Journal article
ABRAXAS (FAM175A) and breast cancer susceptibility: No evidence of association in the breast cancer family registry
AL Renault, F Lesueur, Y Coulombe, S Gobeil, P Soucy, Y Hamdi, S Desjardins, F Le Calvez-Kelm, M Vallï e, C Voegele, JL Hopper, IL Andrulis, MC Southey, EM John, JY Masson, SV Tavtigian, JS Simard, S Buys, M Daly, MB Terry
PLoS ONE | PUBLIC LIBRARY SCIENCE | Published : 2016
Abstract
� 2016 Renault et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Approximately half of the familial aggregation of breast cancer remains unexplained. This proportion is less for early-onset disease where familial aggregation is greater, suggesting that other susceptibility genes remain to be discovered. The majority of known breast cancer susceptibility genes are involved in the DNA double-strand break repair pathway. ABRAXAS is involved in this pathway and mutations in this gene impair BRCA1 recruit..
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Awarded by Canadian Institutes of Health Research for the "CIHR Team in Familial Risks of Breast Cancer" program
Awarded by Ministry of Economic Development, Innovation and Export Trade
Awarded by Canadian Institutes of Health Research
Awarded by National Institute of Health (NIH)
Awarded by National Cancer Institute
Funding Acknowledgements
This work was supported by the Canadian Institutes of Health Research for the "CIHR Team in Familial Risks of Breast Cancer" program - grant # CRN-87521, the Ministry of Economic Development, Innovation and Export Trade - grant # PSR-SIIRI-701 and by the Government of Canada through Genome Canada and the Canadian Institutes of Health Research (GPH-129344), the Ministere de l'Economia, de la Science et de l'Innovation du Quebec through Genome Quebec, the Quebec Breast Cancer Foundation for the PERSPECTIVE project, the National Cancer Institute (NCI) and the National Institute of Health (NIH) grant R01 CA121245. This work was also supported by grant UM1 CA164920 from the National Cancer Institute. The content of this manuscript does not necessarily reflect the views or policies of the National Cancer Institute or any of the collaborating centers in the Breast Cancer Family Registry (BCFR), nor does mention of trade names, commercial products, or organizations imply endorsement by the US Government or the BCFR. J.S. is Chairholder of the Canada Research Chair in Oncogenetics. J-Y.M. is a FQRS chercheur national investigator and was supported by a Canadian Institutes of Health Research operating grant. I.L.A is the Anne and Max Tanenbaum Chair in Molecular Medicine at the University of Toronto. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.