Chronic obstructive pulmonary disease as a risk factor for lung cancer

Abstract

The association between chronic obstructive pulmonary disease (COPD) and lung cancer has long been a subject of intense debate. The high prevalence of COPD in elderly smokers inevitably strengthens their coincidence. In addition to this contingent coincidence, recent studies have revealed a close association between the two diseases that is independent of the smoking history; that is, the existence of COPD is an independent risk factor for the development of lung cancer. Molecular-based evidence has been accumulating as a result of the efforts to explain the underlying mechanisms of this association. These mechanisms may include the following: the retention of airborne carcinogens followed by the activation of oncogenes and the suppression of tumor suppressor genes; the complex molecular mechanism associated with chronic inflammation in the distal airways of patients with COPD; the possible involvement of putative distal airway stem cells; and genetic factors that are common to both COPD and lung cancer. The existence of COPD in patients with lung cancer may potentially affect the process of diagnosis, surgical resection, radiotherapy, chemotherapy, and end-of-life care. The comprehensive management of COPD is extremely important for the appropriate treatment of lung cancer. Surgical resections with the aid of early interventions for COPD are often possible, even for patients with mild-to-moderate COPD. New challenges, such as lung cancer CT screening for individuals at high risk, are now in the process of being implemented. Evaluating the risk of lung cancer in patients with COPD may be warranted in community-based lung cancer screening.

Lung cancer in connective tissue disease-associated interstitial lung disease: clinical features and impact on outcomes

“…Furthermore, inflammatory mediators, such as tumor necrosis factor, interleukin-1, interleukin-6, growth factors, chemokines, and proteases, can promote the development of cancer via proliferative, anti-apoptotic, and pro-angiogenic effects on the epithelium (30). Although just speculation, it is possible that a lack of immunosuppressive therapy might prolong inflammation, leading to repeated epithelial injury and promotion of the destruction, repair, and remodeling of lung tissue, resulting in the development of LC (31). The present results cannot demonstrate whether immunosuppressant therapy leads to improvement or stabilization of ILD resulting in the prevention of LC.…”

Will chronic e-cigarette use cause lung disease?

“…Inflammation may be beneficial in the short term, especially when resolving infection. However, chronic inflammation can act as a precursor to cancer, and continued influx of neutrophils, with the subsequent increase in free elastase levels, can lead to cell damage and denudation of the epithelia (22,143). Tobacco exposure is also associated with cellular cytotoxicity, including increased apoptosis, autophagosome formation, membrane permeability, and mitochondrial damage (46,78,87,129).…”

Ablation of Liver X receptors α and β leads to spontaneous peripheral squamous cell lung cancer in mice

“…The incidence of PSCCa is increasing and is reported to be approximately 50% of squamous cell lung cancer (3)(4)(5)(6). Although the etiology of squamous cell lung cancer is not known, smoking and chronic lung inflammation have been recognized as predisposing factors (7). Smoking is a major risk factor for chronic obstructive pulmonary disease, interstitial lung diseases, and all types of lung cancer, especially squamous cell lung cancer.…”