Although cigarette smoking is considered the main risk factor for lung cancer, others, such as chronic inflammation and oxidative stress, have been identified. Chronic inflammation and oxidative stress also play a crucial role in chronic lung diseases such as COPD and IPF. Furthermore, post-transplant immunosuppressive treatment is often considered a risk factor for lung cancer. Recently, new data on (epi)genetic mechanisms have made the link between lung cancer and other respiratory diseases

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... uch as COPD and IPF) or glucose metabolism. The transcription factor NF-B has been linked to COPD and lung cancer through its role in inflammation, cell proliferation and apoptosis [5] . Epigenetic modifications are molecular mechanisms that regulate gene expression without changing the DNA sequence; DNA methylation, histone acetylation and microRNA expression have received most attention with regard to tumorgenesis and COPD [6, 7] . The association between single nucleotide polymorphism in the ␣ 5 subunit of the nicotinic acetylcholine receptor subunit genes (nAChR) on chromosome 15q25 and lung cancer may be confounded by COPD [8] . It has been observed that nAChR is causally involved in alveolar destruction as a potentially shared pathogenic mechanism in lung cancer and COPD [9] . Activation of the Wnt-␤ -catenin pathway contributes to tumor cell In the first half of 2011 a new thematic review series in Respiration will focus on epithelial cell and lung cancer. Many studies have recently highlighted the potential association between chronic obstructive pulmonary disease (COPD), idiopathic pulmonary fibrosis (IPF), lung transplantation, glucose metabolism and lung cancer, but this raises intriguing scientific questions as it is not yet fully understood. This series will outline the epidemiology, risk factors and potential pathogenesis of the nexus between lung cancer and COPD, IPF, lung transplantation, and glucose metabolism. COPD is associated with an increased risk of developing lung cancer after adjusting for confounders including smoking. An FEV 1 ! 70% of predicted was associated with a 1 2-fold increase in the risk for lung cancer in men and an almost 4-fold increase in women [1] . A 4.7-fold increase in the risk of lung cancer was observed in a large dataset of patients with IPF [2] . Dickson et al. observed that 6.9% of lung transplant recipients developed lung cancer in the native lung, while no lung cancer was observed in matched bilateral lung transplant recipients [3] . Recent findings show that epithelial cell signaling pathways are responsible for both tumor cell proliferation and the regulation of metabolic pathways in lung cancer [4] .