Epidermal Growth Factor Receptor in COPD and Lung Cancer : Is Inflammation the Culprit?
(2025) In Cancer Drug Discovery and Development (CDD&D) p.75-101- Abstract
Chronic obstructive pulmonary disease (COPD) and lung cancer (LC) are recognized as severe diseases of the lungs and are closely linked to cigarette smoking and environmental pollution and share common mechanisms such as oxidative stress, inflammation, matrix degradation, and airway remodeling. Epidermal growth factor receptor (EGFR), a transmembrane receptor featuring an extracellular ligand binding domain and an intracellular tyrosine kinase domain, has been recognized as a crucial player in these processes. EGFR is known to be dysregulated in both COPD and LC. In LC, oncogenic mutations that activate EGFR lead to an increased oncogenic response, positioning EGFR as a key regulator and hub for unregulated cell growth signaling. This... (More)
Chronic obstructive pulmonary disease (COPD) and lung cancer (LC) are recognized as severe diseases of the lungs and are closely linked to cigarette smoking and environmental pollution and share common mechanisms such as oxidative stress, inflammation, matrix degradation, and airway remodeling. Epidermal growth factor receptor (EGFR), a transmembrane receptor featuring an extracellular ligand binding domain and an intracellular tyrosine kinase domain, has been recognized as a crucial player in these processes. EGFR is known to be dysregulated in both COPD and LC. In LC, oncogenic mutations that activate EGFR lead to an increased oncogenic response, positioning EGFR as a key regulator and hub for unregulated cell growth signaling. This signaling promotes tumor cell proliferation, invasion, migration, metastasis, and survival. Conversely, in COPD, dysregulated EGFR signaling in response to different stimuli results in heightened airway inflammation, remodeling, and mucus secretion, contributing to exacerbations of the disease. In this chapter, we explore the intricate connection and shared signaling pathways between COPD and LC, focusing on the EGFR cascade. We discuss how in both these conditions inflammation leads to altered EGFR signaling and examine various therapeutic strategies that can be implemented for better prognosis and treatment options in both conditions.
(Less)
- author
- Agraval, Hina ; Sharma, Jiten LU and Yadav, Umesh C.S.
- organization
- publishing date
- 2025
- type
- Chapter in Book/Report/Conference proceeding
- publication status
- published
- subject
- keywords
- Cigarette smoke, COPD, EGFR, Inflammation, Lung cancer
- host publication
- Receptor Tyrosine Kinases in Cancer
- series title
- Cancer Drug Discovery and Development (CDD&D)
- pages
- 27 pages
- publisher
- Humana Press Inc.
- external identifiers
-
- scopus:105013116503
- DOI
- 10.1007/978-3-031-93894-8_3
- language
- English
- LU publication?
- yes
- id
- 05e04211-3b1a-4f7f-802c-64a9446dafc0
- date added to LUP
- 2026-01-09 08:59:18
- date last changed
- 2026-01-09 08:59:18
@inbook{05e04211-3b1a-4f7f-802c-64a9446dafc0,
abstract = {{<p>Chronic obstructive pulmonary disease (COPD) and lung cancer (LC) are recognized as severe diseases of the lungs and are closely linked to cigarette smoking and environmental pollution and share common mechanisms such as oxidative stress, inflammation, matrix degradation, and airway remodeling. Epidermal growth factor receptor (EGFR), a transmembrane receptor featuring an extracellular ligand binding domain and an intracellular tyrosine kinase domain, has been recognized as a crucial player in these processes. EGFR is known to be dysregulated in both COPD and LC. In LC, oncogenic mutations that activate EGFR lead to an increased oncogenic response, positioning EGFR as a key regulator and hub for unregulated cell growth signaling. This signaling promotes tumor cell proliferation, invasion, migration, metastasis, and survival. Conversely, in COPD, dysregulated EGFR signaling in response to different stimuli results in heightened airway inflammation, remodeling, and mucus secretion, contributing to exacerbations of the disease. In this chapter, we explore the intricate connection and shared signaling pathways between COPD and LC, focusing on the EGFR cascade. We discuss how in both these conditions inflammation leads to altered EGFR signaling and examine various therapeutic strategies that can be implemented for better prognosis and treatment options in both conditions.</p>}},
author = {{Agraval, Hina and Sharma, Jiten and Yadav, Umesh C.S.}},
booktitle = {{Receptor Tyrosine Kinases in Cancer}},
keywords = {{Cigarette smoke; COPD; EGFR; Inflammation; Lung cancer}},
language = {{eng}},
pages = {{75--101}},
publisher = {{Humana Press Inc.}},
series = {{Cancer Drug Discovery and Development (CDD&D)}},
title = {{Epidermal Growth Factor Receptor in COPD and Lung Cancer : Is Inflammation the Culprit?}},
url = {{http://dx.doi.org/10.1007/978-3-031-93894-8_3}},
doi = {{10.1007/978-3-031-93894-8_3}},
year = {{2025}},
}