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dc.contributor.authorCollin, Simon M
dc.contributor.authorMetcalfe, Chris
dc.contributor.authorZuccolo, Luisa
dc.contributor.authorLewis, Sarah J
dc.contributor.authorChen, Lina
dc.contributor.authorCox, Angela
dc.contributor.authorDavis, Michael
dc.contributor.authorLane, J Athene
dc.contributor.authorDonovan, Jenny
dc.contributor.authorSmith, George Davey
dc.contributor.authorNeal, David E
dc.contributor.authorHamdy, Freddie C
dc.contributor.authorGudmundsson, Julius
dc.contributor.authorSulem, Patrick
dc.contributor.authorRafnar, Thorunn
dc.contributor.authorBenediktsdottir, Kristrun R
dc.contributor.authorEeles, Rosalind A
dc.contributor.authorGuy, Michelle
dc.contributor.authorKote-Jarai, Zsofia
dc.contributor.authorMorrison, Jonathan
dc.contributor.authorAl Olama, Ali Amin
dc.contributor.authorStefansson, Kari
dc.contributor.authorEaston, Douglas F
dc.contributor.authorMartin, Richard M
dc.date.accessioned2009-10-20T09:46:51Z
dc.date.available2009-10-20T09:46:51Z
dc.date.issued2009-09-01
dc.date.submitted2009-10-20
dc.identifier.citationCancer Epidemiol. Biomarkers Prev. 2009, 18(9):2528-39en
dc.identifier.issn1055-9965
dc.identifier.pmid19706844
dc.identifier.doi10.1158/1055-9965.EPI-09-0223
dc.identifier.urihttp://hdl.handle.net/2336/84476
dc.descriptionTo access publisher full text version of this article. Please click on the hyperlink in Additional Links fielden
dc.description.abstractFolate-pathway gene polymorphisms have been implicated in several cancers and investigated inconclusively in relation to prostate cancer. We conducted a systematic review, which identified nine case-control studies (eight included, one excluded). We also included data from four genome-wide association studies and from a case-control study nested within the UK population-based Prostate Testing for Cancer and Treatment study. We investigated by meta-analysis the effects of eight polymorphisms: MTHFR C677T (rs1801133; 12 studies; 10,745 cases; 40,158 controls), MTHFR A1298C (rs1801131; 5 studies; 3,176 cases; 4,829 controls), MTR A2756G (rs1805087; 8 studies; 7,810 cases; 37,543 controls), MTRR A66G (rs1801394; 4 studies; 3,032 cases; 4,515 controls), MTHFD1 G1958A (rs2236225; 6 studies; 7,493 cases; 36,941 controls), SLC19A1/RFC1 G80A (rs1051266; 4 studies; 6,222 cases; 35,821 controls), SHMT1 C1420T (rs1979277; 2 studies; 2,689 cases; 4,110 controls), and FOLH1 T1561C (rs202676; 5 studies; 6,314 cases; 35,190 controls). The majority (10 of 13) of eligible studies had 100% Caucasian subjects; only one study had <90% Caucasian subjects. We found weak evidence of dominant effects of two alleles: MTR 2756A>G [random effects pooled odds ratio, 1.06 (1.00-1.12); P = 0.06 (P = 0.59 for heterogeneity across studies)] and SHMT1 1420C>T [random effects pooled odds ratio, 1.11 (1.00-1.22); P = 0.05 (P = 0.38 for heterogeneity across studies)]. We found no effect of MTHFR 677C>T or any of the other alleles in dominant, recessive or additive models, or in comparing a/a versus A/A homozygous. Neither did we find any difference in effects on advanced or localized cancers. Our meta-analysis suggests that known common folate-pathway single nucleotide polymorphisms do not have significant effects on susceptibility to prostate cancer.
dc.language.isoenen
dc.publisherAmerican Association for Cancer Researchen
dc.relation.urlhttp://dx.doi.org/10.1158/1055-9965.EPI-09-0223en
dc.titleAssociation of folate-pathway gene polymorphisms with the risk of prostate cancer: a population-based nested case-control study, systematic review, and meta-analysis.en
dc.typeArticleen
dc.identifier.eissn1538-7755
dc.contributor.departmentDepartment of Social Medicine, University of Bristol, Canynge Hall, 39 Whatley Road, Bristol, BS8 2PS United Kingdom. simon.collin@bristol.ac.uken
dc.identifier.journalCancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncologyen
html.description.abstractFolate-pathway gene polymorphisms have been implicated in several cancers and investigated inconclusively in relation to prostate cancer. We conducted a systematic review, which identified nine case-control studies (eight included, one excluded). We also included data from four genome-wide association studies and from a case-control study nested within the UK population-based Prostate Testing for Cancer and Treatment study. We investigated by meta-analysis the effects of eight polymorphisms: MTHFR C677T (rs1801133; 12 studies; 10,745 cases; 40,158 controls), MTHFR A1298C (rs1801131; 5 studies; 3,176 cases; 4,829 controls), MTR A2756G (rs1805087; 8 studies; 7,810 cases; 37,543 controls), MTRR A66G (rs1801394; 4 studies; 3,032 cases; 4,515 controls), MTHFD1 G1958A (rs2236225; 6 studies; 7,493 cases; 36,941 controls), SLC19A1/RFC1 G80A (rs1051266; 4 studies; 6,222 cases; 35,821 controls), SHMT1 C1420T (rs1979277; 2 studies; 2,689 cases; 4,110 controls), and FOLH1 T1561C (rs202676; 5 studies; 6,314 cases; 35,190 controls). The majority (10 of 13) of eligible studies had 100% Caucasian subjects; only one study had <90% Caucasian subjects. We found weak evidence of dominant effects of two alleles: MTR 2756A>G [random effects pooled odds ratio, 1.06 (1.00-1.12); P = 0.06 (P = 0.59 for heterogeneity across studies)] and SHMT1 1420C>T [random effects pooled odds ratio, 1.11 (1.00-1.22); P = 0.05 (P = 0.38 for heterogeneity across studies)]. We found no effect of MTHFR 677C>T or any of the other alleles in dominant, recessive or additive models, or in comparing a/a versus A/A homozygous. Neither did we find any difference in effects on advanced or localized cancers. Our meta-analysis suggests that known common folate-pathway single nucleotide polymorphisms do not have significant effects on susceptibility to prostate cancer.


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