定量多基因荧光原位杂交检测乳腺癌中c-myc和CCNE2基因扩增
Evaluation of c-myc and CCNE2 amplification in breast cancer with quantitative multi-gene fluorescence in-situ hybridization
摘要目的 探讨c-myc和CCNE2基因在原发乳腺癌中的扩增情况以及二者之间的关系.方法 采用组织芯片、定量多基因荧光原位杂交(QM-FISH)技术检测配对的乳腺导管内癌、浸润性导管癌中c-myc和CCNE2的基因拷贝数,并分析其与临床病理指标之间的关系.结果 2005年1月至2007年12月间收集的66例原发乳腺癌中18例显示c-myc扩增(27.3%),23例显示CCNE2扩增(34.8%),且c-myc扩增与CCNE2扩增两者之间的相关性有统计学差异(P<0.01).c-myc、CCNE2扩增的肿瘤全部为非整倍体,且与HER2基因扩增相关(P<0.05).Ki-67高表达的肿瘤c-myc扩增更为常见(P<0.05).结论 c-myc和CCNE2基因扩增多伴随发生,二者通过相互作用以及相对独立的信号通路在乳腺癌的发生发展中发挥重要作用.
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abstractsObjective To investigate c-myc and CCNE2 gene amplifications and their relationship in breast cancer.Methods Sixty-six infiltrating ductal breast carcinomas with foci of ductal carcinoma in situ components collected from January 2005 to December 2007 were selected for tissue microarray and quantitative multi-gene FISH for c-myc and CCNE2 gene amplification,and the relationship with the clinicopathologic features was analyzed.Results Of the 66 cases,18 (27.3%) showed c-myc amplification and 23 (34.8%) showed CCNE2 amplification.A strong correlation was found between c-myc and CCNE2 amplification (P < 0.01).The breast cancers showing c-myc and CCNE2 amplifications were all aneuploidy,and were HER2 positive (P < 0.05).Tumors with c-myc amplification also showed higher Ki-67 index (P < 0.05).Conclusions C-myc and CCNE2 amplifications are common events in breast cancer,and they often coexist.C-myc and CCNE2 genes may play critical roles in the pathogenesis and development of breast cancer through unique and overlapping signaling pathways.
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