首页> 外文期刊>Breast cancer research and treatment. >Validation of a tissue microarray to study differential protein expression in inflammatory and non-inflammatory breast cancer.
【24h】

Validation of a tissue microarray to study differential protein expression in inflammatory and non-inflammatory breast cancer.

机译:验证组织微阵列以研究炎性和非炎性乳腺癌中差异蛋白表达的方法。

获取原文
获取原文并翻译 | 示例
获取外文期刊封面目录资料

摘要

Aims. Inflammatory breast cancer (IBC) is an aggressive subtype of breast cancer with poor prognosis. The mechanisms responsible for the aggressive clinical evolution are incompletely understood. We constructed a tissue microarray (TMA) and validated its use in translational IBC research. Differential expression of proteins that might play a role in causing the IBC phenotype was studied. Methods and results. A TMA containing 34 IBC and 41 non-stage matched non-IBC tumours was constructed. Five core biopsies were taken for each IBC and three cores for each non-IBC tumour. The TMA was validated using three approaches: (1) the excellent concordance between immunohistochemical results of the initial pathological examination and the results obtained with the TMA for ER, PR and HER2eu (kappa > 0.74); (2) the known differential expression between IBC and non-IBC for four bio-markers in IBC (ER, PR, p53 and HER2eu) was confirmed ( p < 0.01); (3) the HER2eu status using three different antibodies (CB11, TAB250 and HercepTest) was highly concordant (kappa > 0.75). Furthermore, the overexpression of E-Cadherin and RhoC GTPase in IBC ( p < 0.05) was confirmed. We did not find a differential expression pattern for carbonic anhydrase IX (CA IX) and EGFR. Conclusions. Using different approaches, we have validated the use of our TMA for studying differential protein expression in IBC and non-IBC. We confirm the overexpression of E-Cadherin and RhoC GTPase in IBC. The lack of differential expression for CA IX and EGFR might suggest the pathways are equally utilised in both types of breast cancer.
机译:目的炎性乳腺癌(IBC)是一种侵略性乳腺癌,预后较差。导致侵略性临床进化的机制尚不完全清楚。我们构建了组织微阵列(TMA),并验证了其在翻译IBC研究中的用途。研究了可能在引起IBC表型中起作用的蛋白质的差异表达。方法和结果。构建了包含34个IBC和41个非分期匹配的非IBC肿瘤的TMA。每个IBC进行五次核心活检,每个非IBC肿瘤进行三次核心活检。使用以下三种方法验证了TMA:(1)初始病理学检查的免疫组织化学结果与使用TMA获得的ER,PR和HER2 / neu的结果之间的极佳一致性(kappa> 0.74); (2)确认了IBC和非IBC在IBC中的四个生物标记(ER,PR,p53和HER2 / neu)之间的已知差异表达(p <0.01); (3)使用三种不同抗体(CB11,TAB250和HercepTest)的HER2 / neu状态高度一致(kappa> 0.75)。此外,证实了在IBC中E-钙黏着蛋白和RhoC GTP酶的过表达(p <0.05)。我们没有发现碳酸酐酶IX(CA IX)和EGFR的差异表达模式。结论使用不同的方法,我们验证了TMA在研究IBC和非IBC中差异蛋白表达中的应用。我们证实了IBC中E-钙黏着蛋白和RhoC GTPase的过表达。 CA IX和EGFR缺乏差异表达可能表明该途径在两种类型的乳腺癌中均得到了同样的利用。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号