Skip Navigation


Carcinogenesis Advance Access originally published online on August 19, 2004
Carcinogenesis 2004 25(12):2459-2465; doi:10.1093/carcin/bgh259
This Article
Right arrow Full Text Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow All Versions of this Article:
25/12/2459    most recent
bgh259v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrow Search for citing articles in:
ISI Web of Science (12)
Right arrowRequest Permissions
Google Scholar
Right arrow Articles by Peluso, M.
Right arrow Articles by Bonassi, S.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Peluso, M.
Right arrow Articles by Bonassi, S.
Social Bookmarking
 Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Carcinogenesis vol.25 no.12 © Oxford University Press 2004; all rights reserved.

ARTICLE

Comparison of DNA adduct levels in nasal mucosa, lymphocytes and bronchial mucosa of cigarette smokers and interaction with metabolic gene polymorphisms

Marco Peluso, Monica Neri1, Giovanni Margarino2, Carlo Mereu3, Armelle Munnia, Marcello Ceppi1, Marina Buratti4, Raffaella Felletti5, Francesca Stea5, Roberto Quaglia6, Riccardo Puntoni1, Emanuela Taioli7, Seymour Garte8 and Stefano Bonassi1,9

Cancer Risk Factor Branch, Molecular Biology Laboratory, CSPO, Scientific Institute of Tuscany, Florence, Italy, 1 Unit of Environmental Epidemiology and Biostatistics and 2 Unit of Head and Neck Surgery, National Cancer Research Institute, 10-16132 Genoa, Italy, 3 Unit of Pneumology, National Cancer Research Institute, Genoa, Italy, and University of Genoa, Italy, 4 Dipartimento di Medicina del Lavoro, Clinica del Lavoro ‘l. Devoto’, University of Milan, Milan, Italy, 5 U.O. Pneumologia, Azienda Ospedaliera San Martino, Genoa, Italy, 6 Clinica Malattie Apparato Respiratorio & Allergologia DIMI, Azienda Ospedaliera San Martino Università degli Studi, Genoa, Italy, 7 Molecular and Genetic Epidemiology Unit, IRCCS, University of Milan, Milan, Italy, 8 Environmental and Occupational Health Sciences Institute, University of Medicine and Dentistry of New Jersey, Piscataway, New Jersey 08854, USA

9 To whom correspondence should be addressed. Tel: +39 010 5600924; Fax: +39 010 5600501; Email: stefano.bonassi{at}istge.it

The recent introduction of biomarkers in population studies of lung cancer has improved the traditional epidemiological approach, especially in the detection of high risk groups. Many inhalable carcinogens form DNA adducts, an initial event in lung carcinogenesis, and therefore the identification of easily accessible sources of DNA for population studies is considered a leading priority in the field. In this study we compared the frequency of DNA adducts in samples from nasal brushing, bronchial biopsy and peripheral blood lymphocytes (PBL) in a group of 55 subjects, both smokers and non-smokers, undergoing bronchoscopy for diagnostic purposes. Polymorphisms in the CYP1A1, GSTM1 and GSTT1 genes were also evaluated. The level of DNA adducts measured by 32P-labelling assay in nasal mucosa (108 relative adduct level, mean ± SD 1.10 ± 0.66) was higher than in bronchial mucosa (0.82 ± 0.36) and in PBL (0.54 ± 0.39, P < 0.01). DNA adducts measured in nasal mucosa and in PBL were correlated with those in bronchial mucosa (P < 0.01 and P < 0.05, respectively). DNA adducts in smokers were significantly increased in both nasal mucosa and PBL, with a significant dose–response linear trend (P < 0.05). No significant effect on DNA adduction of the genetic polymorphisms investigated was found. Nasal mucosa brushing proved to be a suitable procedure for the 32P-labelling assay and its use in population studies should be further explored.


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
CarcinogenesisHome page
E. Taioli
Gene-environment interaction in tobacco-related cancers
Carcinogenesis, August 1, 2008; 29(8): 1467 - 1474.
[Abstract] [Full Text] [PDF]


Home page
MutagenesisHome page
E. Gyorffy, L. Anna, K. Kovacs, P. Rudnai, and B. Schoket
Correlation between biomarkers of human exposure to genotoxins with focus on carcinogen-DNA adducts
Mutagenesis, January 1, 2008; 23(1): 1 - 18.
[Abstract] [Full Text] [PDF]


Home page
CarcinogenesisHome page
A. G. Schwartz, G. M. Prysak, C. H. Bock, and M. L. Cote
The molecular epidemiology of lung cancer
Carcinogenesis, March 1, 2007; 28(3): 507 - 518.
[Abstract] [Full Text] [PDF]


Home page
J. Virol.Home page
M. L. Gatza and S. J. Marriott
Genotoxic Stress and Cellular Stress Alter the Subcellular Distribution of Human T-Cell Leukemia Virus Type 1 Tax through a CRM1-Dependent Mechanism.
J. Virol., July 1, 2006; 80(13): 6657 - 6668.
[Abstract] [Full Text] [PDF]


Home page
MutagenesisHome page
H. Hoffmann, C. Isner, J. Hogel, and G. Speit
Genetic polymorphisms and the effect of cigarette smoking in the comet assay
Mutagenesis, September 1, 2005; 20(5): 359 - 364.
[Abstract] [Full Text] [PDF]



Disclaimer:
Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.