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Published on: August 11, 2017
Inflammation, epithelial to mesenchymal transition, and epidermal growth factor receptor tyrosine kinase inhibitor
Kostyantyn Krysan1, Jay M Lee, Mariam Dohadwala
1Department of Medicine, David Geffen School of Medicine at UCLA, Los Angeles, California, USA. KKrysan@mednet.ucla.edu
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.
Insights
Inflammation fuels lung tumor growth and resistance to therapies. Targeting inflammatory pathways and using biomarkers may improve treatment effectiveness for lung cancer patients.
Area of Science:
- Oncology
- Molecular Biology
- Immunology
Background:
- Inflammation significantly contributes to lung tumor development and progression.
- Inflammatory signaling pathways are implicated in promoting aggressive tumor phenotypes, metastasis, and therapeutic resistance.
- Emerging research highlights the role of inflammation in resistance to targeted therapies, particularly epidermal growth factor receptor tyrosine kinase inhibitors.
Purpose of the Study:
- To explore the contribution of inflammation to lung cancer progression.
- To investigate the role of inflammatory mediators in resistance to epidermal growth factor receptor tyrosine kinase inhibitors.
- To underscore the importance of combination therapies and biomarker selection for effective lung cancer treatment.
Main Methods:
- Review of current literature on inflammation and lung cancer.
- Analysis of signaling pathways involved in inflammation-induced resistance.
- Discussion of therapeutic strategies targeting inflammatory mediators.
Main Results:
- Inflammation promotes key processes in lung cancer, including epithelial to mesenchymal transition and metastasis.
- Inflammatory mediators can induce resistance to targeted therapies like epidermal growth factor receptor tyrosine kinase inhibitors.
- Combination therapies targeting both cancer cells and inflammatory pathways show promise.
Conclusions:
- Targeting inflammation is a crucial strategy for overcoming lung cancer progression and therapeutic resistance.
- Biomarker-driven patient selection will be essential for the success of combination therapies.
- Further research into inflammatory pathways is needed to optimize lung cancer treatment.
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