Dana-Farber Cancer Institute, Boston, MA 02115, USA.
Clin Breast Cancer. 2010 Feb;10(1):27-32. doi: 10.3816/CBC.2010.n.003.
The treatment of inflammatory breast cancer (IBC) has been hampered by the diagnostic rarity of the disease and its consequent inclusion in clinical trials of preoperative treatment for the more indolent locally advanced breast cancer (LABC). Patients with IBC have a 2-fold greater probability of dying of their disease compared with patients diagnosed with LABC. The aggressive clinical portrait of IBC supports the recent investigative focus on determining molecular changes specific to IBC and developing novel systemic therapies that will favorably affect its poor disease prognosis. A significant amount of laboratory research has been involved in defining a specific "inflammatory signature" for IBC, denoting molecular changes consistently found in IBC. This work has involved human IBC tissue and cell lines and has demonstrated overexpression of several molecules governing metastatic dissemination, such as overexpression of E-cadherin concurrent with a dysfunctional mucin 1. An increased prevalence of mutant TP53, overexpression of RhoC, and vascular endothelial growth factor-A has been found to contribute to the dominant influence of angiogenesis in this disease. A greater understanding of the molecular mechanisms governing the pathophysiology of IBC has led to the development and clinical application of novel targeting agents for preoperative therapy. This study reviews the advances in molecular understanding of IBC and focuses on the efficacy of therapies that target the epidermal growth factor pathway and angiogenesis as well as early investigational therapies involving RhoC and TP53.
炎性乳腺癌(IBC)的治疗受到以下因素的阻碍:该疾病的诊断罕见,以及其被纳入更惰性的局部晚期乳腺癌(LABC)术前治疗临床试验中。与诊断为 LABC 的患者相比,IBC 患者死于该病的可能性要高出 2 倍。IBC 具有侵袭性的临床特征,这支持了最近对确定 IBC 特定分子变化的研究重点,并开发新的系统疗法,以改善其不良预后。大量的实验室研究涉及定义 IBC 的特定“炎症特征”,表示在 IBC 中一致发现的分子变化。这项工作涉及人 IBC 组织和细胞系,并证明了几种控制转移扩散的分子的过表达,例如 E-钙粘蛋白的过表达同时伴有功能失调的粘蛋白 1。突变型 TP53 的高发生率、RhoC 的过表达和血管内皮生长因子-A 的过表达被认为导致了该疾病中血管生成的主导影响。对 IBC 病理生理学的分子机制有了更深入的了解,导致了新型术前治疗靶向药物的开发和临床应用。本研究综述了对 IBC 的分子认识的进展,并重点介绍了针对表皮生长因子途径和血管生成的治疗方法的疗效,以及涉及 RhoC 和 TP53 的早期研究性治疗方法。