Molecular profiling of inflammatory breast cancer:: Identification of a poor-prognosis gene expression signature
Molecular profiling of inflammatory breast cancer:: Identification of a poor-prognosis gene expression signature
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DOI：
10.1158/1078-0432.ccr-04-0306
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发表时间：
2004-10-15
影响因子：
11.5
通讯作者：
Lidereau, R
中科院分区：
文献类型：
--
作者：
Bièche, I;Lerebours, F;Lidereau, R
目的：炎性乳腺癌（IBC）是一种罕见但特别侵袭性的原发性乳腺癌。实验设计：为了进一步了解IBC的分子发病机制，我们使用实时定量逆转录（RT）-PCR定量的mRNA表达的538个选定的基因在IBC相对于非IBC。结果：27（5.0%）的538个基因在IBC与非IBC相比，显着上调。没有一个被下调。27个上调基因主要编码转录因子（JUN、EGR 1、JUNB、FOS、FOSB、MYCN和SNAIL 1）、生长因子（VEGF、DTR/HB-EGF、IGFBP 7、IL 6、ANGPT 2、EREG、CCL 3/MIP 1A和CCL 5/RANTES）和生长因子受体（TBXA 2 R、TNFRSF 10 A/TRAILR 1和ROBO 2）。我们还确定了一个基因表达谱，基于MYCN，EREG，和SHH，区分亚组的IBC患者良好，中间，和穷人output.Conclusion：我们的研究已经确定了数量有限的信号通路，需要不适当的激活IBC的发展。在此鉴定的一些上调基因可以提供有用的诊断或预后标志物，并可以形成新的治疗策略的基础。
Purpose: Inflammatory breast cancer (IBC) is a rare but particularly aggressive form of primary breast cancer. The molecular mechanisms responsible for IBC are largely unknown.Experimental Design: To obtain further insight into the molecular pathogenesis of IBC, we used real-time quantitative reverse transcription (RT)-PCR to quantify the mRNA expression of 538 selected genes in IBC relative to non-IBC.Results: Twenty-seven (5.0%) of the 538 genes were significantly up-regulated in IBC compared with non-IBC. None were down-regulated. The 27 up-regulated genes mainly encoded transcription factors (JUN, EGR1, JUNB, FOS, FOSB, MYCN, and SNAIL1), growth factors (VEGF, DTR/HB-EGF, IGFBP7, IL6, ANGPT2, EREG, CCL3/MIP1A, and CCL5/RANTES) and growth factor receptors (TBXA2R, TNFRSF10A/TRAILR1, and ROBO2). We also identified a gene expression profile, based on MYCN, EREG, and SHH, which discriminated subgroups of IBC patients with good, intermediate, and poor outcome.Conclusion: Our study has identified a limited number of signaling pathways that require inappropriate activation for IBC development. Some of the up-regulated genes identified here could offer useful diagnostic or prognostic markers and could form the basis of novel therapeutic strategies.