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[Cancer Research 63, 4327-4330, August 1, 2003]
© 2003 American Association for Cancer Research

Advances in Brief

Functional FAS Promoter Polymorphisms Are Associated with Increased Risk of Acute Myeloid Leukemia1

Kathryn Sibley2, Sara Rollinson, James M. Allan, Alexandra G. Smith, Graham R. Law, Philippa L. Roddam, Christine F. Skibola3, Martyn T. Smith3 and Gareth J. Morgan

Leukaemia Research Fund, Epidemiology and Genetics Unit, School of Medicine, University of Leeds, Leeds LS2 9JT, United Kingdom

The FAS (TNFRSF6/CD95/APO-1) gene is silenced in many tumor types, resulting in an inability to respond to proapoptotic signals. The FAS promoter is polymorphic, including a G to A substitution at -1377 bp and an A to G substitution at -670 bp, which occur within SP1 and signal transducers and activators of transcription 1 transcription factor binding sites, respectively. In a case-control study of adult acute myeloid leukemia (AML), we show a significantly increased risk of AML associated with heterozygotes (GA) and homozygote variants (AA) at position -1377 bp (32.3% in cases versus 22.0% in controls; odds ratio, 1.69; 95% confidence interval, 1.32–2.16). Extended haplotype analysis revealed that the -1377A/-670A haplotype was significantly associated with disease (3% versus 0.5%; odds ratio, 6.72; 95% confidence interval, 3.13–14.51). These data suggest that variation in the FAS gene promoter may affect FAS gene expression and modulate apoptotic signaling, contributing to an increased risk of AML.




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