TY - JOUR
T1 - Expression of an X-family DNA polymerase, pol lambda, in the respiratory epithelium of non-small cell lung cancer patients with habitual smoking
AU - Ohba, Taro
AU - Kometani, Takurou
AU - Shoji, Fumihiro
AU - Yano, Tokujiro
AU - Ichiro, Yoshino
AU - Taguchi, Kenichi
AU - Kuraoka, Isao
AU - Oda, Shinya
AU - Maehara, Yoshihiko
N1 - Funding Information:
We are most grateful to T. Yamanaka, H. Ohmori, E. Ohashi, Z. Wang and E.K. Braithwaite for their helpful advice. The expert assistance in immunohistochemistry by Y. Kubota is also gratefully acknowledged. This study was supported by a Grant-in-aid for Cancer Research from the Ministry of Health, Labour and Welfare and grants from the Ministry of Education, Science, Sports and Culture of Japan.
PY - 2009
Y1 - 2009
N2 - DNA polymerase lambda, pol λ, is a eukaryotic member of the X-family DNA polymerases that is involved in two modes of DNA repair, i.e. base excision repair (BER) or non-homologous end joining (NHEJ). Using immunohistochemical approaches, we have observed pol λ expression in human tissues, particularly in the respiratory system of lung cancer patients. pol λ proteins were distributed in the nuclei of the epithelial cells in the bronchi, bronchioles and alveoli. Intriguingly, the level of pol λ expression in the bronchiolar epithelia significantly correlated with the amount of habitual smoking in the individuals. Conversely, pol λ expression in cancer tissues did not correlate with the smoking status of the patients. Pol λ expression was sometimes discrepant between the tumor tissues and adjacent bronchioles. More importantly, tumors without pol λ expression that occurred in heavy smokers significantly tended to be at an advanced clinical stage. Pol λ may thus be involved in the DNA repair processes counteracting DNA damage caused by tobacco smoke in the respiratory system.
AB - DNA polymerase lambda, pol λ, is a eukaryotic member of the X-family DNA polymerases that is involved in two modes of DNA repair, i.e. base excision repair (BER) or non-homologous end joining (NHEJ). Using immunohistochemical approaches, we have observed pol λ expression in human tissues, particularly in the respiratory system of lung cancer patients. pol λ proteins were distributed in the nuclei of the epithelial cells in the bronchi, bronchioles and alveoli. Intriguingly, the level of pol λ expression in the bronchiolar epithelia significantly correlated with the amount of habitual smoking in the individuals. Conversely, pol λ expression in cancer tissues did not correlate with the smoking status of the patients. Pol λ expression was sometimes discrepant between the tumor tissues and adjacent bronchioles. More importantly, tumors without pol λ expression that occurred in heavy smokers significantly tended to be at an advanced clinical stage. Pol λ may thus be involved in the DNA repair processes counteracting DNA damage caused by tobacco smoke in the respiratory system.
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U2 - 10.1016/j.mrgentox.2009.05.008
DO - 10.1016/j.mrgentox.2009.05.008
M3 - Article
C2 - 19467344
AN - SCOPUS:67650021428
SN - 1383-5718
VL - 677
SP - 66
EP - 71
JO - Mutation Research - Genetic Toxicology and Environmental Mutagenesis
JF - Mutation Research - Genetic Toxicology and Environmental Mutagenesis
IS - 1-2
ER -