An intergenic risk locus containing an enhancer deletion in 2q35 modulates breast cancer risk by deregulating IGFBP5 expression.
暂无分享,去创建一个
M. Beckmann | P. Fasching | K. Czene | P. Hall | J. Olson | F. Couch | H. Brenner | J. Chang-Claude | M. García-Closas | J. Benítez | T. Wong | Sofia Khan | G. Giles | J. Hopper | B. Henderson | C. Haiman | T. Dörk | M. Southey | A. Lophatananon | A. Cox | D. Easton | Chen-Yang Shen | A. Broeks | P. Pharoah | D. Lambrechts | J. Peto | C. Amos | N. Orr | H. Brauch | V. Kristensen | J. Long | X. Shu | W. Zheng | P. Guénel | L. Signorello | W. Blot | A. Dunning | S. Sangrajrang | Pei-Ei Wu | G. Chenevix-Trench | S. Bojesen | B. Nordestgaard | H. Nevanlinna | D. Kang | N. Bogdanova | P. Devilee | R. Milne | A. González-Neira | U. Hamann | A. Mannermaa | V. Kosma | M. Shah | M. Cole | K. Muir | A. Lindblom | K. Michailidou | J. Dennis | M. Schmidt | M. Bolla | Qin Wang | A. Meindl | R. Schmutzler | A. Rudolph | T. Truong | F. Marmé | B. Burwinkel | E. Sawyer | I. Tomlinson | I. Andrulis | J. Knight | S. Margolin | M. Hooning | A. Swerdlow | J. Figueroa | M. Dumont | R. Winqvist | K. Pylkäs | P. Radice | P. Peterlongo | C. Seynaeve | A. Jakubowska | J. Lubiński | A. Toland | K. Matsuo | Hidemi Ito | A. Wu | S. Teo | M. Hartman | H. Miao | J. Mckay | J. Simard | H. Darabi | I. Dos-Santos-Silva | H. Wildiers | S. Neuhausen | A. V. D. van den Ouweland | D. Yannoukakos | S. Yao | D. J. Van Den Berg | C. Ambrosone | E. Bandera | A. K. Dieffenbach | C. Hong | D. Klevebring | Ji-Yeob Choi | Yu-Tang Gao | Asaf Wyszynski | Yali Zhang | C. Lytle | K. Lam | I. dos-Santos-Silva | Pei‐Ei Wu | Chang-Claude Jenny | Thérèse Truong | P. Hall | Hatef Darabi | Yu-Tang Gao | T. Wong
[1] S. Cross,et al. Evidence that breast cancer risk at the 2q35 locus is mediated through IGFBP5 regulation , 2014, Nature Communications.
[2] A. Ashworth,et al. Unbiased analysis of potential targets of breast cancer susceptibility loci by Capture Hi-C , 2014, Genome research.
[3] L. Berthiaume,et al. Wnt acylation: seeing is believing. , 2014, Nature chemical biology.
[4] A. Dunning,et al. Beyond GWASs: illuminating the dark road from association to function. , 2013, American journal of human genetics.
[5] N. Boyd,et al. Longitudinal Changes in IGF-I and IGFBP-3, and Mammographic Density among Postmenopausal Women , 2013, Cancer Epidemiology, Biomarkers & Prevention.
[6] Yarden Katz,et al. Multiplexed activation of endogenous genes by CRISPR-on, an RNA-guided transcriptional activator system , 2013, Cell Research.
[7] H. Werner,et al. Insulin-like growth factor binding protein-4 and -5 modulate ligand-dependent estrogen receptor-α activation in breast cancer cells in an IGF-independent manner. , 2013, Cellular signalling.
[8] C. Ambrosone,et al. Rethinking sources of representative controls for the conduct of case–control studies in minority populations , 2013, BMC Medical Research Methodology.
[9] Jaana M. Hartikainen,et al. Large-scale genotyping identifies 41 new loci associated with breast cancer risk , 2013, Nature Genetics.
[10] Patrick Neven,et al. Genome-wide association studies identify four ER negative–specific breast cancer risk loci , 2013, Nature Genetics.
[11] A. Jemal,et al. Cancer statistics, 2013 , 2013, CA: a cancer journal for clinicians.
[12] O. Delaneau,et al. Supplementary Information for ‘ Improved whole chromosome phasing for disease and population genetic studies ’ , 2012 .
[13] Data production leads,et al. An integrated encyclopedia of DNA elements in the human genome , 2012 .
