Genome-wide association studies in women of African ancestry identified 3q26.21 as a novel susceptibility locus for oestrogen receptor negative breast cancer.

التفاصيل البيبلوغرافية
العنوان:	Genome-wide association studies in women of African ancestry identified 3q26.21 as a novel susceptibility locus for oestrogen receptor negative breast cancer.
المؤلفون:	Huo D; Department of Public Health Sciences, University of Chicago, Chicago, IL, USA., Feng Y; Department of Preventive Medicine, Keck School of Medicine and Norris Comprehensive Cancer Center, University of Southern California, Los Angeles, CA, USA., Haddad S; Slone Epidemiology Center, Boston University, Boston, MA, USA., Zheng Y; Center for Clinical Cancer Genetics and Global Health, Department of Medicine, University of Chicago, Chicago, IL, USA., Yao S; Roswell Park Cancer Institute, Buffalo, NY, USA., Han YJ; Center for Clinical Cancer Genetics and Global Health, Department of Medicine, University of Chicago, Chicago, IL, USA., Ogundiran TO; Department of Surgery, College of Medicine, University of Ibadan, Ibadan, Nigeria., Adebamowo C; Department of Epidemiology & Preventive Medicine, University of Maryland, Baltimore, MD, USA., Ojengbede O; Center for Population and Reproductive Health, College of Medicine, University of Ibadan, Ibadan, Nigeria., Falusi AG; Institute for Medical Research and Training, College of Medicine, University of Ibadan, Ibadan, Nigeria., Zheng W; Division of Epidemiology, Department of Medicine, Vanderbilt Epidemiology Center, Vanderbilt-Ingram Cancer Center, Vanderbilt University, Nashville, TN, USA., Blot W; Division of Epidemiology, Department of Medicine, Vanderbilt Epidemiology Center, Vanderbilt-Ingram Cancer Center, Vanderbilt University, Nashville, TN, USA., Cai Q; Division of Epidemiology, Department of Medicine, Vanderbilt Epidemiology Center, Vanderbilt-Ingram Cancer Center, Vanderbilt University, Nashville, TN, USA., Signorello L; Cancer Prevention Fellowship Program, National Cancer Institute, Bethesda, MD, USA., John EM; Division of Epidemiology, Department of Medicine, Vanderbilt Epidemiology Center, Vanderbilt-Ingram Cancer Center, Vanderbilt University, Nashville, TN, USA.; Cancer Prevention Fellowship Program, National Cancer Institute, Bethesda, MD, USA., Bernstein L; Division of Cancer Etiology, Department of Population Sciences, Beckman Research Institute of City of Hope, Duarte, CA, USA., Hu JJ; Sylvester Comprehensive Cancer Center and Department of Public Health Sciences, University of Miami Miller School of Medicine, Miami, FL, USA., Ziegler RG; Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, MA, USA., Nyante S; Department of Epidemiology, Gillings School of Global Public Health, and Lineberger Comprehensive Cancer Center, University of North Carolina, Chapel Hill, NC, USA., Bandera EV; The Cancer Institute of New Jersey, New Brunswick, NJ, USA., Ingles SA; Department of Preventive Medicine, Keck School of Medicine and Norris Comprehensive Cancer Center, University of Southern California, Los Angeles, CA, USA., Press MF; Department of Pathology, Keck School of Medicine and Norris Comprehensive Cancer Center, University of Southern California, Los Angeles, CA, USA., Deming SL; Division of Epidemiology, Department of Medicine, Vanderbilt Epidemiology Center, Vanderbilt-Ingram Cancer Center, Vanderbilt University, Nashville, TN, USA., Rodriguez-Gil JL; Sylvester Comprehensive Cancer Center and Department of Public Health Sciences, University of Miami Miller School of Medicine, Miami, FL, USA., Nathanson KL; Department of Medicine, University of Pennsylvania, Philadelphia, PA, USA., Domchek SM; Department of Medicine, University of Pennsylvania, Philadelphia, PA, USA., Rebbeck TR; Dana Farber Cancer Institute & Harvard T.H. Chan School of Public Health, Boston, MA, USA., Ruiz-Narváez EA; Slone Epidemiology Center, Boston University, Boston, MA, USA., Sucheston-Campbell LE; Colleges of Pharmacy and Veterinary Medicine, Ohio State University, Columbus, OH, USA., Bensen JT; Department of Epidemiology, Gillings School of Global Public Health, and Lineberger Comprehensive Cancer Center, University of North Carolina, Chapel Hill, NC, USA., Simon MS; Karmanos Cancer Institute, Department of Oncology, Wayne State University, Detroit, MI, USA., Hennis A; Division of Cancer Etiology, Department of Population Sciences, Beckman Research Institute of City of Hope, Duarte, CA, USA.; Sylvester Comprehensive Cancer Center and Department of Public Health Sciences, University of Miami Miller School of Medicine, Miami, FL, USA., Nemesure B; Department of Preventive Medicine, State University of New York at Stony Brook, Stony Brook, NY, USA., Leske MC; Department of Preventive Medicine, State University of New York at Stony Brook, Stony Brook, NY, USA., Ambs S; Laboratory of Human Carcinogenesis, National Cancer Institute, Bethesda, MD, USA., Chen LS; Department of Public Health Sciences, University of Chicago, Chicago, IL, USA., Qian F; Center for Clinical Cancer Genetics and Global Health, Department of Medicine, University of Chicago, Chicago, IL, USA., Gamazon ER; Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, MA, USA.; Department of Epidemiology, Gillings School of Global Public Health, and Lineberger Comprehensive Cancer Center, University of North Carolina, Chapel Hill, NC, USA., Lunetta KL; Department of Biostatistics, Boston University School of Public Health, Boston, MA, USA., Cox NJ; Division of Genetic Medicine, Department of Medicine, Vanderbilt University, Nashville, TN, USA., Chanock SJ; Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, MA, USA., Kolonel LN; Epidemiology Program, University of Hawaii Cancer Center, Honolulu, HI, USA., Olshan AF; Department of Epidemiology, Gillings School of Global Public Health, and Lineberger Comprehensive Cancer Center, University of North Carolina, Chapel Hill, NC, USA., Ambrosone CB; Roswell Park Cancer Institute, Buffalo, NY, USA., Olopade OI; Center for Clinical Cancer Genetics and Global Health, Department of Medicine, University of Chicago, Chicago, IL, USA., Palmer JR; Slone Epidemiology Center, Boston University, Boston, MA, USA., Haiman CA; Department of Preventive Medicine, Keck School of Medicine and Norris Comprehensive Cancer Center, University of Southern California, Los Angeles, CA, USA.
