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Carcinogenesis Advance Access published online on June 19, 2008
Carcinogenesis, doi:10.1093/carcin/bgn140
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© The Author 2008. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Double strand breaks repair in lymphoblastoid cell lines from sisters discordant for breast cancer from the New York site of the BCFR

Nicola Machella1, Mary Beth Terry2, Jennifer Zipprich1, Irina Gurvich1, Yuyan Liao2, Ruby T. Senie2, David O. Kennedy1 and Regina M. Santella1

1 Departments of Environmental Health Sciences
2 Epidemiology, Mailman School of Public Health, Columbia University, New York, NY

Author for correspondence: Regina M. Santella, Department of Environmental Health Sciences, Mailman School of Public Health, Columbia University, 630 West 168th Street, P & S 19-418, New York, NY 10032, USA. Phone: 212-305-8158, Fax: 212-305-5328. Email: rps1{at}columbia.edu

Unrepaired DNA double strand breaks (DSB) may have serious consequences for cells by inducing chromosomal aberrations, thereby increasing genetic instability and cancer risk. One's capacity to repair DSB is therefore an important factor to consider when estimating cancer risk. We assessed DNA end-joining (EJ) capacity in cell lines derived from sisters discordant for breast cancer to determine if individual differences in DSB repair are a significant risk factor. We used an in vitro phenotypic assay on nuclear extracts from lymphoblasts of 179 subjects including 86 cases and 93 controls. EJ activity was functionally estimated as the ability of extracts to join together monomers of the plasmid pUC18 linearized either with sticky (EcoRI) or blunt ends (HincII). Mean percentage of EJ capacity was slightly lower in cases than controls, both for EcoRI (Cases 27.9 ± 11.1; Controls 29.6 ± 10.7, p = .28) and HincII substrates (Cases 28.8 ± 12.2; Controls 30.6 ± 13.0, p = .36); however, no significant differences were observed. Categorizing EJ capacity into tertiles and using the highest activity as the referent, we observed elevated associations for each tertile of decreased repair (OR = 2.20, 95% CI = 0.77-6.22 and OR = 4.22, 95% CI = 1.22-14.0, p = .02) respectively, for EcoRI. Results were not statistically significant for HincII (OR = 1.37, 95% CI =0.51-3.70 and OR = 2.32, 95% CI = 0.57-9.38, p = .24). These data suggest that individual differences in EJ capacity may represent a risk factor predisposing women to breast cancer.

Received January 24, 2008; revised June 4, 2008; accepted June 5, 2008.


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