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WFRF:(Brookes A)
 

Sökning: WFRF:(Brookes A) > Mälardalens universitet > Comprehensive genet...

LIBRIS Formathandbok  (Information om MARC21)
FältnamnIndikatorerMetadata
00004647naa a2200481 4500
001oai:DiVA.org:mdh-40725
003SwePub
008180906s2005 | |||||||||||000 ||eng|
009oai:DiVA.org:umu-14471
009oai:prod.swepub.kib.ki.se:1934655
024a https://urn.kb.se/resolve?urn=urn:nbn:se:mdh:diva-407252 URI
024a https://doi.org/10.1007/s00439-005-0060-62 DOI
024a https://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-144712 URI
024a http://kipublications.ki.se/Default.aspx?queryparsed=id:19346552 URI
040 a (SwePub)mdhd (SwePub)umud (SwePub)ki
041 a engb eng
042 9 SwePub
072 7a ref2 swepub-contenttype
072 7a art2 swepub-publicationtype
100a Lindström, Sarau Umeå universitet,Onkologi4 aut0 (Swepub:umu)sralom02
2451 0a Comprehensive genetic evaluation of common E-cadherin sequence variants and prostate cancer risk :b strong confirmation of functional promoter SNP
264 c 2005-09-28
264 1a Umea Univ, Dept Radiat Sci, S-90187 Umea, Sweden. Karolinska Inst, Dept Med Epidemiol & Biostat, Stockholm, Sweden. Karolinska Inst, Ctr Genom & Bioinformat, Stockholm, Sweden. Univ Leicester, Dept Genet, Leicester LE1 7RH, Leics, England. Wake Forest Univ, Sch Med, Ctr Human Genom, Winston Salem, NC USA. Johns Hopkins Med Inst, Dept Urol, Baltimore, MD USA. CLINTECH, Karolinska Inst, Ctr Oncol, Stockholm, Sweden.b SPRINGER,c 2005
338 a print2 rdacarrier
520 a The E-cadherin gene (CDH1) has been proposed as a prostate cancer (PC) susceptibility gene in several studies. Aberrant protein expression has been related to prognosis and progression in PC. In addition, a functional promoter SNP (rsl6260) has been found to associate with PC risk. We performed a comprehensive genetic analysis of CDH1 by using the method of haplotype tagged SNPs in a large Swedish population-based case-control study consisting of 801 controls and 1,636 cases. In addition, Swedish PC families comprising a total of 157 cases sampled for DNA were analyzed for selected SNPs. Seven SNPs, including the promoter SNP rsl6260, that captured over 96% of CDH1 haplotype variation were selected as haplotype tagging SNPs and analyzed for associated PC risk. We observed significant confirmation of rsl6260 (P=0.003) for cases with a positive family history of PC (FH+) both in an independent case-control population and in PC families. In addition, a common haplotype (HapB, 25%) including the variant allele of rsl6260 was associated (P=0.004) with PC risk among FH+ cases. The promoter SNP rsl6260 as well as HapB were significantly transmitted to affected offspring in PC families. We report strong confirmation of the association between PC risk in FH+ cases and a functional CDH1 promoter SNP in an independent population. In conjunction with the biological importance of CDH1 our findings encourage further evaluation of genetic variation in CDH1 in relation to PC etiology. Due to the difficulties in replication of genetic association studies. this finding is unusual and novel.
650 7a MEDICIN OCH HÄLSOVETENSKAPx Hälsovetenskap0 (SwePub)3032 hsv//swe
650 7a MEDICAL AND HEALTH SCIENCESx Health Sciences0 (SwePub)3032 hsv//eng
700a Wiklund, Fu Karolinska Institutet,Umeå universitet,Onkologi4 aut
700a Jonsson, B Au Karolinska Institutet,Umeå universitet,Onkologi4 aut
700a Adami, H Ou Karolinska Institutet4 aut
700a Bälter, Katarinau Karolinska Institutet4 aut0 (Swepub:mdh)kbr01
700a Brookes, A J4 aut
700a Xu, J F4 aut
700a Zheng, S L4 aut
700a Isaacs, W B4 aut
700a Adolfsson, J4 aut
700a Gronberg, Hu Karolinska Institutet,Umeå universitet,Onkologi4 aut
710a Umeå universitetb Onkologi4 org
773t Human Geneticsd Umea Univ, Dept Radiat Sci, S-90187 Umea, Sweden. Karolinska Inst, Dept Med Epidemiol & Biostat, Stockholm, Sweden. Karolinska Inst, Ctr Genom & Bioinformat, Stockholm, Sweden. Univ Leicester, Dept Genet, Leicester LE1 7RH, Leics, England. Wake Forest Univ, Sch Med, Ctr Human Genom, Winston Salem, NC USA. Johns Hopkins Med Inst, Dept Urol, Baltimore, MD USA. CLINTECH, Karolinska Inst, Ctr Oncol, Stockholm, Sweden. : SPRINGERg 118:3-4, s. 339-347q 118:3-4<339-347x 0340-6717x 1432-1203
8564 8u https://urn.kb.se/resolve?urn=urn:nbn:se:mdh:diva-40725
8564 8u https://doi.org/10.1007/s00439-005-0060-6
8564 8u https://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-14471
8564 8u http://kipublications.ki.se/Default.aspx?queryparsed=id:1934655

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