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

被引：36

作者：

Krysan, Kostyantyn ^{[1
]}

Lee, Jay M. ^{[2
,3
]}

Dohadwala, Mariam ^{[1
]}

Gardner, Brian K. ^{[1
]}

Reckamp, Karen L. ^{[4
]}

Garon, Edward ^{[1
]}

John, Maie St. ^{[2
]}

Sharma, Sherven ^{[5
]}

Dubinett, Steven M. ^{[3
,5
,6
]}

机构：

[1] Univ Calif Los Angeles, David Geffen Sch Med, Dept Med, Los Angeles, CA 90095 USA

[2] Univ Calif Los Angeles, David Geffen Sch Med, Dept Surg, Los Angeles, CA 90095 USA

[3] Univ Calif Los Angeles, David Geffen Sch Med, Jonsson Comprehens Canc Ctr, Lung Canc Res Program, Los Angeles, CA 90095 USA

[4] City Hope Natl Med Ctr, Beckman Res Inst, Dept Med Oncol & Therapeut Res, Duarte, CA 91010 USA

[5] Vet Affairs Greater Los Angeles Healthcare Syst, Los Angeles, CA USA

[6] Univ Calif Los Angeles, David Geffen Sch Med, Dept Pathol, Los Angeles, CA 90095 USA

来源：

JOURNAL OF THORACIC ONCOLOGY | 2008年 / 3卷 / 02期

关键词：

EGFR TK inhibitor; G-protein coupled receptors; inflammation; cyclooxygenase-2; PGE2; epithelial to mesenchymal transition; drug resistance; NSCLC;

D O I：

10.1097/JTO.0b013e3181630ece

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

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.

引用

页码：107 / 110

页数：4

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