التفاصيل البيبلوغرافية
العنوان: |
Identification of multiple risk loci and regulatory mechanisms influencing susceptibility to multiple myeloma |
المؤلفون: |
Went, M, Sud, A, Försti, A, Halvarsson, BM, Weinhold, N, Kimber, S, van Duin, M, Thorleifsson, G, Holroyd, A, Johnson, DC, Li, N, Orlando, G, Law, PJ, Ali, M, Chen, B, Mitchell, JS, Gudbjartsson, DF, Kuiper, R, Stephens, OW, Bertsch, U, Broderick, P, Campo, C, Bandapalli, OR, Einsele, H, Gregory, WA, Gullberg, U, Hillengass, J, Hoffmann, P, Jackson, GH, Jöckel, KH, Johnsson, E, Kristinsson, SY, Mellqvist, UH, Nahi, H, Easton, D, Pharoah, P, Dunning, A, Peto, J, Canzian, F, Swerdlow, A, Eeles, RA, Kote-Jarai, ZS, Muir, K, Pashayan, N, Nickel, J, Nöthen, MM, Rafnar, T, Ross, FM, da Silva Filho, MI, Thomsen, H, Turesson, I, Vangsted, A, Andersen, NF, Waage, A, Walker, BA, Wihlborg, AK, Broyl, A, Davies, FE, Thorsteinsdottir, U, Langer, C, Hansson, M, Goldschmidt, H, Kaiser, M, Sonneveld, P, Stefansson, K, Morgan, GJ, Hemminki, K, Nilsson, B, Houlston, RS, Henderson, BE, Haiman, CA, Benlloch, S, Schumacher, FR, Olama, AAA, Berndt, SI, Conti, DV, Wiklund, F, Chanock, S, Stevens, VL, Tangen, CM, The PRACTICAL Consortium |
المساهمون: |
Claessens, Frank |
بيانات النشر: |
Nature Publishing Group, 2018. |
سنة النشر: |
2018 |
مصطلحات موضوعية: |
Male, Quality Control, Risk, Chromatin Immunoprecipitation, Genotype, European Continental Ancestry Group, Quantitative Trait Loci, Bayes Theorem, Polymorphism, Single Nucleotide, Chromatin, Gene Expression Regulation, Humans, Female, Genetic Predisposition to Disease, Multiple Myeloma, Promoter Regions, Genetic, Genome-Wide Association Study |
الوصف: |
© 2018, The Author(s). Genome-wide association studies (GWAS) have transformed our understanding of susceptibility to multiple myeloma (MM), but much of the heritability remains unexplained. We report a new GWAS, a meta-analysis with previous GWAS and a replication series, totalling 9974 MM cases and 247,556 controls of European ancestry. Collectively, these data provide evidence for six new MM risk loci, bringing the total number to 23. Integration of information from gene expression, epigenetic profiling and in situ Hi-C data for the 23 risk loci implicate disruption of developmental transcriptional regulators as a basis of MM susceptibility, compatible with altered B-cell differentiation as a key mechanism. Dysregulation of autophagy/apoptosis and cell cycle signalling feature as recurrently perturbed pathways. Our findings provide further insight into the biological basis of MM. ispartof: Nature Communications vol:9 issue:1 ispartof: location:England status: published |
وصف الملف: |
Electronic |
اللغة: |
English |
الوصول الحر: |
https://explore.openaire.eu/search/publication?articleId=od______1131::f7734f9e27f34106bbe3f4a96df7e407Test https://lirias.kuleuven.be/handle/123456789/633372Test |
حقوق: |
OPEN |
رقم الانضمام: |
edsair.od......1131..f7734f9e27f34106bbe3f4a96df7e407 |
قاعدة البيانات: |
OpenAIRE |