Inflammation, Epithelial to Mesenchymal Transition, and Epidermal Growth Factor Receptor Tyrosine Kinase Inhibitor Resistance

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 inflam...

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Bibliographic Details
Published in:Journal of thoracic oncology 2008-02, Vol.3 (2), p.107-110
Main Authors: Krysan, Kostyantyn, Lee, Jay M., Dohadwala, Mariam, Gardner, Brian K., Reckamp, Karen L., Garon, Edward, John, Maie St, Sharma, Sherven, Dubinett, Steven M.
Format: Article
Language:English
Subjects:
Biomarkers, Tumor - metabolism
Carcinoma, Non-Small-Cell Lung - drug therapy
Carcinoma, Non-Small-Cell Lung - physiopathology
Cell Transformation, Neoplastic
Cyclooxygenase 2 - metabolism
Cyclooxygenase-2
Dinoprostone - metabolism
Drug resistance
Drug Resistance, Neoplasm
EGFR TK inhibitor
Epithelial to mesenchymal transition
G-protein coupled receptors
Humans
Inflammation
Lung Neoplasms - drug therapy
Lung Neoplasms - physiopathology
MAP Kinase Signaling System - drug effects
NSCLC
PGE2
Protein Kinase Inhibitors - administration & dosage
Protein Kinase Inhibitors - pharmacology
Receptor, Epidermal Growth Factor - antagonists & inhibitors
Receptor, Epidermal Growth Factor - metabolism
Receptors, G-Protein-Coupled - metabolism
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Summary: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.
ISSN:1556-0864
1556-1380
DOI:10.1097/JTO.0b013e3181630ece