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Sökning: L773:0007 0920 OR L773:1532 1827 > (2005-2009) > Mälardalens universitet > Interleukin-1 recep...

LIBRIS Formathandbok  (Information om MARC21)
FältnamnIndikatorerMetadata
00005302naa a2200589 4500
001oai:DiVA.org:mdh-40726
003SwePub
008180906s2005 | |||||||||||000 ||eng|
009oai:DiVA.org:umu-14460
009oai:prod.swepub.kib.ki.se:1935291
0247 a https://urn.kb.se/resolve?urn=urn:nbn:se:mdh:diva-407262 URI
0247 a https://doi.org/10.1038/sj.bjc.66027292 DOI
0247 a https://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-144602 URI
0247 a http://kipublications.ki.se/Default.aspx?queryparsed=id:19352912 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
1001 a Lindmark, Fu Umeå universitet,Onkologi4 aut
2451 0a Interleukin-1 receptor antagonist haplotype associated with prostate cancer risk
264 c 2005-08-02
264 1a Umea Univ, Dept Radiat Sci Oncol, S-90187 Umea, Sweden. Wake Forest Univ, Bowman Gray Sch Med, Ctr Human Genom, Winston Salem, NC USA. Karolinska Inst, Dept Med Epidemiol & Biostat, Stockholm, Sweden. Johns Hopkins Med Inst, Dept Urol, Baltimore, MD 21205 USA. Orebro Univ Hosp, Dept Urol & Clin Med, Orebro, Sweden. Univ Hosp, Reg Oncol Ctr, Uppsala, Sweden.b NATURE PUBLISHING GROUP,c 2005
338 a print2 rdacarrier
520 a IL1-RN is an important anti-inflammatory cytokine that modulate the inflammation response by binding to IL1 receptors, and as a consequence inhibits the action of proinflammatory cytokines IL1 alpha and IL1 beta. In this study, we hypothesise that sequence variants in the IL1-RN gene are associated with prostate cancer risk. The study population, a population-based case - control study in Sweden, consisted of 1383 prostate cancer case patients and 779 control subjects. We first selected 18 sequence variants covering the IL1-RN gene and genotyped these single-nucleotide polymorphisms ( SNPs) in 96 control subjects. Gene-specific haplotypes of IL1-RN were constructed and four haplotype-tagging single-nucleotide polymorphisms (htSNPs) were identified (rs878972, rs315934, rs3087263 and rs315951) that could uniquely describe 495% of the haplotypes. All study subjects were genotyped for the four htSNPs. No significant difference in genotype frequencies between cases and controls were observed for any of the four SNPs based on a multiplicative genetic model. Overall there was no significant difference in haplotype frequencies between cases and controls; however, the prevalence of the most common haplotype (ATGC) was significantly higher among cases (38.7%) compared to controls (33.5%) ( haplotype-specific P = 0.009). Evaluation of the prostate cancer risk associated with carrying the 'ATGC' haplotype revealed that homozygous carriers were at significantly increased risk ( odds ratio (OR) = 1.6, 95% confidence interval (CI) = 1.2 - 2.2), compared to noncarriers, while no significant association was found among subjects heterozygous for the haplotype ( OR = 1.0, 95% CI = 0.8 - 1.2). Restricting analyses to advanced prostate cancer strengthened the association between the 'ATGC' haplotype and disease risk (OR for homozygous carriers vs noncarriers 1.8, 95% CI = 1.3 - 2.5). In conclusion, the results from this study support the hypothesis that inflammation has a role of in the development of prostate cancer, but further studies are needed to identify the causal variants in this region and to elucidate the biological mechanism for this association.
650 7a MEDICIN OCH HÄLSOVETENSKAPx Hälsovetenskap0 (SwePub)3032 hsv//swe
650 7a MEDICAL AND HEALTH SCIENCESx Health Sciences0 (SwePub)3032 hsv//eng
653 a prostate cancer
653 a inflammation
653 a IL1-RN
653 a association
653 a SNPs
7001 a Zheng, S L4 aut
7001 a Wiklund, Fu Karolinska Institutet,Umeå universitet,Onkologi4 aut
7001 a Bälter Augustsson, Katarinau Karolinska Institutet4 aut0 (Swepub:mdh)kbr01
7001 a Sun, J4 aut
7001 a Chang, B4 aut
7001 a Hedelin, Mu Karolinska Institutet4 aut
7001 a Clark, J4 aut
7001 a Johansson, J E4 aut
7001 a Meyers, D A4 aut
7001 a Adami, H Ou Karolinska Institutet4 aut
7001 a Isaacs, W4 aut
7001 a Gronberg, Hu Karolinska Institutet,Umeå universitet,Onkologi4 aut
7001 a Xu, J4 aut
7102 a Umeå universitetb Onkologi4 org
7730 t British Journal of Cancerd Umea Univ, Dept Radiat Sci Oncol, S-90187 Umea, Sweden. Wake Forest Univ, Bowman Gray Sch Med, Ctr Human Genom, Winston Salem, NC USA. Karolinska Inst, Dept Med Epidemiol & Biostat, Stockholm, Sweden. Johns Hopkins Med Inst, Dept Urol, Baltimore, MD 21205 USA. Orebro Univ Hosp, Dept Urol & Clin Med, Orebro, Sweden. Univ Hosp, Reg Oncol Ctr, Uppsala, Sweden. : NATURE PUBLISHING GROUPg 93:4, s. 493-497q 93:4<493-497x 0007-0920x 1532-1827
8564 u https://www.nature.com/articles/6602729.pdf
8564 8u https://urn.kb.se/resolve?urn=urn:nbn:se:mdh:diva-40726
8564 8u https://doi.org/10.1038/sj.bjc.6602729
8564 8u https://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-14460
8564 8u http://kipublications.ki.se/Default.aspx?queryparsed=id:1935291

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