Both COPD and lung cancer are
major global health concerns owing to cigarette smoking, and represent a vast,
global, preventable disease problem. Patients with COPD are at high risk for
both the development of primary lung cancer, as well as poor result after lung cancer
diagnosis and treatment. As a result of existing impairments in lung
function, patients with COPD frequently
do not meet traditional criteria for tolerance of definitive surgical lung
cancer therapy. The risk of lung cancer in patients with COPD is two to five
fold greater when compared with smokers without COPD.
On the other hand COPD could
be a driving factor in lung cancer, by increasing oxidative stress and the
resulting DNA damage, chronic exposure to pro-inflammatory cytokines,
repression of the DNA repair mechanisms and increased cellular proliferation.
Understanding the mechanisms that drive these processes in primary cells from
patients with these diseases along with better disease models is fundamental
for the advancement of new treatments.