[14] J. Marchini,et al. Fast and accurate genotype imputation in genome-wide association studies through pre-phasing , 2012, Nature Genetics.
[15] ENCODEConsortium,et al. An Integrated Encyclopedia of DNA Elements in the Human Genome , 2012, Nature.
[16] S. Weroha,et al. IGFBP Ratio Confers Resistance to IGF Targeting and Correlates with Increased Invasion and Poor Outcome in Breast Tumors , 2012, Clinical Cancer Research.
[17] S. Yao,et al. Variants in the vitamin D pathway, serum levels of vitamin D, and estrogen receptor negative breast cancer among African-American women: a case-control study , 2012, Breast Cancer Research.
[18] Ryan E. Mills,et al. Natural genetic variation caused by small insertions and deletions in the human genome. , 2011, Genome research.
[19] David Reich,et al. Validation of a small set of ancestral informative markers for control of population admixture in African Americans. , 2011, American journal of epidemiology.
[20] N. D. Clarke,et al. Integrative model of genomic factors for determining binding site selection by estrogen receptor-α , 2010, Molecular systems biology.
[21] G. Abecasis,et al. MaCH: using sequence and genotype data to estimate haplotypes and unobserved genotypes , 2010, Genetic epidemiology.
[22] Yun Li,et al. METAL: fast and efficient meta-analysis of genomewide association scans , 2010, Bioinform..
[23] J. Marchini,et al. Genotype imputation for genome-wide association studies , 2010, Nature Reviews Genetics.
[24] Yurii S. Aulchenko,et al. ProbABEL package for genome-wide association analysis of imputed data , 2010, BMC Bioinformatics.
[25] H. Valdimarsdottir,et al. Conducting Molecular Epidemiological Research in the Age of HIPAA: A Multi-Institutional Case-Control Study of Breast Cancer in African-American and European-American Women , 2009, Journal of oncology.
[26] I. Amit,et al. Comprehensive mapping of long range interactions reveals folding principles of the human genome , 2011 .
[27] E. Liu,et al. An Oestrogen Receptor α-bound Human Chromatin Interactome , 2009, Nature.
[28] M. Beckmann,et al. Risk of estrogen receptor-positive and -negative breast cancer and single-nucleotide polymorphism 2q35-rs13387042. , 2009, Journal of the National Cancer Institute.
[29] P. Donnelly,et al. A Flexible and Accurate Genotype Imputation Method for the Next Generation of Genome-Wide Association Studies , 2009, PLoS genetics.
[30] I. Gram,et al. Genotypes and haplotypes in the insulin-like growth factors, their receptors and binding proteins in relation to plasma metabolic levels and mammographic density , 2008, BMC Medical Genomics.
[31] D. Gudbjartsson,et al. Common variants on chromosomes 2q35 and 16q12 confer susceptibility to estrogen receptor–positive breast cancer , 2007, Nature Genetics.
[32] Bao Hoang,et al. Delayed mammary gland involution in mice with mutation of the insulin-like growth factor binding protein 5 gene. , 2007, Endocrinology.
[33] Romayne A. Thompson,et al. Age-related lobular involution and risk of breast cancer. , 2006, Journal of the National Cancer Institute.
[34] A. Miele,et al. Mapping Chromatin Interactions by Chromosome Conformation Capture , 2006, Current protocols in molecular biology.
[35] R. Baxter,et al. Insulin-like Growth Factor-binding Protein-5 Inhibits the Growth of Human Breast Cancer Cells in Vitro and in Vivo* , 2003, Journal of Biological Chemistry.
[36] D. Flint,et al. Insulin-like growth factor binding protein 5 and apoptosis in mammary epithelial cells , 2003, Journal of Cell Science.
[37] J. Beattie,et al. Insulin-like growth factor binding protein-5 (IGFBP-5) induces premature cell death in the mammary glands of transgenic mice. , 2002, Development.
[38] Tom H. Pringle,et al. The human genome browser at UCSC. , 2002, Genome research.
[39] H. Berkel,et al. Free insulin-like growth factor-I and breast cancer risk. , 2001, International journal of cancer.
[40] P. Donnelly,et al. Association mapping in structured populations. , 2000, American journal of human genetics.
[41] W. Thilly,et al. Mismatch amplification mutation assay (MAMA): application to the c-H-ras gene. , 1992, PCR methods and applications.
[42] N. Dubrawsky. Cancer statistics , 1989, CA: a cancer journal for clinicians.