studies conducted to date, the known genetic alterations do not fully explain the processes but, based on the re sults from our study, perhaps methylation is the key to explaining, at least in part, some of the observations. Also, given that methylation is a reversible event, analyz ing this reversibility can be useful in identifying the cru cial point in the success, or otherwise, of hormonal treatment of breast cancer. Conclusions Our results indicate that the silencing of gene expression by methylation of the promoter region of the ESR1 gene of the estrogen receptor has an important role in the ex pression of the protein for which this gene codes in the primary tumor.