Validation of prostate cancer risk-related loci identified from genome-wide association studies using family-based association analysis: evidence from the International Consortium for Prostate Cancer Genetics (ICPCG)

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Fältnamn	Indikatorer	Metadata
000		04728naa a2200841 4500
001		oai:DiVA.org:umu-52482
003		SwePub
008		120222s2012 \| \|\|\|\|\|\|\|\|\|\|\|000 \|\|eng\|
009		oai:prod.swepub.kib.ki.se:124759858
024	7	a https://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-524822 URI
024	7	a https://doi.org/10.1007/s00439-011-1136-02 DOI
024	7	a http://kipublications.ki.se/Default.aspx?queryparsed=id:1247598582 URI
040		a (SwePub)umud (SwePub)ki
041		a engb eng
042		9 SwePub
072	7	a ref2 swepub-contenttype
072	7	a art2 swepub-publicationtype
100	1	a Jin, Guangfu4 aut
245	1 0	a Validation of prostate cancer risk-related loci identified from genome-wide association studies using family-based association analysis :b evidence from the International Consortium for Prostate Cancer Genetics (ICPCG)
264		c 2011-12-25
264	1	b Springer Science and Business Media LLC,c 2012
338		a print2 rdacarrier
520		a Multiple prostate cancer (PCa) risk-related loci have been discovered by genome-wide association studies (GWAS) based on case-control designs. However, GWAS findings may be confounded by population stratification if cases and controls are inadvertently drawn from different genetic backgrounds. In addition, since these loci were identified in cases with predominantly sporadic disease, little is known about their relationships with hereditary prostate cancer (HPC). The association between seventeen reported PCa susceptibility loci was evaluated with a family-based association test using 1,979 hereditary PCa families of European descent collected by members of the International Consortium for Prostate Cancer Genetics, with a total of 5,730 affected men. The risk alleles for 8 of the 17 loci were significantly over-transmitted from parents to affected offspring, including SNPs residing in 8q24 (regions 1, 2 and 3), 10q11, 11q13, 17q12 (region 1), 17q24 and Xp11. In subgroup analyses, three loci, at 8q24 (regions 1 and 2) plus 17q12, were significantly over-transmitted in hereditary PCa families with five or more affected members, while loci at 3p12, 8q24 (region 2), 11q13, 17q12 (region 1), 17q24 and Xp11 were significantly over-transmitted in HPC families with an average age of diagnosis at 65 years or less. Our results indicate that at least a subset of PCa risk-related loci identified by case-control GWAS are also associated with disease risk in HPC families.
700	1	a Lu, Lingyi4 aut
700	1	a Cooney, Kathleen A4 aut
700	1	a Ray, Anna M4 aut
700	1	a Zuhlke, Kimberly A4 aut
700	1	a Lange, Ethan M4 aut
700	1	a Cannon-Albright, Lisa A4 aut
700	1	a Camp, Nicola J4 aut
700	1	a Teerlink, Craig C4 aut
700	1	a Fitzgerald, Liesel M4 aut
700	1	a Stanford, Janet L4 aut
700	1	a Wiley, Kathleen E4 aut
700	1	a Isaacs, Sarah D4 aut
700	1	a Walsh, Patrick C4 aut
700	1	a Foulkes, William D4 aut
700	1	a Giles, Graham G4 aut
700	1	a Hopper, John L4 aut
700	1	a Severi, Gianluca4 aut
700	1	a Eeles, Ros4 aut
700	1	a Easton, Doug4 aut
700	1	a Kote-Jarai, Zsofia4 aut
700	1	a Guy, Michelle4 aut
700	1	a Rinckleb, Antje4 aut
700	1	a Maier, Christiane4 aut
700	1	a Vogel, Walther4 aut
700	1	a Cancel-Tassin, Geraldine4 aut
700	1	a Egrot, Christophe4 aut
700	1	a Cussenot, Olivier4 aut
700	1	a Thibodeau, Stephen N4 aut
700	1	a McDonnell, Shannon K4 aut
700	1	a Schaid, Daniel J4 aut
700	1	a Wiklund, Fredriku Karolinska Institutet4 aut
700	1	a Grönberg, Henriku Karolinska Institutet4 aut
700	1	a Emanuelsson, Monicau Umeå universitet,Onkologi4 aut0 (Swepub:umu)moem0001
700	1	a Whittemore, Alice S4 aut
700	1	a Oakley-Girvan, Ingrid4 aut
700	1	a Hsieh, Chih-Lin4 aut
700	1	a Wahlfors, Tiina4 aut
700	1	a Tammela, Teuvo4 aut
700	1	a Schleutker, Johanna4 aut
700	1	a Catalona, William J4 aut
700	1	a Zheng, S Lilly4 aut
700	1	a Ostrander, Elaine A4 aut
700	1	a Isaacs, William B4 aut
700	1	a Xu, Jianfeng4 aut
710	2	a Karolinska Institutetb Onkologi4 org
773	0	t Human Geneticsd : Springer Science and Business Media LLCg 131:7, s. 1095-1103q 131:7<1095-1103x 0340-6717x 1432-1203
856	4	u https://europepmc.org/articles/pmc3535428?pdf=render
856	4 8	u https://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-52482
856	4 8	u https://doi.org/10.1007/s00439-011-1136-0
856	4 8	u http://kipublications.ki.se/Default.aspx?queryparsed=id:124759858

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Av författaren/redakt...: Jin, Guangfu; Lu, Lingyi; Cooney, Kathleen ...; Ray, Anna M; Zuhlke, Kimberly ...; Lange, Ethan M; visa fler...; Cannon-Albright, ...; Camp, Nicola J; Teerlink, Craig ...; Fitzgerald, Lies ...; Stanford, Janet ...; Wiley, Kathleen ...; Isaacs, Sarah D; Walsh, Patrick C; Foulkes, William ...; Giles, Graham G; Hopper, John L; Severi, Gianluca; Eeles, Ros; Easton, Doug; Kote-Jarai, Zsof ...; Guy, Michelle; Rinckleb, Antje; Maier, Christian ...; Vogel, Walther; Cancel-Tassin, G ...; Egrot, Christoph ...; Cussenot, Olivie ...; Thibodeau, Steph ...; McDonnell, Shann ...; Schaid, Daniel J; Wiklund, Fredrik; Grönberg, Henrik; Emanuelsson, Mon ...; Whittemore, Alic ...; Oakley-Girvan, I ...; Hsieh, Chih-Lin; Wahlfors, Tiina; Tammela, Teuvo; Schleutker, Joha ...; Catalona, Willia ...; Zheng, S Lilly; Ostrander, Elain ...; Isaacs, William ...; Xu, Jianfeng; visa färre...

Artiklar i publikationen: Human Genetics

Av lärosätet: Umeå universitet; Karolinska Institutet

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