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  • Poster Presentation
  • Open Access

Association of NCOA3 (AIB1) polymorphisms with breast cancer risk

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Breast Cancer Research20057 (Suppl 2) :P1.20

  • Published:


  • Breast Cancer
  • Tamoxifen
  • Breast Cancer Risk
  • Nuclear Receptor
  • Human Breast Tumour

The nuclear receptor coactivator 3 (NCOA3, also known as AIB1) is a coactivator of nuclear receptors like the estrogen receptor. NCOA3 is overexpressed in ~60% of primary human breast tumours, and high levels of NCOA3 expression are associated with tamoxifen resistance and worse survival rate. In contrast, NCOA3 deficiency suppresses v-Ha-ras-induced breast cancer initiation and progression in mice. Here we analysed the influence of NCOA3 coding single nucleotide polymorphisms on breast cancer risk by performing a case–control study using a German and a Polish study population, and identified an association between NCOA3 polymorphisms and breast cancer. A joint analysis of the German and Polish study population revealed a significant protective effect for the 1758G>C (Q586H) and 2880A>G (T960T) variants. In addition, haplotype analysis showed a protective effect of the 1758C-2880A and 1758G-2880G haplotypes (odds ratio = 0.79, 95% confidence interval = 0.67-0.93, P = 0.004). Due to the impact of NCOA3 in anti-estrogen therapy resistance, these polymorphisms might also influence therapy outcome in breast cancer.



BB and MW contributed equally to this work.

Authors’ Affiliations

Division of Molecular Genetic Epidemiology, German Cancer Research Center, Heidelberg, Germany
Institute of Human Genetics, University of Heidelberg, Germany
Department of Molecular Gynaeco-Oncology, Division of Gynaecology and Obstetrics, Clinical Center University of Cologne, Germany
Department of Tumor Biology, Center of Oncology, Maria Sklodowska-Curie Institute, Gliwice, Poland
Department at Biosciences at Novum, Karolinska Institute, Huddinge, Sweden
Institute of Transfusion Medicine and Immunology, Red Cross Blood Service of Baden–Württemberg–Hessia, University of Heidelberg, Faculty of Clinical Medicine, Mannheim, Germany
Department of Genetic Toxicology, Institute of Occupational Medicine and Environmental Health, Sosnowiec, Poland


© BioMed Central 2005