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首页> 外文期刊>Oncology reports >Molecular profiling to identify molecular mechanism in esophageal cancer with familial clustering.
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Molecular profiling to identify molecular mechanism in esophageal cancer with familial clustering.

机译:分子谱分析以鉴定家族性食管癌的分子机制。

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To identify the genes and molecular functional pathways involved in esophageal cancer, we analyzed the gene expression profile of esophageal tumor tissue from patients having family history of esophageal cancer by cDNA microarray. Three hundred and fifty differentially expressed genes (26 up-regulated and 324 down-regulated) were identified. Genes involved in humoral immune response (PF4), extracellular matrix organization (COL4A4), metabolism of xenobiotics (EPHX1), TGF-beta signaling (SMAD1) and calcium signaling pathways (VDAC1) were down-regulated and genes involved in regulation of actin cytoskeleton (WASL), neuroactive ligand receptor interaction (GRM3), Toll-like receptor (CD14), B-cell receptor (IFITM1) and insulin signaling pathways (FOXO1A) were up-regulated. Validation of differential expression of subset of genes by QRT-PCR and tissue microarray in familial and non-familial cases showed no significant difference in expression of these genes in two groups suggesting familial clustering occurs as result of sharing of common environmental factors. Gene expression profiling of clinical specimens from well characterized populations that have familial clustering of cancer identified molecular mechanism associated with progression of esophageal cancer.
机译:为了确定食管癌的相关基因和分子功能途径,我们通过cDNA芯片分析了具有食管癌家族史的患者的食管肿瘤组织的基因表达谱。鉴定了350个差异表达的基因(26个上调和324个下调)。涉及体液免疫应答(PF4),细胞外基质组织(COL4A4),异源生物代谢(EPHX1),TGF-β信号传导(SMAD1)和钙信号传导途径(VDAC1)的基因被下调,而参与调节肌动蛋白细胞骨架的基因(WASL),神经活性配体受体相互作用(GRM3),Toll样受体(CD14),B细胞受体(IFITM1)和胰岛素信号通路(FOXO1A)上调。通过QRT-PCR和组织微阵列对家族性和非家族性病例中基因亚群的差异表达进行验证,结果表明两组中这些基因的表达没有显着差异,表明家族性聚集是由于共同环境因素的共享而发生的。来自特征明确的具有家族性癌症聚类的人群的临床标本的基因表达谱鉴定了与食道癌进展相关的分子机制。

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