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Carcinogenesis Advance Access published online on December 19, 2005
Carcinogenesis, doi:10.1093/carcin/bgi288
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© The Author 2005. Published by Oxford University Press. All rights reserved. For permissions, please email: journals.permissions@oxfordjournals.org
Received June 15, 2005
Revised November 20, 2005
Accepted November 22, 2005

MOLECULAR EPIDEMIOLOGY AND CANCER PREVENTION

DNA damage levels in prostate cancer cases and controls

Kristin L. Lockett 1, M. Craig Hall 2, Peter E. Clark 2, Shu-Chun Chuang 1, Brittany Robinson 1, Hui-Yi Lin 3, L. Joseph Su 4, and Jennifer J. Hu 5 *

1 Department of Cancer Biology, Wake Forest University School of Medicine, Winston-Salem, NC 27157, USA
2 Department of Urology, Wake Forest University School of Medicine, Winston-Salem, NC 27157, USA; Comprehensive Cancer Center, Wake Forest University School of Medicine, Winston-Salem, NC 27157, USA
3 School of Public Health, Louisiana State University Health Sciences Center, New Orleans, LA 70112
4 School of Public Health, Louisiana State University Health Sciences Center, New Orleans, LA 70112; Stanley S. Scott Cancer Center, Louisiana State University Health Sciences Center, New Orleans, LA 70112
5 Department of Cancer Biology, Wake Forest University School of Medicine, Winston-Salem, NC 27157, USA; Comprehensive Cancer Center, Wake Forest University School of Medicine, Winston-Salem, NC 27157, USA; School of Public Health, Louisiana State University Health Sciences Center, New Orleans, LA 70112; Stanley S. Scott Cancer Center, Louisiana State University Health Sciences Center, New Orleans, LA 70112

* To whom correspondence should be addressed.
Jennifer J. Hu, E-mail: jenhu{at}lsuhsc.edu


  Abstract

This study used the alkaline Comet assay to evaluate whether basal or H2O2-induced DNA damage is associated with prostate cancer (CaP) risk. Using lymphocyte samples from 158 CaP cases and 128 controls, collected in an ongoing case-control study, our results showed that basal DNA damage did not differ between cases and controls. However, the H2O2-induced DNA damage level was significantly higher in incident cases (mean±SD; 6.61±4.43, n=102) than controls (5.30±3.60, n=128) or prevalent cases (4.47±3.19; n=56). Incident cases with a positive smoking history had significantly higher H2O2-induced DNA damage than never-smokers (7.57±4.82 vs. 4.52±2.40; p<0.001). Above-median H2O2-induced DNA damage was associated with a 1.61-fold increase in CaP risk (95% confidence interval [CI]=0.92-2.81), after adjustment for age, race, benign prostatic hyperplasia, smoking history, and family history (FH). Using the lowest quartile of H2O2-induced DNA damage as the referent group, the adjusted ORs for the 25th, 50th, and 75th quartiles were 0.90 (95% CI=0.39-2.05), 1.06 (95% CI=0.48-2.35), and 2.05 (95% CI=0.96-4.37), respectively (p=0.046, test for linear trend). The association between CaP and DNA damage was modified by age, smoking history, family history, and body mass index. Our results suggest that DNA damage may be associated with CaP risk. However, larger case-control and follow-up studies are warranted to further evaluate the potential application of the alkaline Comet assay in CaP risk assessment and prevention.


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