Inflammation and lung cancer: The link to angiogenesis Chapter uri icon

Overview

MeSH Major

  • Dietary Supplements
  • Liver Failure, Acute
  • Obesity
  • Phytotherapy
  • Plant Preparations

abstract

  • © Springer Science+Business Media New York 2015. Emerging studies have begun to strengthen the link between chronic inflammation and cancer. Inflammation is now accepted as an underlying or enabling characteristic that contributes to key hallmarks of cancer, and nonsteroidal antiinflammatory drugs (NSAID) have shown a reduction in the risk of several cancers. In lung cancer patients, pulmonary disorders, such as chronic obstructive pulmonary disease (COPD) and emphysema, constitute comorbid conditions and comprise an independent risk factor for lung cancer. Despite the clinical association, the mechanistic link between COPD and lung cancer is not completely understood and constitutes an area of intense investigation. Notably, chronic inflammation appears to be a pivotal pathological feature in both COPD and lung cancer. The inflammatory microenvironment encountered in COPD/emphysema may contribute to tumorigenesis via several possible signaling pathways, including angiogenesis. Accumulating evidence suggests that angiogenesis is closely linked to inflammation, with regulators of angiogenesis playing key roles in various inflammatory conditions and vice versa. Inflammatory cells, namely neutrophils, mast cells, monocytes/macrophages, and lymphocytes, play an active role in enhancing tumor angiogenesis by secreting chemokines, inflammatory cytokines, and proteases into the local microenvironment that control endothelial cell (EC) activation by virtue of regulating proliferation, survival and apoptosis, and migration. Therefore, targeting the inflammatory and angiogenic pathways provides unique opportunities for both prevention and treatment of lung cancer.

publication date

  • January 2015

Research

keywords

  • Book Chapter

Identity

Digital Object Identifier (DOI)

  • 10.1007/978-1-4939-2724-1_5

Additional Document Info

start page

  • 137

end page

  • 159