TY - JOUR
T1 - MnSOD Val-9Ala genotype, pro- and anti-oxidant environmental modifiers, and breast cancer among women on Long Island, New York
AU - Gaudet, Mia M.
AU - Gammon, Marilie D.
AU - Santella, Regina M.
AU - Britton, Julie A.
AU - Teitelbaum, Susan L.
AU - Eng, Sybil M.
AU - Terry, Mary Beth
AU - Bensen, Jeannette T.
AU - Schroeder, Jane
AU - Olshan, Andrew F.
AU - Neugut, Alfred I.
AU - Ambrosone, Christine B.
N1 - Funding Information:
For their valuable contributions to the Long Island Breast Cancer Study Project the authors thank: members of the Long Island Breast Cancer Network; the 31 participating institutions on Long Island and in New York City, NY; our National Institutes of Health collaborators, Gwen Colman, Ph.D., National Institutes of Environmental Health Sciences; G. Iris Obrams, M.D., Ph.D. formerly of the National Cancer Institute; members of the External Advisory Committee to the population-based case-control study: Leslie Bernstein, Ph.D., (Committee chair); Gerald Akland, M.S.; Barbara Bal-aban, MSW; Blake Cady, M.D.; Dale Sandler, Ph.D.; Roy Shore, Ph.D.; and Gerald Wogan, Ph.D.; as well as other collaborators who assisted with various aspects of our data collection efforts including Mary Wolff, Ph.D.; Steve Stellman, Ph.D.; Maureen Hatch, Ph.D.; Gail Garbowski, MPH; H. Leon Bradlow, Ph.D.; David Camann, B.S.; Martin Trent, B.S.; Jan Beyea, Ph.D.; Ruby Senie, Ph.D.; Carla Maffeo, Ph.D.; Pat Montal-van; Gertrud Berkowitz, Ph.D.; Margaret Kemeny, M.D.; Mark Citron, M.D.; Freya Schnabel, M.D.; Allen Schuss, M.D.; Steven Hajdu, M.D.; and Vincent Vinceguerra, M.D. This work was supported in part by grants from the National Cancer Institute and the National Institutes of Environmental Health and Sciences (Grant No. UO1CA/ES66572, UO1CA66572, P50CA55283, P30ES09089, and P30ES10126), and from the Department of Defense (Grant No. BC021366).
PY - 2005/12
Y1 - 2005/12
N2 - Excessive oxidative stress may induce and promote breast carcinogenesis. Manganese superoxide dismutase (MnSOD) is critical to management of oxidative stress by catalyzing the formation of hydrogen peroxide from two superoxide anions. To examine the relationship between MnSOD Val-9Ala polymorphism, breast cancer and potential modifiers, we analyzed data from a large population-based case-control study. Study participants com-pleted an in-home interviewer-administered questionnaire, and self-completed a Block food frequency questionnaire. Age-adjusted unconditional logistic models included 1034 cases and 1084 controls. As compared with Val/Val genotype, we found no association between MnSOD Ala/Val (OR = 0.98, 95% CI: 0.79-1.21) and Ala/Ala (OR = 1.00, 95% CI: 0.79-1.28) genotypes and breast cancer. Results did not differ by menopausal status, stage of tumor, or estrogen and progesterone receptor status. No discernable patterns of interaction were found between this MnSOD variant and anti-oxidative exposures, including fruit and vegetable intake or NSAID use, or pro-oxidant exposures, including smoking and alcohol. This study provides little evidence that variation in Val-9Ala polymorphism of MnSOD alone or through substantial interaction with key exposures believed to be pro- or antioxidant properties influences breast cancer risk.
AB - Excessive oxidative stress may induce and promote breast carcinogenesis. Manganese superoxide dismutase (MnSOD) is critical to management of oxidative stress by catalyzing the formation of hydrogen peroxide from two superoxide anions. To examine the relationship between MnSOD Val-9Ala polymorphism, breast cancer and potential modifiers, we analyzed data from a large population-based case-control study. Study participants com-pleted an in-home interviewer-administered questionnaire, and self-completed a Block food frequency questionnaire. Age-adjusted unconditional logistic models included 1034 cases and 1084 controls. As compared with Val/Val genotype, we found no association between MnSOD Ala/Val (OR = 0.98, 95% CI: 0.79-1.21) and Ala/Ala (OR = 1.00, 95% CI: 0.79-1.28) genotypes and breast cancer. Results did not differ by menopausal status, stage of tumor, or estrogen and progesterone receptor status. No discernable patterns of interaction were found between this MnSOD variant and anti-oxidative exposures, including fruit and vegetable intake or NSAID use, or pro-oxidant exposures, including smoking and alcohol. This study provides little evidence that variation in Val-9Ala polymorphism of MnSOD alone or through substantial interaction with key exposures believed to be pro- or antioxidant properties influences breast cancer risk.
KW - Breast cancer
KW - Gene-environment interaction
KW - MnSOD
UR - http://www.scopus.com/inward/record.url?scp=33644874895&partnerID=8YFLogxK
U2 - 10.1007/s10552-005-0375-6
DO - 10.1007/s10552-005-0375-6
M3 - Article
C2 - 16215873
AN - SCOPUS:33644874895
SN - 0957-5243
VL - 16
SP - 1225
EP - 1234
JO - Cancer Causes and Control
JF - Cancer Causes and Control
IS - 10
ER -