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炎症、上皮-间质转化与表皮生长因子受体酪氨酸激酶抑制剂耐药性

Inflammation, epithelial to mesenchymal transition, and epidermal growth factor receptor tyrosine kinase inhibitor resistance.

作者信息

Krysan Kostyantyn, Lee Jay M, Dohadwala Mariam, Gardner Brian K, Reckamp Karen L, Garon Edward, St John Maie, Sharma Sherven, Dubinett Steven M

机构信息

Department of Medicine, David Geffen School of Medicine at UCLA, Los Angeles, California, USA.

出版信息

J Thorac Oncol. 2008 Feb;3(2):107-10. doi: 10.1097/JTO.0b013e3181630ece.

Abstract

Inflammation is an important contributor to lung tumor development and progression. In addition, inflammatory signaling may promote epithelial to mesenchymal transition, development of aggressive metastatic tumor phenotypes, and play a role in resistance to targeted therapies. New insights in inflammatory signaling have led to the evaluation of combination therapies that target these specific pathways. In addition to developing the optimal combination of targeted agents, biomarker-based selection of patients who will likely benefit will be critical to the success of this strategy. Here we focus on the potential contribution of inflammatory mediator-induced resistance to epidermal growth factor receptor tyrosine kinase inhibitors.

摘要

炎症是肺肿瘤发生和发展的重要促成因素。此外,炎症信号可能促进上皮-间质转化、侵袭性转移肿瘤表型的发展,并在对靶向治疗的耐药性中发挥作用。炎症信号方面的新见解促使人们对靶向这些特定途径的联合疗法进行评估。除了开发靶向药物的最佳组合外,基于生物标志物选择可能受益的患者对于该策略的成功至关重要。在这里,我们重点关注炎症介质诱导的对表皮生长因子受体酪氨酸激酶抑制剂耐药性的潜在影响。

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