Interaction of Cigarette Exposure and Airway Epithelial Cell Gene Expression

被引:22
作者
Brody, Jerome S. [1 ]
Steiling, Katrina [1 ]
机构
[1] Boston Univ, Sch Med, Ctr Pulm, Boston, MA 02218 USA
来源
ANNUAL REVIEW OF PHYSIOLOGY, VOL 73 | 2011年 / 73卷
关键词
field of injury; lung cancer; COPD; OBSTRUCTIVE PULMONARY-DISEASE; ABERRANT PROMOTER METHYLATION; LUNG-CANCER; BRONCHIAL EPITHELIUM; OXIDATIVE STRESS; MOLECULAR ALTERATIONS; DNA METHYLATION; SMOKING; TOBACCO; INFLAMMATION;
D O I
10.1146/annurev-physiol-012110-142219
中图分类号
Q4 [生理学];
学科分类号
071003 ;
摘要
Cigarette smoking is responsible for lung cancer and chronic obstructive pulmonary disease (COPD), the leading cause of death from cancer and the second-leading cause of death in the United States. In the United States, 46 million people smoke, with an equal number of former smokers. Moreover, 20-25% of current or former smokers will develop either disease, and smokers with one disease are at increased risk for developing the other. There are no tools for predicting risk of developing either disease; no accepted tools for early diagnosis of potentially curable lung cancer; and no tools for defining molecular pathways or molecular subtypes of these diseases, for predicting rate of progression, or for assessing response to therapy at a biochemical or molecular level. This review discusses current studies and the future potential of measuring global gene expression in epithelial cells that are in the airway field of injury and of using the genomic information derived to begin to answer some of the above questions.
引用
收藏
页码:437 / 456
页数:20
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