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Sökning: (WFRF:(Wiley Kathleen E)) pers:(Cooney Kathleen A) > (2012) > Analysis of Xq27-28...

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FältnamnIndikatorerMetadata
00005959naa a2200961 4500
001oai:DiVA.org:umu-62806
003SwePub
008121218s2012 | |||||||||||000 ||eng|
009oai:prod.swepub.kib.ki.se:125590654
0247 a https://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-628062 URI
0247 a https://doi.org/10.1186/1471-2350-13-462 DOI
0247 a http://kipublications.ki.se/Default.aspx?queryparsed=id:1255906542 URI
040 a (SwePub)umud (SwePub)ki
041 a engb eng
042 9 SwePub
072 7a ref2 swepub-contenttype
072 7a art2 swepub-publicationtype
1001 a Bailey-Wilson, Joan E4 aut
2451 0a Analysis of Xq27-28 linkage in the international consortium for prostate cancer genetics (ICPCG) families
264 c 2012-06-19
264 1a London :b BioMed Central,c 2012
338 a electronic2 rdacarrier
520 a Background: Genetic variants are likely to contribute to a portion of prostate cancer risk. Full elucidation of the genetic etiology of prostate cancer is difficult because of incomplete penetrance and genetic and phenotypic heterogeneity. Current evidence suggests that genetic linkage to prostate cancer has been found on several chromosomes including the X; however, identification of causative genes has been elusive.Methods: Parametric and non-parametric linkage analyses were performed using 26 microsatellite markers in each of 11 groups of multiple-case prostate cancer families from the International Consortium for Prostate Cancer Genetics (ICPCG). Meta-analyses of the resultant family-specific linkage statistics across the entire 1,323 families and in several predefined subsets were then performed.Results: Meta-analyses of linkage statistics resulted in a maximum parametric heterogeneity lod score (HLOD) of 1.28, and an allele-sharing lod score (LOD) of 2.0 in favor of linkage to Xq27-q28 at 138 cM. In subset analyses, families with average age at onset less than 65 years exhibited a maximum HLOD of 1.8 (at 138 cM) versus a maximum regional HLOD of only 0.32 in families with average age at onset of 65 years or older. Surprisingly, the subset of families with only 2-3 affected men and some evidence of male-to-male transmission of prostate cancer gave the strongest evidence of linkage to the region (HLOD = 3.24, 134 cM). For this subset, the HLOD was slightly increased (HLOD = 3.47 at 134 cM) when families used in the original published report of linkage to Xq27-28 were excluded.Conclusions: Although there was not strong support for linkage to the Xq27-28 region in the complete set of families, the subset of families with earlier age at onset exhibited more evidence of linkage than families with later onset of disease. A subset of families with 2-3 affected individuals and with some evidence of male to male disease transmission showed stronger linkage signals. Our results suggest that the genetic basis for prostate cancer in our families is much more complex than a single susceptibility locus on the X chromosome, and that future explorations of the Xq27-28 region should focus on the subset of families identified here with the strongest evidence of linkage to this region.
650 7a NATURVETENSKAPx Biologix Genetik0 (SwePub)106092 hsv//swe
650 7a NATURAL SCIENCESx Biological Sciencesx Genetics0 (SwePub)106092 hsv//eng
7001 a Childs, Erica J4 aut
7001 a Cropp, Cheryl D4 aut
7001 a Schaid, Daniel J4 aut
7001 a Xu, Jianfeng4 aut
7001 a Camp, Nicola J4 aut
7001 a Cannon-Albright, Lisa A4 aut
7001 a Farnham, James M4 aut
7001 a George, Asha4 aut
7001 a Powell, Isaac4 aut
7001 a Carpten, John D4 aut
7001 a Giles, Graham G4 aut
7001 a Hopper, John L4 aut
7001 a Severi, Gianluca4 aut
7001 a English, Dallas R4 aut
7001 a Foulkes, William D4 aut
7001 a Maehle, Lovise4 aut
7001 a Moller, Pal4 aut
7001 a Eeles, Rosalind4 aut
7001 a Easton, Douglas4 aut
7001 a Guy, Michelle4 aut
7001 a Edwards, Steve4 aut
7001 a Badzioch, Michael D4 aut
7001 a Whittemore, Alice S4 aut
7001 a Oakley-Girvan, Ingrid4 aut
7001 a Hsieh, Chih-Lin4 aut
7001 a Dimitrov, Latchezar4 aut
7001 a Stanford, Janet L4 aut
7001 a Karyadi, Danielle M4 aut
7001 a Deutsch, Kerry4 aut
7001 a McIntosh, Laura4 aut
7001 a Ostrander, Elaine A4 aut
7001 a Wiley, Kathleen E4 aut
7001 a Isaacs, Sarah D4 aut
7001 a Walsh, Patrick C4 aut
7001 a Thibodeau, Stephen N4 aut
7001 a McDonnell, Shannon K4 aut
7001 a Hebbring, Scott4 aut
7001 a Lange, Ethan M4 aut
7001 a Cooney, Kathleen A4 aut
7001 a Tammela, Teuvo LJ4 aut
7001 a Schleutker, Johanna4 aut
7001 a Maier, Christiane4 aut
7001 a Bochum, Sylvia4 aut
7001 a Hoegel, Josef4 aut
7001 a Gronberg, Henriku Karolinska Institutet4 aut
7001 a Wiklund, Fredriku Karolinska Institutet4 aut
7001 a Emanuelsson, Monicau Umeå universitet,Onkologi4 aut0 (Swepub:umu)moem0001
7001 a Cancel-Tassin, Geraldine4 aut
7001 a Valeri, Antoine4 aut
7001 a Cussenot, Olivier4 aut
7001 a Isaacs, William B4 aut
7102 a Karolinska Institutetb Onkologi4 org
7730 t BMC Medical Geneticsd London : BioMed Centralg 13, s. 46-q 13<46-x 1471-2350
8564 u https://umu.diva-portal.org/smash/get/diva2:581082/FULLTEXT02.pdfx primaryx Raw objecty fulltext:print
8564 u https://bmcmedgenet.biomedcentral.com/track/pdf/10.1186/1471-2350-13-46
8564 8u https://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-62806
8564 8u https://doi.org/10.1186/1471-2350-13-46
8564 8u http://kipublications.ki.se/Default.aspx?queryparsed=id:125590654

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