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.
Publication types
-
Research Support, N.I.H., Extramural
-
Research Support, Non-U.S. Gov't
-
Research Support, U.S. Gov't, Non-P.H.S.
-
Review
MeSH terms
-
Biomarkers, Tumor / metabolism
-
Carcinoma, Non-Small-Cell Lung / drug therapy*
-
Carcinoma, Non-Small-Cell Lung / physiopathology
-
Cell Transformation, Neoplastic
-
Cyclooxygenase 2 / metabolism
-
Dinoprostone / metabolism
-
Drug Resistance, Neoplasm*
-
ErbB Receptors / antagonists & inhibitors*
-
ErbB Receptors / metabolism
-
Humans
-
Inflammation
-
Lung Neoplasms / drug therapy*
-
Lung Neoplasms / physiopathology
-
MAP Kinase Signaling System / drug effects
-
Protein Kinase Inhibitors / administration & dosage
-
Protein Kinase Inhibitors / pharmacology*
-
Receptors, G-Protein-Coupled / metabolism
Substances
-
Biomarkers, Tumor
-
Protein Kinase Inhibitors
-
Receptors, G-Protein-Coupled
-
Cyclooxygenase 2
-
ErbB Receptors
-
Dinoprostone