Inflammatory breast cancer (IBC): clues for targeted therapies.
Inflammatory breast cancer (IBC): clues for targeted therapies.
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DOI：
10.1007/s10549-013-2600-4
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发表时间：
2013-07
影响因子：
3.8
通讯作者：
Cristofanilli, Massimo
中科院分区：
文献类型：
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作者：
Fernandez, Sandra V.;Robertson, Fredika M.;Pei, Jianming;Aburto-Chumpitaz, Lucy;Mu, Zhaomei;Chu, Khoi;Alpaugh, R. K.;Huang, Yong;Cao, Yu;Ye, Zaiming;Cai, Kathy Q.;Boley, Kimberly M.;Klein-Szanto, Andres J.;Devarajan, Karthik;Addya, Sankar;Cristofanilli, Massimo
炎性乳腺癌（IBC）是最具侵袭性的晚期乳腺癌，其特点是增殖快、转移发展早、预后差。由于 IBC 的临床前模型很少，人们普遍对该疾病的复杂性缺乏了解。最近，我们开发了一种新的 IBC 模型，该模型源自一名患有转移性继发性 IBC 的女性的胸腔积液。 FC-IBC02 细胞呈三阴性，并在悬浮液中形成簇（乳腺球），这些簇对 E-钙粘蛋白、β-连环蛋白和 TSPAN24 呈强阳性，所有粘附分子在细胞迁移和侵袭中发挥重要作用。 FC-IBC02 细胞表达干细胞标记物以及经历上皮间质转化 (EMT) 的细胞的一些但不是全部特征。乳腺肿瘤 FC-IBC02 异种移植物在 SCID 小鼠中快速发育，存在肿瘤栓塞以及淋巴结和肺转移的发展。值得注意的是，FC-IBC02 细胞通过心内或腹膜内注射能够在小鼠体内产生脑转移。 FC-IBC02 和其他 IBC 细胞系的基因组研究表明，IBC 细胞的 8q24 具有重要扩增，其中 MYC、ATAD2 和粘着斑激酶 FAK1 位于此处。 MYC 和 ATAD2 在 IBC 细胞中显示出 2.5 至 7 个拷贝。 FAK1 在失巢凋亡抵抗和肿瘤转移中发挥重要作用，在 IBC 细胞中显示有 6-4 个拷贝。此外，CD44 在三阴性 IBC 细胞（10-3 个拷贝）中被扩增。此外，FC-IBC02 显示 ALK 和 NOTCH3 的扩增。这些结果表明 MYC、ATAD2、CD44、NOTCH3、ALK 和/或 FAK1 可用作针对 IBC 的潜在靶向疗法。本文的在线版本 (doi:10.1007/s10549-013-2600-4) 包含补充材料，可供授权用户使用。
Inflammatory breast cancer (IBC) is the most aggressive type of advanced breast cancer characterized by rapid proliferation, early metastatic development and poor prognosis. Since there are few preclinical models of IBC, there is a general lack of understanding of the complexity of the disease. Recently, we have developed a new model of IBC derived from the pleural effusion of a woman with metastatic secondary IBC. FC-IBC02 cells are triple negative and form clusters (mammospheres) in suspension that are strongly positive for E-cadherin, β-catenin and TSPAN24, all adhesion molecules that play an important role in cell migration and invasion. FC-IBC02 cells expressed stem cell markers and some, but not all of the characteristics of cells undergoing epithelial mesenchymal transition (EMT). Breast tumor FC-IBC02 xenografts developed quickly in SCID mice with the presence of tumor emboli and the development of lymph node and lung metastases. Remarkably, FC-IBC02 cells were able to produce brain metastasis in mice on intracardiac or intraperitoneal injections. Genomic studies of FC-IBC02 and other IBC cell lines showed that IBC cells had important amplification of 8q24 where MYC, ATAD2 and the focal adhesion kinase FAK1 are located. MYC and ATAD2 showed between 2.5 and 7 copies in IBC cells. FAK1, which plays important roles in anoikis resistance and tumor metastasis, showed 6–4 copies in IBC cells. Also, CD44 was amplified in triple-negative IBC cells (10–3 copies). Additionally, FC-IBC02 showed amplification of ALK and NOTCH3. These results indicate that MYC, ATAD2, CD44, NOTCH3, ALK and/or FAK1 may be used as potential targeted therapies against IBC. The online version of this article (doi:10.1007/s10549-013-2600-4) contains supplementary material, which is available to authorized users.
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影响因子：
50.3
作者：
Hu G;Chong RA;Yang Q;Wei Y;Blanco MA;Li F;Reiss M;Au JL;Haffty BG;Kang Y
通讯作者：
Kang Y
影响因子：
10.5
作者：
Dontu, G;Abdallah, WM;Wicha, MS
通讯作者：
Wicha, MS
影响因子：
6.2
作者：
Bertucci, Francois;Finetti, Pascal;Viens, Patrice
通讯作者：
Viens, Patrice
影响因子：
8.8
作者：
Forozan, F;Veldman, R;Ammerman, CA;Parsa, NZ;Kallioniemi, A;Kallioniemi, OP;Ethier, SP
通讯作者：
Ethier, SP
选择性抑制BET溴结构域。
影响因子：
64.8
作者：
通讯作者：
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