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Article: Pathway analyses identify TGFBR2 as potential breast cancer susceptibility gene: results from a consortium study among Asians

TitlePathway analyses identify TGFBR2 as potential breast cancer susceptibility gene: results from a consortium study among Asians
Authors
Issue Date2012
PublisherAmerican Association for Cancer Research. The Journal's web site is located at http://cebp.aacrjournals.org/
Citation
Cancer Epidemiology, Biomarkers & Prevention, 2012, v. 21 n. 7, p. 1176-84 How to Cite?
AbstractBACKGROUND: The TGF-beta signaling pathway plays a significant role in the carcinogenic process of breast cancer. METHODS: We systematically evaluated associations of common variants in TGF-beta signaling pathway genes with breast cancer risk using a multistage, case-control study among Asian women. RESULTS: In the first stage, 341 single-nucleotide polymorphisms with minor allele frequencies >/= 0.05 across 11 genes were evaluated among 2,926 cases and 2,380 controls recruited as a part of the Shanghai Breast Cancer Genetics Study (SBCGS). In the second stage, 20 SNPs with promising associations were evaluated among an additional 1,890 cases and 2,000 controls from the SBCGS. One variant, TGFBR2 rs1078985, had highly consistent and significant associations with breast cancer risk among participants in both study stages, as well as promising results from in silico analysis. Additional genotyping was carried out among 2,475 cases and 2,343 controls from the SBCGS, as well as among 5,077 cases and 5,384 controls from six studies in the Asian Breast Cancer Consortium (stage III). Pooled analysis of all data indicated that minor allele homozygotes (GG) of TGFBR2 rs1078985 had a 24% reduced risk of breast cancer compared with major allele carriers (AG or AA; OR, 0.76; 95% CI, 0.65-0.89; P = 8.42 x 10(-4)). CONCLUSION: These findings support a role for common genetic variation in TGF-beta signaling pathway genes, specifically in TGFBR2, in breast cancer susceptibility. IMPACT: These findings may provide new insights into the etiology of breast cancer as well as future potential therapeutic targets.
Persistent Identifierhttp://hdl.handle.net/10722/186464
ISSN
2015 Impact Factor: 3.622
2015 SCImago Journal Rankings: 2.579
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorMa, Xen_US
dc.contributor.authorBeeghly-Fadiel, Aen_US
dc.contributor.authorLu, Wen_US
dc.contributor.authorShi, Jen_US
dc.contributor.authorXiang, YBen_US
dc.contributor.authorCai, Qen_US
dc.contributor.authorShen, Hen_US
dc.contributor.authorShen, CYen_US
dc.contributor.authorRen, Zen_US
dc.contributor.authorMatsuo, Ken_US
dc.contributor.authorKhoo, USen_US
dc.contributor.authorIwasaki, Men_US
dc.contributor.authorLong, Jen_US
dc.contributor.authorZhang, Ben_US
dc.contributor.authorJi, BTen_US
dc.contributor.authorZheng, Yen_US
dc.contributor.authorWang, Wen_US
dc.contributor.authorHu, Zen_US
dc.contributor.authorLiu, Yen_US
dc.contributor.authorWu, PEen_US
dc.contributor.authorShieh, YLen_US
dc.contributor.authorWang, Sen_US
dc.contributor.authorXie, Xen_US
dc.contributor.authorIto, Hen_US
dc.contributor.authorKasuga, Yen_US
dc.contributor.authorChan, KYKen_US
dc.contributor.authorIwata, Hen_US
dc.contributor.authorTsugane, Sen_US
dc.contributor.authorGao, YTen_US
dc.contributor.authorShu, XOen_US
dc.contributor.authorMoses, HLen_US
dc.contributor.authorZheng, Wen_US
dc.date.accessioned2013-08-20T12:09:13Z-
dc.date.available2013-08-20T12:09:13Z-
dc.date.issued2012en_US
dc.identifier.citationCancer Epidemiology, Biomarkers & Prevention, 2012, v. 21 n. 7, p. 1176-84en_US
dc.identifier.issn1055-9965en_US
dc.identifier.urihttp://hdl.handle.net/10722/186464-
dc.description.abstractBACKGROUND: The TGF-beta signaling pathway plays a significant role in the carcinogenic process of breast cancer. METHODS: We systematically evaluated associations of common variants in TGF-beta signaling pathway genes with breast cancer risk using a multistage, case-control study among Asian women. RESULTS: In the first stage, 341 single-nucleotide polymorphisms with minor allele frequencies >/= 0.05 across 11 genes were evaluated among 2,926 cases and 2,380 controls recruited as a part of the Shanghai Breast Cancer Genetics Study (SBCGS). In the second stage, 20 SNPs with promising associations were evaluated among an additional 1,890 cases and 2,000 controls from the SBCGS. One variant, TGFBR2 rs1078985, had highly consistent and significant associations with breast cancer risk among participants in both study stages, as well as promising results from in silico analysis. Additional genotyping was carried out among 2,475 cases and 2,343 controls from the SBCGS, as well as among 5,077 cases and 5,384 controls from six studies in the Asian Breast Cancer Consortium (stage III). Pooled analysis of all data indicated that minor allele homozygotes (GG) of TGFBR2 rs1078985 had a 24% reduced risk of breast cancer compared with major allele carriers (AG or AA; OR, 0.76; 95% CI, 0.65-0.89; P = 8.42 x 10(-4)). CONCLUSION: These findings support a role for common genetic variation in TGF-beta signaling pathway genes, specifically in TGFBR2, in breast cancer susceptibility. IMPACT: These findings may provide new insights into the etiology of breast cancer as well as future potential therapeutic targets.en_US
dc.languageengen_US
dc.publisherAmerican Association for Cancer Research. The Journal's web site is located at http://cebp.aacrjournals.org/en_US
dc.relation.ispartofCancer Epidemiology, Biomarkers & Preventionen_US
dc.subject.meshBreast - pathologyen_US
dc.subject.meshBreast Neoplasms - diagnosis - epidemiology - geneticsen_US
dc.subject.meshGenetic Predisposition to Diseaseen_US
dc.subject.meshPolymorphism, Single Nucleotideen_US
dc.subject.meshProtein-Serine-Threonine Kinases - geneticsen_US
dc.titlePathway analyses identify TGFBR2 as potential breast cancer susceptibility gene: results from a consortium study among Asiansen_US
dc.typeArticleen_US
dc.identifier.emailKhoo, US: uskhoo@hku.hken_US
dc.identifier.emailChan, KYK: ykchanc@hku.hken_US
dc.identifier.authorityKhoo, US=rp00362en_US
dc.identifier.authorityChan, KYK=rp00453en_US
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1158/1055-9965.EPI-12-0118en_US
dc.identifier.pmid22539603-
dc.identifier.scopuseid_2-s2.0-84863572566-
dc.identifier.hkuros220090en_US
dc.identifier.volume21en_US
dc.identifier.issue7en_US
dc.identifier.spage1176en_US
dc.identifier.epage84en_US
dc.identifier.isiWOS:000306210100022-
dc.publisher.placeUnited Statesen_US

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