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Sökning: WFRF:(Pasaniuc Bogdan) > (2018) > Large-scale transcr...

LIBRIS Formathandbok  (Information om MARC21)
FältnamnIndikatorerMetadata
00004121naa a2200409 4500
001oai:DiVA.org:uu-419404
003SwePub
008200910s2018 | |||||||||||000 ||eng|
0247 a https://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-4194042 URI
0247 a https://doi.org/10.1038/s41467-018-06302-12 DOI
040 a (SwePub)uu
041 a engb eng
042 9 SwePub
072 7a ref2 swepub-contenttype
072 7a art2 swepub-publicationtype
1001 a Mancuso, Nicholasu Univ Calif Los Angeles, David Geffen Sch Med, Dept Pathol & Lab Med, Los Angeles, CA 90095 USA.4 aut
2451 0a Large-scale transcriptome-wide association study identifies new prostate cancer risk regions
264 c 2018-10-04
264 1b NATURE PUBLISHING GROUP,c 2018
338 a print2 rdacarrier
520 a Although genome-wide association studies (GWAS) for prostate cancer (PrCa) have identified more than 100 risk regions, most of the risk genes at these regions remain largely unknown. Here we integrate the largest PrCa GWAS (N = 142,392) with gene expression measured in 45 tissues (N = 4458), including normal and tumor prostate, to perform a multi-tissue transcriptome-wide association study (TWAS) for PrCa. We identify 217 genes at 84 independent 1 Mb regions associated with PrCa risk, 9 of which are regions with no genome-wide significant SNP within 2 Mb. 23 genes are significant in TWAS only for alternative splicing models in prostate tumor thus supporting the hypothesis of splicing driving risk for continued oncogenesis. Finally, we use a Bayesian probabilistic approach to estimate credible sets of genes containing the causal gene at a pre-defined level; this reduced the list of 217 associations to 109 genes in the 90% credible set. Overall, our findings highlight the power of integrating expression with PrCa GWAS to identify novel risk loci and prioritize putative causal genes at known risk loci.
650 7a MEDICIN OCH HÄLSOVETENSKAPx Medicinska och farmaceutiska grundvetenskaperx Medicinsk genetik0 (SwePub)301072 hsv//swe
650 7a MEDICAL AND HEALTH SCIENCESx Basic Medicinex Medical Genetics0 (SwePub)301072 hsv//eng
7001 a Gayther, Simonu Cedars Sinai Med Ctr, Ctr Bioinformat & Funct Genom, Los Angeles, CA 90048 USA.4 aut
7001 a Gusev, Alexanderu Dana Farber Canc Inst, Boston, MA 02215 USA.4 aut
7001 a Zheng, Weiu Vanderbilt Univ, Sch Med, Vanderbilt Ingram Canc Ctr, Vanderbilt Epidemiol Ctr,Dept Med,Div Epidemiol, Nashville, TN 37232 USA.4 aut
7001 a Penney, Kathryn L.u Harvard TH Chan Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA.;Harvard Med Sch, Brigham & Womens Hosp, Dept Med, Channing Div Network Med, Boston, MA 02115 USA.4 aut
7001 a Kote-Jarai, Zsofiau Inst Canc Res, Div Genet & Epidemiol, London SW7 3RP, England.;Royal Marsden NHS Fdn Trust, London SW3 6JJ, England.4 aut
7001 a Eeles, Rosalindu Inst Canc Res, Div Genet & Epidemiol, London SW7 3RP, England.;Royal Marsden NHS Fdn Trust, London SW3 6JJ, England.4 aut
7001 a Freedman, Matthewu Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02215 USA.;Harvard Med Sch, Boston, MA 02215 USA.4 aut
7001 a Haiman, Christopheru Univ Southern Calif, Keck Sch Med, Norris Comprehens Canc Ctr, Dept Prevent Med, Los Angeles, CA 90015 USA.4 aut
7001 a Pasaniuc, Bogdanu Univ Calif Los Angeles, David Geffen Sch Med, Dept Pathol & Lab Med, Los Angeles, CA 90095 USA.;Univ Calif Los Angeles, David Geffen Sch Med, Dept Human Genet, Los Angeles, CA 90095 USA.;Univ Calif Los Angeles, Bioinformat Interdept Program, Los Angeles, CA 90095 USA.4 aut
7102 a Univ Calif Los Angeles, David Geffen Sch Med, Dept Pathol & Lab Med, Los Angeles, CA 90095 USA.b Cedars Sinai Med Ctr, Ctr Bioinformat & Funct Genom, Los Angeles, CA 90048 USA.4 org
7730 t Nature Communicationsd : NATURE PUBLISHING GROUPg 9q 9x 2041-1723
8564 u https://www.nature.com/articles/s41467-018-06302-1.pdf
8564 8u https://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-419404
8564 8u https://doi.org/10.1038/s41467-018-06302-1

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