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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
1
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pubmed:dateCreated |
2006-1-25
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pubmed:abstractText |
This is by far the largest study of its kind to date, and further suggests that AIB1 does not play a substantial role in modifying the phenotype of BRCA1 and BRCA2 carriers. The AIB1 gene encodes the AIB1/SRC-3 steroid hormone receptor coactivator, and amplification of the gene and/or protein occurs in breast and ovarian tumors. A CAG/CAA repeat length polymorphism encodes a stretch of 17 to 29 glutamines in the HR-interacting carboxyl-terminal region of the protein which is somatically unstable in tumor tissues and cell lines. There is conflicting evidence regarding the role of this polymorphism as a modifier of breast cancer risk in BRCA1 and BRCA2 carriers. To further evaluate the evidence for an association between AIB1 glutamine repeat length and breast cancer risk in BRCA1 and BRCA2 mutation carriers, we have genotyped this polymorphism in 1,090 BRCA1 and 661 BRCA2 mutation carriers from Australia, Europe, and North America. There was no evidence for an increased risk associated with AIB1 glutamine repeat length. Given the large sample size, with more than adequate power to detect previously reported effects, we conclude that the AIB1 glutamine repeat does not substantially modify risk of breast cancer in BRCA1 and BRCA2 mutation carriers.
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pubmed:grant |
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
Jan
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pubmed:issn |
1055-9965
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pubmed:author |
pubmed-author:AndrulisIrene LIL,
pubmed-author:AntoniouAntonis CAC,
pubmed-author:Australian Breast Cancer Family Study,
pubmed-author:Australian Jewish Breast Cancer Study,
pubmed-author:BeckJeanneJ,
pubmed-author:Breast Cancer Family Registry,
pubmed-author:Chenevix-TrenchGeorgiaG,
pubmed-author:CookMargaret RMR,
pubmed-author:DalyMary BMB,
pubmed-author:DurocherFrancineF,
pubmed-author:EastonDouglas FDF,
pubmed-author:Epidemiological Study of Familial Breast Cancer Study Collaborators,
pubmed-author:GodwinAndrew KAK,
pubmed-author:GreeneMark HMH,
pubmed-author:HollandHeleneH,
pubmed-author:HopperJohn LJL,
pubmed-author:Interdisciplinary Health Research International Team on Breast Cancer...,
pubmed-author:JohnEsther MEM,
pubmed-author:Kathleen Cunningham Foundation Consortium for Research into Familial...,
pubmed-author:KelemenLiviaL,
pubmed-author:MironAlexanderA,
pubmed-author:PeockSusanS,
pubmed-author:PlourdeMarieM,
pubmed-author:SantellaRegina MRM,
pubmed-author:SimardJacquesJ,
pubmed-author:SmithPaula LPL,
pubmed-author:SoutheyMelissa CMC,
pubmed-author:SpurdleAmanda BAB,
pubmed-author:StruewingJeffery PJP
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pubmed:copyrightInfo |
(Cancer Epidemiol Biomarkers Prev 2006;15(1):76-9).
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pubmed:issnType |
Print
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pubmed:volume |
15
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
76-9
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pubmed:dateRevised |
2009-11-19
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pubmed:meshHeading |
pubmed-meshheading:16434590-Acetyltransferases,
pubmed-meshheading:16434590-Breast Neoplasms,
pubmed-meshheading:16434590-Female,
pubmed-meshheading:16434590-Genes, BRCA1,
pubmed-meshheading:16434590-Genes, BRCA2,
pubmed-meshheading:16434590-Genetic Predisposition to Disease,
pubmed-meshheading:16434590-Genotype,
pubmed-meshheading:16434590-Histone Acetyltransferases,
pubmed-meshheading:16434590-Humans,
pubmed-meshheading:16434590-Mutation,
pubmed-meshheading:16434590-Nuclear Receptor Coactivator 3,
pubmed-meshheading:16434590-Oncogene Proteins,
pubmed-meshheading:16434590-Peptides,
pubmed-meshheading:16434590-Polymorphism, Genetic,
pubmed-meshheading:16434590-Proportional Hazards Models,
pubmed-meshheading:16434590-Repetitive Sequences, Nucleic Acid,
pubmed-meshheading:16434590-Risk,
pubmed-meshheading:16434590-Trans-Activators
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pubmed:year |
2006
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pubmed:articleTitle |
The AIB1 polyglutamine repeat does not modify breast cancer risk in BRCA1 and BRCA2 mutation carriers.
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pubmed:affiliation |
The Queensland Institute of Medical Research, Brisbane, Australia. Amanda.Spurdle@qimr.edu.au
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't,
Research Support, N.I.H., Extramural
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