TY - JOUR
T1 - DNA damage levels in prostate cancer cases and controls
AU - Lockett, Kristin L.
AU - Hall, M. Craig
AU - Clark, Peter E.
AU - Chuang, Shu Chun
AU - Robinson, Brittany
AU - Lin, Hui Yi
AU - Su, L. Joseph
AU - Hu, Jennifer J.
N1 - Funding Information:
The authors are grateful to study participants. We also want to acknowledge the contributions of Frank M.Torti, MD; Robert Lee, MD; Charles J.Rosser, MD; Dean G.Assimos, MD; Elizabeth Albertson, MD; Dominck J.Carbone, MD; William Rice, MD; Francis O’Brien, MD; Ray Morrow, MD; Franklyn Millman, MD; Nadine Shelton, Joel Anderson, Shirley Cothren, Eunkyung Chang, the General Clinical Research Center, the Urology Clinic and the Internal Medicine Clinic. This study was supported by a grant from the American Cancer Society (No. CNE-101119 to J.J.H.), a pilot grant from the Comprehensive Cancer Center of Wake Forest University (CA12197 to J.J.H.) and a grant from the National Research Foundation to the Wake Forest University’s General Clinical Research Center (M01-RR07122).
PY - 2006/6
Y1 - 2006/6
N2 - 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 H2 O2-induced DNA damage than never-smokers (7.57 ± 4.82 versus 4.52 ± 2.40; P < 0.001). Above-median H2 O2-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 (BPH), 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.
AB - 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 H2 O2-induced DNA damage than never-smokers (7.57 ± 4.82 versus 4.52 ± 2.40; P < 0.001). Above-median H2 O2-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 (BPH), 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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U2 - 10.1093/carcin/bgi288
DO - 10.1093/carcin/bgi288
M3 - Article
C2 - 16364923
AN - SCOPUS:33745588556
SN - 0143-3334
VL - 27
SP - 1187
EP - 1193
JO - Carcinogenesis
JF - Carcinogenesis
IS - 6
ER -