Polymorphisms in oxidative stress and inflammation pathway genes, low-dose ionizing radiation, and the risk of breast cancer among US radiologic technologists

Sara J. Schonfeld; Parveen Bhatti; Elizabeth E. Brown; Martha S. Linet; Steven L. Simon; Robert M. Weinstock; Amy A. Hutchinson; Marilyn Stovall; Dale L. Preston; Bruce H. Alexander; Michele M. Doody; Alice J. Sigurdson

doi:10.1007/s10552-010-9613-7

Polymorphisms in oxidative stress and inflammation pathway genes, low-dose ionizing radiation, and the risk of breast cancer among US radiologic technologists

Sara J. Schonfeld, Parveen Bhatti, Elizabeth E. Brown, Martha S. Linet, Steven L. Simon, Robert M. Weinstock, Amy A. Hutchinson, Marilyn Stovall, Dale L. Preston, Bruce H. Alexander, Michele M. Doody, Alice J. Sigurdson

Environmental Health Sciences

Research output: Contribution to journal › Article › peer-review

34 Scopus citations

Abstract

Objective: Ionizing radiation, an established breast cancer risk factor, has been shown to induce oxidative damage and chronic inflammation. Polymorphic variation in oxidative stress and inflammatory-mediated pathway genes may modify radiation-related breast cancer risk. Methods: We estimated breast cancer risk for 28 common variants in 16 candidate genes involved in these pathways among 859 breast cancer cases and 1,083 controls nested within the US Radiologic Technologists cohort. We estimated associations between occupational and personal diagnostic radiation exposures with breast cancer by modeling the odds ratio (OR) as a linear function in logistic regression models and assessed heterogeneity of the dose-response across genotypes. Results: There was suggestive evidence of an interaction between the rs5277 variant in PTGS2 and radiation-related breast cancer risk. The excess OR (EOR)/Gy from occupational radiation exposure = 5.5 (95%CI 1.2-12.5) for the GG genotype versus EOR/Gy < 0 (95%CI < 0-3.8) and EOR/Gy < 0 (95%CI < 0-14.8) for the GC and CC genotypes, respectively, (p _interaction = 0.04). The association between radiation and breast cancer was not modified by other SNPs examined. Conclusions: This study suggests that variation in PTGS2 may modify the breast cancer risk from occupational radiation exposure, but replication in other populations is needed to confirm this result.

Original language	English (US)
Pages (from-to)	1857-1866
Number of pages	10
Journal	Cancer Causes and Control
Volume	21
Issue number	11
DOIs	https://doi.org/10.1007/s10552-010-9613-7
State	Published - Nov 2010

Bibliographical note

Funding Information:
Acknowledgments We are grateful to the radiologic technologists who participated in the USRT Study; Jerry Reid of the American Registry of Radiologic Technologists for continued support of this study; Diane Kampa and Allison Iwan of the University of Minnesota for data collection and study coordination; Laura Bowen of Information Management Systems for biomedical computing statistical support; and Chu-Ling Yu of the National Cancer Institute for editorial and scientific review. This research was supported by the Intramural Research Program of the National Cancer Institute, National Institutes of Health. This project has been funded in part with federal funds from the National Cancer Institute, National Institutes of Health, under Contract No. HHSN261200800001E. The content of this publication does not necessarily reflect the views or policies of the Department of Health and Human Services, nor does mention of trade names, commercial products, or organizations imply endorsement by the US Government.