المصدر:	Human molecular genetics [Hum Mol Genet] 2016 Nov 01; Vol. 25 (21), pp. 4835-4846.
نوع المنشور:	Journal Article; Meta-Analysis
اللغة:	English
بيانات الدورية:	Publisher: IRL Press at Oxford University Press Country of Publication: England NLM ID: 9208958 Publication Model: Print Cited Medium: Internet ISSN: 1460-2083 (Electronic) Linking ISSN: 09646906 NLM ISO Abbreviation: Hum Mol Genet Subsets: MEDLINE
أسماء مطبوعة:	Original Publication: Oxford, England ; New York : IRL Press at Oxford University Press, c1992-
مواضيع طبية MeSH:	Breast Neoplasms/genetics , Chromosomes, Human, Pair 3/genetics, Black or African American/genetics ; Alleles ; Black People/genetics ; Case-Control Studies ; Female ; Gene Frequency/genetics ; Genetic Loci ; Genetic Predisposition to Disease/genetics ; Genome-Wide Association Study/methods ; Humans ; Polymorphism, Single Nucleotide/genetics ; Receptors, Estrogen/genetics ; Risk Factors ; TNF-Related Apoptosis-Inducing Ligand/genetics ; TNF-Related Apoptosis-Inducing Ligand/metabolism
مستخلص:	Multiple breast cancer loci have been identified in previous genome-wide association studies, but they were mainly conducted in populations of European ancestry. Women of African ancestry are more likely to have young-onset and oestrogen receptor (ER) negative breast cancer for reasons that are unknown and understudied. To identify genetic risk factors for breast cancer in women of African descent, we conducted a meta-analysis of two genome-wide association studies of breast cancer; one study consists of 1,657 cases and 2,029 controls genotyped with Illumina’s HumanOmni2.5 BeadChip and the other study included 3,016 cases and 2,745 controls genotyped using Illumina Human1M-Duo BeadChip. The top 18,376 single nucleotide polymorphisms (SNP) from the meta-analysis were replicated in the third study that consists of 1,984 African Americans cases and 2,939 controls. We found that SNP rs13074711, 26.5 Kb upstream of TNFSF10 at 3q26.21, was significantly associated with risk of oestrogen receptor (ER)-negative breast cancer (odds ratio [OR]=1.29, 95% CI: 1.18-1.40; P = 1.8 × 10 − 8). Functional annotations suggest that the TNFSF10 gene may be involved in breast cancer aetiology, but further functional experiments are needed. In addition, we confirmed SNP rs10069690 was the best indicator for ER-negative breast cancer at 5p15.33 (OR = 1.30; P = 2.4 × 10 − 10) and identified rs12998806 as the best indicator for ER-positive breast cancer at 2q35 (OR = 1.34; P = 2.2 × 10 − 8) for women of African ancestry. These findings demonstrated additional susceptibility alleles for breast cancer can be revealed in diverse populations and have important public health implications in building race/ethnicity-specific risk prediction model for breast cancer.
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معلومات مُعتمدة:	P30 CA016086 United States CA NCI NIH HHS; P30 ES010126 United States ES NIEHS NIH HHS; T32 GM008692 United States GM NIGMS NIH HHS; R01 CA092447 United States CA NCI NIH HHS; UM1 CA164974 United States CA NCI NIH HHS
المشرفين على المادة:	0 (Receptors, Estrogen) 0 (TNF-Related Apoptosis-Inducing Ligand) 0 (TNFSF10 protein, human)
تواريخ الأحداث:	Date Created: 20170208 Date Completed: 20180131 Latest Revision: 20221207
رمز التحديث:	20231215
مُعرف محوري في PubMed:	PMC5975608
DOI:	10.1093/hmg/ddw305
PMID:	28171663
قاعدة البيانات:	MEDLINE

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تدمد:	1460-2083
DOI:	10.1093/hmg/ddw305