Thaiparambil J, Dong L, Jasso D, et al. - Researchers sought to clarify how chronic obstructive pulmonary disease (COPD) contributes to lung cancer risk by investigating whether tobacco smoke carcinogens cause mitotic spindle apparatus abnormalities and change expression of vital genes, resulting in increased genomic instability and finally tumorigenesis. They used bronchial epithelial cells from patients with COPD and normal bronchial epithelial cells in order to determine the genotoxic impacts of a potent tobacco-smoke carcinogen [4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone, (NNK)] on these cells. It was found that COPD cells vs normal epithelial cells exhibited a significantly altered spindle orientation, centrosome amplification, and chromosome misalignment when exposed to NNK. Additionally, several upregulated genes (such as AURKA, AURKB, and MAD2L2) that were also shown to overlap with lung cancer were found in this study, indicating a possible common pathway in the transition from COPD to lung cancer.