Keywords

Breast cancer
COX-2
Inflammation
PTGS2
Radiation

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

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10.1007/s10552-010-9613-7

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Schonfeld, S. J., Bhatti, P., Brown, E. E., Linet, M. S., Simon, S. L., Weinstock, R. M., Hutchinson, A. A., Stovall, M., Preston, D. L., Alexander, B. H., Doody, M. M., & Sigurdson, A. J. (2010). Polymorphisms in oxidative stress and inflammation pathway genes, low-dose ionizing radiation, and the risk of breast cancer among US radiologic technologists. Cancer Causes and Control, 21(11), 1857-1866. https://doi.org/10.1007/s10552-010-9613-7

Schonfeld, SJ, Bhatti, P, Brown, EE, Linet, MS, Simon, SL, Weinstock, RM, Hutchinson, AA, Stovall, M, Preston, DL, Alexander, BH, Doody, MM & Sigurdson, AJ 2010, 'Polymorphisms in oxidative stress and inflammation pathway genes, low-dose ionizing radiation, and the risk of breast cancer among US radiologic technologists', Cancer Causes and Control, vol. 21, no. 11, pp. 1857-1866. https://doi.org/10.1007/s10552-010-9613-7

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title = "Polymorphisms in oxidative stress and inflammation pathway genes, low-dose ionizing radiation, and the risk of breast cancer among US radiologic technologists",

abstract = "Objective: Ionizing radiation, an established breast cancer risk factor, has been shown to induce oxidative damage and chronic inflammation. Polymorphic variation in oxidative stress and inflammatory-mediated pathway genes may modify radiation-related breast cancer risk. Methods: We estimated breast cancer risk for 28 common variants in 16 candidate genes involved in these pathways among 859 breast cancer cases and 1,083 controls nested within the US Radiologic Technologists cohort. We estimated associations between occupational and personal diagnostic radiation exposures with breast cancer by modeling the odds ratio (OR) as a linear function in logistic regression models and assessed heterogeneity of the dose-response across genotypes. Results: There was suggestive evidence of an interaction between the rs5277 variant in PTGS2 and radiation-related breast cancer risk. The excess OR (EOR)/Gy from occupational radiation exposure = 5.5 (95%CI 1.2-12.5) for the GG genotype versus EOR/Gy < 0 (95%CI < 0-3.8) and EOR/Gy < 0 (95%CI < 0-14.8) for the GC and CC genotypes, respectively, (p interaction = 0.04). The association between radiation and breast cancer was not modified by other SNPs examined. Conclusions: This study suggests that variation in PTGS2 may modify the breast cancer risk from occupational radiation exposure, but replication in other populations is needed to confirm this result.",

keywords = "Breast cancer, COX-2, Inflammation, PTGS2, Radiation",

author = "Schonfeld, {Sara J.} and Parveen Bhatti and Brown, {Elizabeth E.} and Linet, {Martha S.} and Simon, {Steven L.} and Weinstock, {Robert M.} and Hutchinson, {Amy A.} and Marilyn Stovall and Preston, {Dale L.} and Alexander, {Bruce H.} and Doody, {Michele M.} and Sigurdson, {Alice J.}",

note = "Funding Information: Acknowledgments We are grateful to the radiologic technologists who participated in the USRT Study; Jerry Reid of the American Registry of Radiologic Technologists for continued support of this study; Diane Kampa and Allison Iwan of the University of Minnesota for data collection and study coordination; Laura Bowen of Information Management Systems for biomedical computing statistical support; and Chu-Ling Yu of the National Cancer Institute for editorial and scientific review. This research was supported by the Intramural Research Program of the National Cancer Institute, National Institutes of Health. This project has been funded in part with federal funds from the National Cancer Institute, National Institutes of Health, under Contract No. HHSN261200800001E. The content of this publication does not necessarily reflect the views or policies of the Department of Health and Human Services, nor does mention of trade names, commercial products, or organizations imply endorsement by the US Government.",

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T1 - Polymorphisms in oxidative stress and inflammation pathway genes, low-dose ionizing radiation, and the risk of breast cancer among US radiologic technologists

AU - Schonfeld, Sara J.

AU - Bhatti, Parveen

AU - Brown, Elizabeth E.

AU - Linet, Martha S.

AU - Simon, Steven L.

AU - Weinstock, Robert M.

AU - Hutchinson, Amy A.

