Invited commentary: genes, environment, and hybrid vigor.
In the 1950s, case-control studies of smoking and lung cancer established a paradigm for epidemiologic studies of risk factors for chronic diseases. Since then, thousands of case-control studies have examined possible associations of countless risk factors with numerous diseases, rarely finding associations as strong or consistent as that of smoking with lung cancer. Recently, researchers have applied advances in molecular genetics to conduct candidate gene and genome-wide association studies of lung cancer. Skeptics among both epidemiologists and geneticists have argued that genomic research adds little value when most cases of disease can be attributed to a preventable exposure; however, well-conducted studies of gene-environment interactions that draw on data from more than 50 years of research in toxicology, pathophysiology, and behavioral science offer important models for the development of more comprehensive approaches to understanding the etiology of chronic diseases.
Gwinn
Marta
M
Office of Public Health Genomics, Centers for Disease Control and Prevention, Atlanta, Georgia 30341 , USA. mgwinn@cdc.gov
Guessous
Idris
I
Khoury
Muin J
MJ
D045647:DNA Glycosylases / Q000235:genetics* / Q000378:metabolism; D004777:Environment; D020022:Genetic Predisposition to Disease; D006801:Humans; D006823:Hybrid Vigor / Q000235:genetics; D008175:Lung Neoplasms / Q000201:enzymology / Q000453:epidemiology / Q000235:genetics*; D012307:Risk Factors; D012907:Smoking / Q000009:adverse effects*; D013624:Taiwan / Q000453:epidemiology
D045647:DNA Glycosylases; C479058:oxoguanine glycosylase 1, human