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Journal of the National Cancer Institute Advance Access originally published online on October 28, 2008
JNCI Journal of the National Cancer Institute 2008 100(21):1488-1491; doi:10.1093/jnci/djn380
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© The Author 2008. Published by Oxford University Press.

EDITORIALS

Intermediacy and Gene–Environment Interaction: The Example of CHRNA5-A3 Region, Smoking, Nicotine Dependence, and Lung Cancer

Sholom Wacholder, Nilanjan Chatterjee, Neil Caporaso

Affiliation of authors: Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, MD

Correspondence to: Sholom Wacholder, Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, MD 20892 (e-mail: WacholdS@mail.NIH.gov).

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During the "candidate gene era," many studies with a small number of cases investigated a small number of variants in a limited number of genes chosen on the basis of partial knowledge of their function. These studies established only a few genetic risk factors for cancer (1) and other diseases. Remarkably, recent genome-wide association (GWA) studies have produced strong evidence that variation in a number of genomic regions affects risk of disease (2). Successful GWA studies most often used an agnostic approach to interrogating as many of the more common genetic variants as feasible (up to a million now) and large numbers of cases. They adopted a de facto criterion for genome-wide statistical significance of P values below 10–7 (3), thus guaranteeing a low chance of reporting a false positive even for quite low prior probabilities of association and weak effects (4), . . . [Full Text of this Article]


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J Natl Cancer Inst 2008 100: 1485. [Extract] [Full Text] [PDF]



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