AU - Stovall, Marilyn

AU - Preston, Dale L.

AU - Alexander, Bruce H.

AU - Doody, Michele M.

AU - Sigurdson, Alice J.

N1 - Funding Information: Acknowledgments We are grateful to the radiologic technologists who participated in the USRT Study; Jerry Reid of the American Registry of Radiologic Technologists for continued support of this study; Diane Kampa and Allison Iwan of the University of Minnesota for data collection and study coordination; Laura Bowen of Information Management Systems for biomedical computing statistical support; and Chu-Ling Yu of the National Cancer Institute for editorial and scientific review. This research was supported by the Intramural Research Program of the National Cancer Institute, National Institutes of Health. This project has been funded in part with federal funds from the National Cancer Institute, National Institutes of Health, under Contract No. HHSN261200800001E. The content of this publication does not necessarily reflect the views or policies of the Department of Health and Human Services, nor does mention of trade names, commercial products, or organizations imply endorsement by the US Government.

PY - 2010/11

Y1 - 2010/11

N2 - Objective: Ionizing radiation, an established breast cancer risk factor, has been shown to induce oxidative damage and chronic inflammation. Polymorphic variation in oxidative stress and inflammatory-mediated pathway genes may modify radiation-related breast cancer risk. Methods: We estimated breast cancer risk for 28 common variants in 16 candidate genes involved in these pathways among 859 breast cancer cases and 1,083 controls nested within the US Radiologic Technologists cohort. We estimated associations between occupational and personal diagnostic radiation exposures with breast cancer by modeling the odds ratio (OR) as a linear function in logistic regression models and assessed heterogeneity of the dose-response across genotypes. Results: There was suggestive evidence of an interaction between the rs5277 variant in PTGS2 and radiation-related breast cancer risk. The excess OR (EOR)/Gy from occupational radiation exposure = 5.5 (95%CI 1.2-12.5) for the GG genotype versus EOR/Gy < 0 (95%CI < 0-3.8) and EOR/Gy < 0 (95%CI < 0-14.8) for the GC and CC genotypes, respectively, (p interaction = 0.04). The association between radiation and breast cancer was not modified by other SNPs examined. Conclusions: This study suggests that variation in PTGS2 may modify the breast cancer risk from occupational radiation exposure, but replication in other populations is needed to confirm this result.

AB - Objective: Ionizing radiation, an established breast cancer risk factor, has been shown to induce oxidative damage and chronic inflammation. Polymorphic variation in oxidative stress and inflammatory-mediated pathway genes may modify radiation-related breast cancer risk. Methods: We estimated breast cancer risk for 28 common variants in 16 candidate genes involved in these pathways among 859 breast cancer cases and 1,083 controls nested within the US Radiologic Technologists cohort. We estimated associations between occupational and personal diagnostic radiation exposures with breast cancer by modeling the odds ratio (OR) as a linear function in logistic regression models and assessed heterogeneity of the dose-response across genotypes. Results: There was suggestive evidence of an interaction between the rs5277 variant in PTGS2 and radiation-related breast cancer risk. The excess OR (EOR)/Gy from occupational radiation exposure = 5.5 (95%CI 1.2-12.5) for the GG genotype versus EOR/Gy < 0 (95%CI < 0-3.8) and EOR/Gy < 0 (95%CI < 0-14.8) for the GC and CC genotypes, respectively, (p interaction = 0.04). The association between radiation and breast cancer was not modified by other SNPs examined. Conclusions: This study suggests that variation in PTGS2 may modify the breast cancer risk from occupational radiation exposure, but replication in other populations is needed to confirm this result.

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KW - COX-2

KW - Inflammation

KW - PTGS2

KW - Radiation

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Polymorphisms in oxidative stress and inflammation pathway genes, low-dose ionizing radiation, and the risk of breast cancer among US radiologic technologists

Abstract

Bibliographical note

Keywords

UN SDGs

Access

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