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Cellular, Molecular, and Tumor Biology 28: Functional Genomics

BRCA1 mediates the repression of select X chromosome genes

Amir A. Jazaeri, Chandramouli Gadisetti, Olga Aprelikova, Ulrike A. Nuber, Christos Sotiriou, Edison T. Liu, Hans H. Ropers, Cindy J. Yee, Jeff Boyd and J. C. Barrett
Amir A. Jazaeri
MD Anderson Cancer Center, Houston, TX, National Cancer Institute, Bethesda, MD, Max Planck Institute for Molecular Genetics, Berlin, Germany, Jules Bordet Institute, Brussels, Belgium, Genome Institute of Singapore, Singapore, Singapore, Memorial Sloan-Kettering Cancer Center, New York, NY
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Chandramouli Gadisetti
MD Anderson Cancer Center, Houston, TX, National Cancer Institute, Bethesda, MD, Max Planck Institute for Molecular Genetics, Berlin, Germany, Jules Bordet Institute, Brussels, Belgium, Genome Institute of Singapore, Singapore, Singapore, Memorial Sloan-Kettering Cancer Center, New York, NY
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Olga Aprelikova
MD Anderson Cancer Center, Houston, TX, National Cancer Institute, Bethesda, MD, Max Planck Institute for Molecular Genetics, Berlin, Germany, Jules Bordet Institute, Brussels, Belgium, Genome Institute of Singapore, Singapore, Singapore, Memorial Sloan-Kettering Cancer Center, New York, NY
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Ulrike A. Nuber
MD Anderson Cancer Center, Houston, TX, National Cancer Institute, Bethesda, MD, Max Planck Institute for Molecular Genetics, Berlin, Germany, Jules Bordet Institute, Brussels, Belgium, Genome Institute of Singapore, Singapore, Singapore, Memorial Sloan-Kettering Cancer Center, New York, NY
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Christos Sotiriou
MD Anderson Cancer Center, Houston, TX, National Cancer Institute, Bethesda, MD, Max Planck Institute for Molecular Genetics, Berlin, Germany, Jules Bordet Institute, Brussels, Belgium, Genome Institute of Singapore, Singapore, Singapore, Memorial Sloan-Kettering Cancer Center, New York, NY
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Edison T. Liu
MD Anderson Cancer Center, Houston, TX, National Cancer Institute, Bethesda, MD, Max Planck Institute for Molecular Genetics, Berlin, Germany, Jules Bordet Institute, Brussels, Belgium, Genome Institute of Singapore, Singapore, Singapore, Memorial Sloan-Kettering Cancer Center, New York, NY
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Hans H. Ropers
MD Anderson Cancer Center, Houston, TX, National Cancer Institute, Bethesda, MD, Max Planck Institute for Molecular Genetics, Berlin, Germany, Jules Bordet Institute, Brussels, Belgium, Genome Institute of Singapore, Singapore, Singapore, Memorial Sloan-Kettering Cancer Center, New York, NY
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Cindy J. Yee
MD Anderson Cancer Center, Houston, TX, National Cancer Institute, Bethesda, MD, Max Planck Institute for Molecular Genetics, Berlin, Germany, Jules Bordet Institute, Brussels, Belgium, Genome Institute of Singapore, Singapore, Singapore, Memorial Sloan-Kettering Cancer Center, New York, NY
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Jeff Boyd
MD Anderson Cancer Center, Houston, TX, National Cancer Institute, Bethesda, MD, Max Planck Institute for Molecular Genetics, Berlin, Germany, Jules Bordet Institute, Brussels, Belgium, Genome Institute of Singapore, Singapore, Singapore, Memorial Sloan-Kettering Cancer Center, New York, NY
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J. C. Barrett
MD Anderson Cancer Center, Houston, TX, National Cancer Institute, Bethesda, MD, Max Planck Institute for Molecular Genetics, Berlin, Germany, Jules Bordet Institute, Brussels, Belgium, Genome Institute of Singapore, Singapore, Singapore, Memorial Sloan-Kettering Cancer Center, New York, NY
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DOI:  Published April 2004
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Proc Amer Assoc Cancer Res, Volume 45, 2004

Abstract

1620

Objectives: Recently it has been proposed that BRCA1 may be involved in the regulation of gene expression from the X chromosome. This hypothesis is based on newly discovered interactions between BRCA1 and XIST, a non-translated RNA that normally coats the inactive X chromosome. In this study the influence of BRCA1 on the expression of X chromosome genes was investigated in ovarian cancer samples. Methods: Complementary DNA microarrays were used to compare the expression levels of X chromosome genes in 18 BRCA1-associated ovarian cancers to those of the 13 “BRCA1-like” and 14 “BRCA2-like” sporadic tumors (as defined by previously reported expression profiling). Significance was determined using parametric statistics with P<0.005 as a cutoff. Virally-mediated BRCA1 re-expression in HCC1937 BRCA1-deficient breast cancer cells was also performed to complement our in vivo studies. Results: Forty of 178 total X-chromosome transcripts were differentially expressed between the BRCA1-associated tumors and sporadic cancers with a BRCA2-like molecular profile. Thirty of these 40 genes showed higher mean expression in the BRCA1-associated samples including all 11 transcripts that mapped to Xp11. In contrast, four of 178 total X chromosome transcripts showed significant differential expression between BRCA1-associated and sporadic tumors with a BRCA1-like molecular profile. All four mapped to Xp11 and showed higher mean expression in BRCA1-associated tumors. Re-expression of BRCA1 in HCC1937 BRCA1-deficient breast cancer cell resulted in the repression of 21 transcripts. Eleven of the 21 (54.5%) transcripts mapped to Xp11. Conclusions: These findings demonstrate that wild-type BRCA1 mediates the repression of several X chromosome genes, many of which map to the Xp11 locus. In addition, tumors from patients with BRCA1 germ-line mutations show significantly higher mean expression levels of genes mapped to Xp11. Future investigations are needed to address the mechanism for this repression.

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April 2004
Volume 64, Issue 7 Supplement
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BRCA1 mediates the repression of select X chromosome genes
Amir A. Jazaeri, Chandramouli Gadisetti, Olga Aprelikova, Ulrike A. Nuber, Christos Sotiriou, Edison T. Liu, Hans H. Ropers, Cindy J. Yee, Jeff Boyd and J. C. Barrett
Cancer Res April 1 2004 (64) (7 Supplement) 373;

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BRCA1 mediates the repression of select X chromosome genes
Amir A. Jazaeri, Chandramouli Gadisetti, Olga Aprelikova, Ulrike A. Nuber, Christos Sotiriou, Edison T. Liu, Hans H. Ropers, Cindy J. Yee, Jeff Boyd and J. C. Barrett
Cancer Res April 1 2004 (64) (7 Supplement) 373;
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