首页> 外文期刊>Proceedings of the Romanian Academy, Series B. Chemistry, life sciences and geosciences >EPIGENETIC MODIFICATIONS OF p16, E-CADHERIN, RARβ AND DAPK GENEPROMOTERS IN BREAST CANCER
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EPIGENETIC MODIFICATIONS OF p16, E-CADHERIN, RARβ AND DAPK GENEPROMOTERS IN BREAST CANCER

机译:乳腺癌中p16,E-钙粘蛋白,RARβ和DAPK基因表位的表位修饰

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摘要

The breast cancer is the result of multiple associations of genetic and epigenetic alterations, whichlead to overexpression of the proto-oncogenes and loss of expression of tumor suppressor genes. Suchnew expression patterns determine the cell genetic reprogramming results in the oncogenesis processand therefore may represent possible important markers for diagnostic and prognostic in cancertherapy. The epigenetic process is frequently associated with the aberrant silencing of tumorsuppressor genes through the CpG islands located in their promoter region. These regions arenormally unmethylated while in tumor cells are abnormally hypermethylated and associated withtranscriptional silencing. Such local hypermethylation processes represent frequently an alternativemechanism for mutations of tumor suppressor genes, being an early and ordinary process for manytumor types, including breast cancer. The aim of this study is to analyze the promoter methylation pattern of some tumor suppressor genes(p1 6, E-cadherin, RARβ and DAPK) in invasive ductal breast cancers, in order to identify newmolecular markers for diagnosis and prognosis.
机译:乳腺癌是遗传和表观遗传学改变的多种关联的结果,其导致原癌基因的过表达和肿瘤抑制基因表达的丧失。这种新的表达方式决定了肿瘤发生过程中细胞遗传重编程的结果,因此可能代表了癌症治疗中诊断和预后的重要标志。表观遗传过程通常与位于其启动子区域的CpG岛与肿瘤抑制基因的异常沉默有关。这些区域通常未被甲基化,而在肿瘤细胞中被异常地高度甲基化并与转录沉默相关。这样的局部高甲基化过程通常代表肿瘤抑制基因突变的替代机制,这是包括乳腺癌在内的许多肿瘤类型的早期且普通的过程。这项研究的目的是分析侵袭性导管癌中某些抑癌基因(p1、6,E-cadherin,RARβ和DAPK)的启动子甲基化模式,以鉴定用于诊断和预后的新分子标记。

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