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Published ahead of print on February 21, 2003, doi:10.1165/rcmb.2002-0183RC

Am. J. Respir. Cell Mol. Biol., Volume 29, Number 2, August 2003, 157-162

A more recent version of this article appeared on August 1, 2003
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Submitted on September 11, 2002
Revised on February 21, 2003

GENE EXPRESSION IN LUNG ADENOCARCINOMAS OF SMOKERS AND NON-SMOKERS

Charles A Powell1, Avrum Spira2, Adnan Derti3, Charles DeLisi3, Gang Liu4, Alain Borczuk5, Steve Busch6, Sudhir Sahasrabudhe6, Yangde Chen6, David Sugarbaker7, Raphael Bueno7, William G Richards7, and Jerome S Brody4*

1 Department of Medicine, Columbia College of Physicians and Surgeons, New York, NY, 2 Pulmonary Center and Department of Medicine, Boston University School of Medicine, Boston, Ma; Bioinformatics Program, College of Engineering, Boston University, Boston, Ma., 3 Bioinformatics Program, College of Engineering, Boston University, Boston, Ma., 4 Pulmonary Center and Department of Medicine, Boston University School of Medicine, Boston, Ma, 5 Department of Pathology, Columbia University School of Medicine, New York, NY, 6 Aventis Pharmaceuticals, NJ, 7 Division of Thoracic Surgery, Brigham and Women's Hospital and Harvard Medical School, Boston, Ma.

* To whom correspondence should be addressed. E-mail: jbrody{at}bu.edu.

Adenocarcinoma (AC) has become the most frequent type of lung cancer in men and women and is the major form of lung cancer in non-smokers. Our goal in this paper was to determine if AC in smokers and non-smokers represents the same genetic disease. We compared gene expression profiles in resected samples of non-malignant lung tissue and tumor tissue in six never smokers with AC and in six smokers with AC, who were matched for clinical staging and histologic criteria of cell differentiation. Results were analyzed using a variety of bioinformatic tools. Four times as many genes changed expression in the transition from non-involved lung to tumor in non-smokers as in smokers, suggesting that AC in non-smokers evolves locally while AC in smokers evolves in a field of genetically altered tissue. There were some similarities in gene expression in smokers and non-smokers but many differences, suggesting different pathways of cell transformation and tumor formation. Gene expression in the non-involved lungs of smokers differed from non-smokers and multidemensional scaling showed that non-involved lungs of smokers groups with tumors rather than non-involved lungs of non-smokers. In addition, expression of a number of genes correlated with smoking intensity. Our findings, while limited by small sample size, suggest that additional studies comparing non-involved to tumor tissue may identify pathogenetic mechanisms and therapeutic targets that differ in AC of smokers and non-smokers.




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