Title | Circulating Antioxidant Levels and Risk of Prostate Cancer by TMPRSS2:ERG. |
Publication Type | Journal Article |
Year of Publication | 2017 |
Authors | Graff RE, Judson G, Ahearn TU, Fiorentino M, Loda M, Giovannucci EL, Mucci LA, Pettersson A |
Journal | Prostate |
Volume | 77 |
Issue | 6 |
Pagination | 647-653 |
Date Published | 2017 May |
ISSN | 1097-0045 |
Keywords | Adult, Aged, Aged, 80 and over, Antioxidants, Biomarkers, Tumor, Case-Control Studies, Double-Blind Method, Follow-Up Studies, Humans, Male, Middle Aged, Prospective Studies, Prostatic Neoplasms, Risk Factors, Serine Endopeptidases, Transcriptional Regulator ERG |
Abstract | BACKGROUND: Few studies have considered etiological differences across molecular subtypes of prostate cancer, despite potential to improve opportunities for precision prevention of a disease for which modifiable risk factors have remained elusive. Factors that lead to DNA double-strand breaks, such as oxidative stress, may promote the formation of the TMPRSS2:ERG gene fusion in prostate cancer. We tested the hypothesis that increasing levels of pre-diagnostic circulating antioxidants, which may reduce oxidative stress, are associated with lower risk of developing TMPRSS2:ERG positive prostate cancer. METHODS: We conducted a nested case-control study, including 370 cases and 2,470 controls, to evaluate associations between pre-diagnostic α- and β-carotene, α- and γ-tocopherol, β-cryptoxanthin, lutein, lycopene, retinol, and selenium with the risk of prostate cancer by ERG protein expression status (a marker of TMPRSS2:ERG). Multivariable unconditional polytomous logistic regression was used to calculate odds ratios and 95% confidence intervals. RESULTS: We did not find any of the antioxidants to be significantly associated with the risk of prostate cancer according to ERG status. CONCLUSIONS: The results do not support the hypothesis that circulating pre-diagnostic antioxidant levels protect against developing TMPRSS2:ERG positive prostate cancer. Additional studies are needed to explore mechanisms for the development of TMPRSS2:ERG positive disease. Prostate 77: 647-653, 2017. © 2017 Wiley Periodicals, Inc. |
DOI | 10.1002/pros.23312 |
Alternate Journal | Prostate |
PubMed ID | 28102015 |
PubMed Central ID | PMC5354965 |
Grant List | P50 CA090381 / CA / NCI NIH HHS / United States P01 CA087969 / CA / NCI NIH HHS / United States R25 CA112355 / CA / NCI NIH HHS / United States T32 CA009001 / CA / NCI NIH HHS / United States UM1 CA167552 / CA / NCI NIH HHS / United States R01 CA136578 / CA / NCI NIH HHS / United States |
Related Faculty:
Massimo Loda, M.D.