Relationships between chronic obstructive pulmonary disease and lung cancer: biological insights

Abstract

Lung cancer (LC) has become one of the leading causes of preventable death in the last few decades. Cigarette smoking (CS) stays as the main etiologic factor of LC despite that many other causes such as occupational exposures, air pollution, asbestos, or radiation have also been implicated. Patients with chronic obstructive pulmonary disease (COPD), which also represents a major cause of morbidity and mortality in developed countries, exhibit a significantly greater risk of LC. The study of the underlying biological mechanisms that may predispose patients with chronic respiratory diseases to a higher incidence of LC has also gained much attention in the last few years. The present review has been divided into three major sections in which different aspects have been addressed: (I) relevant etiologic agents of LC; (II) studies confirming the hypothesis that COPD patients are exposed to a greater risk of developing LC; and (III) evidence on the most relevant underlying biological mechanisms that support the links between COPD and LC. Several carcinogenic agents have been described in the last decades but CS remains to be the leading etiologic agent in most geographical regions in which the incidence of LC is very high. Growing evidence has put the line forward the implications of COPD and especially of emphysema in LC development. Hence, COPD represents a major risk factor of LC in patients. Different avenues of research have demonstrated the presence of relevant biological mechanisms that may predispose COPD patients to develop LC. Importantly, the so far identified biological mechanisms offer targets for the design of specific therapeutic strategies that will further the current treatment options for patients with LC. Prospective screening studies, in which patients with COPD should be followed up for several years will help identify biomarkers that may predict the risk of LC among these patients.

Neoantigens in Chronic Obstructive Pulmonary Disease and Lung Cancer: A Point of View

“…Lung cancer has become one of the leading causes of death with smoke inhalation as the main etiologic factor . Lung cancer is caused by mutations in oncogenes, leading to the proliferation of mutated cells and the formation of a tumor.…”

“…Chronic inflammation through the induction of several interleukins and cyclooxygenase‐2 activity may be an important player in the lung tumor formation among patients with COPD. For instance, CCL21 may favor cancer cell migration in the lungs of patients with COPD . Oxidative damage and antioxidant depletion may contribute to a greater risk to lung carcinogenis, especially in patients with underlying COPD .…”

“…For instance, CCL21 may favor cancer cell migration in the lungs of patients with COPD . Oxidative damage and antioxidant depletion may contribute to a greater risk to lung carcinogenis, especially in patients with underlying COPD . An epigenome wide association study identified that DNA methylation and repression of two genes—CCDC37 and MAP1B—was significantly associated with both COPD and lung cancer .…”

Myocyte enhancer factor 2D provides a cross-talk between chronic inflammation and lung cancer

“…Chronic obstructive pulmonary disease (COPD), a chronic inflammatory lung disease, is closely related to susceptibility to lung cancer and stands as the most important risk factor of lung cancer among smokers [8]. Patients with moderate-to-severe COPD have a fivefold higher risk of developing lung cancer than smokers without the disease [9]. Chronic inflammation associated with COPD seems to play a critical role in cancer evolution.…”

From biological mechanisms to clinical implications: the role of mineral dust-induced gene in lung cancers

“…While lung cancer has been a leading cause of death for humans with highest morbidity among all types of cancers, air pollution poses an increasing impact on the incidence of this catastrophe (1)(2)(3). Mineral dust-induced gene (Mdig ) is a lung cancer-related gene found in alveolar macrophages from coal miners exposed to mineral dusts in 2005 (4).…”