Journal Article

DNA double-strand break repair capacity and risk of breast cancer

Da-Tian Bau, Yi-Chien Mau, Shian-ling Ding, Pei-Ei Wu and Chen-Yang Shen

in Carcinogenesis

Volume 28, issue 8, pages 1726-1730
Published in print August 2007 | ISSN: 0143-3334
Published online May 2007 | e-ISSN: 1460-2180 | DOI:
DNA double-strand break repair capacity and risk of breast cancer

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A tumorigenic role of the non-homologous end-joining (NHEJ) pathway for the repair of DNA double-strand breaks (DSBs) has been suggested by our finding of a significant association between increased breast cancer risk and a cooperative effect of single-nucleotide polymorphisms in NHEJ genes. To confirm this finding, this case–control study detected both in vivo and in vitro DNA end-joining (EJ) capacities in Epstein-Barr virus-immortalized peripheral blood mononuclear cells (PBMCs) of 112 breast cancer patients and 108 healthy controls to identify individual differences in EJ capacity to repair DSB as a risk factor predisposing women to breast cancer. PBMCs from breast cancer patients consistently showed lower values of in vivo and in vitro EJ capacities than those from healthy women (P < 0.05). Logistic regression, simultaneously considering the effect of known risk factors of breast cancer, shows that the in vitro EJ capacity above the median of control subjects was associated with nearly 3-fold increased risks for breast cancer (adjusted odds ratio, 2.98; 95% confidence interval, 1.64–5.43). Furthermore, a dose–response relationship was evident between risk for breast cancer and EJ capacity, which was analyzed as a continuous variable (every unit decrease of EJ capacity being associated with an 1.09-fold increase of breast cancer risk) and was divided into tertiles based on the EJ capacity values of the controls (P for trend < 0.01). The findings support the conclusion that NHEJ may play a role in susceptibility to breast cancer.

Journal Article.  4054 words.  Illustrated.

Subjects: Clinical Cytogenetics and Molecular Genetics

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