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Article: Single nucleotide polymorphisms of follicle-stimulating hormone receptor are associated with ovarian cancer susceptibility

TitleSingle nucleotide polymorphisms of follicle-stimulating hormone receptor are associated with ovarian cancer susceptibility
Authors
Issue Date2006
PublisherOxford University Press. The Journal's web site is located at http://carcin.oxfordjournals.org/
Citation
Carcinogenesis, 2006, v. 27 n. 7, p. 1502-1506 How to Cite?
AbstractEpidemiological studies suggested that ovulation was associated with ovarian carcinogenesis. Follicle-stimulating hormone (FSH) played an important role in follicular development and was recently found to affect growth of ovarian epithelial cells. Single nucleotide polymorphisms (SNPs) Thr307Ala and Asn680Ser were two non-synonymous variations in the coding region of the FSH receptor (FSHR) gene. This hitherto first case-control study investigating the association between these two FSHR SNPs and the risk of ovarian cancer involved 202 histopathologically confirmed ovarian cancer patients and 266 age-matched cancer-free control subjects using restriction fragment length polymorphism assay and direct sequencing. Our results demonstrated that the 307Ala and 680Ser carriers were associated with significantly increased risk of developing serous and mucinous types of ovarian cancers (P < 0.0005, OR = 2.60, 95% CI = 1.56-4.34; and P < 0.0005, OR = 2.89, 95% CI = 1.73-4.84, adjusted for age, respectively) but not endometrioid and clear cell types. The two SNPs were found to be in modest linkage disequilibrium, D′ = 0.804 and 0.701, r 2 = 0.581 and 0.406 for the cancer and control groups, respectively. The major haplotype of 307Ala-680Ser was also associated with higher cancer risk (P = 0.033, OR = 1.39, 95% CI = 1.03-1.88), especially for the serous and mucinous carcinomas (P = 0.001, OR = 1.82, 95% CI = 1.27-2.60). Our results suggested that the two FSHR SNPs might affect the susceptibility of women to specific subtypes of ovarian cancer. Different types of ovarian cancer might adopt distinct carcinogenetic pathways. Such understanding may be important in selecting patients for ovulation induction therapy. © 2006 Oxford University Press.
Persistent Identifierhttp://hdl.handle.net/10722/87255
ISSN
2015 Impact Factor: 4.874
2015 SCImago Journal Rankings: 2.439
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorYang, CQen_HK
dc.contributor.authorChan, KYKen_HK
dc.contributor.authorNgan, HYSen_HK
dc.contributor.authorKhoo, USen_HK
dc.contributor.authorChiu, PMen_HK
dc.contributor.authorChan, QKYen_HK
dc.contributor.authorXue, WCen_HK
dc.contributor.authorCheung, ANYen_HK
dc.date.accessioned2010-09-06T09:27:20Z-
dc.date.available2010-09-06T09:27:20Z-
dc.date.issued2006en_HK
dc.identifier.citationCarcinogenesis, 2006, v. 27 n. 7, p. 1502-1506en_HK
dc.identifier.issn0143-3334en_HK
dc.identifier.urihttp://hdl.handle.net/10722/87255-
dc.description.abstractEpidemiological studies suggested that ovulation was associated with ovarian carcinogenesis. Follicle-stimulating hormone (FSH) played an important role in follicular development and was recently found to affect growth of ovarian epithelial cells. Single nucleotide polymorphisms (SNPs) Thr307Ala and Asn680Ser were two non-synonymous variations in the coding region of the FSH receptor (FSHR) gene. This hitherto first case-control study investigating the association between these two FSHR SNPs and the risk of ovarian cancer involved 202 histopathologically confirmed ovarian cancer patients and 266 age-matched cancer-free control subjects using restriction fragment length polymorphism assay and direct sequencing. Our results demonstrated that the 307Ala and 680Ser carriers were associated with significantly increased risk of developing serous and mucinous types of ovarian cancers (P < 0.0005, OR = 2.60, 95% CI = 1.56-4.34; and P < 0.0005, OR = 2.89, 95% CI = 1.73-4.84, adjusted for age, respectively) but not endometrioid and clear cell types. The two SNPs were found to be in modest linkage disequilibrium, D′ = 0.804 and 0.701, r 2 = 0.581 and 0.406 for the cancer and control groups, respectively. The major haplotype of 307Ala-680Ser was also associated with higher cancer risk (P = 0.033, OR = 1.39, 95% CI = 1.03-1.88), especially for the serous and mucinous carcinomas (P = 0.001, OR = 1.82, 95% CI = 1.27-2.60). Our results suggested that the two FSHR SNPs might affect the susceptibility of women to specific subtypes of ovarian cancer. Different types of ovarian cancer might adopt distinct carcinogenetic pathways. Such understanding may be important in selecting patients for ovulation induction therapy. © 2006 Oxford University Press.en_HK
dc.languageengen_HK
dc.publisherOxford University Press. The Journal's web site is located at http://carcin.oxfordjournals.org/en_HK
dc.relation.ispartofCarcinogenesisen_HK
dc.rightsCarcinogenesis. Copyright © Oxford University Press.en_HK
dc.subject.meshBase Sequenceen_HK
dc.subject.meshCase-Control Studiesen_HK
dc.subject.meshFemaleen_HK
dc.subject.meshGenetic Predisposition to Diseaseen_HK
dc.subject.meshHumansen_HK
dc.subject.meshOvarian Neoplasms - geneticsen_HK
dc.subject.meshPolymerase Chain Reactionen_HK
dc.subject.meshPolymorphism, Restriction Fragment Lengthen_HK
dc.subject.meshPolymorphism, Single Nucleotide - geneticsen_HK
dc.subject.meshReceptors, FSH - geneticsen_HK
dc.subject.meshRisk Factorsen_HK
dc.titleSingle nucleotide polymorphisms of follicle-stimulating hormone receptor are associated with ovarian cancer susceptibilityen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0143-3334&volume=27&spage=1502&epage=6&date=2006&atitle=Single+nucleotide+polymorphisms+of+follicle-stimulating+hormone+receptor+are+associated+with+ovarian+cancer+susceptibilityen_HK
dc.identifier.emailChan, KYK: kelvinc@pathology.hku.hken_HK
dc.identifier.emailNgan, HYS: hysngan@hkucc.hku.hken_HK
dc.identifier.emailKhoo, US: uskhoo@hku.hken_HK
dc.identifier.emailCheung, ANY: anycheun@hkucc.hku.hken_HK
dc.identifier.authorityChan, KYK=rp00453en_HK
dc.identifier.authorityNgan, HYS=rp00346en_HK
dc.identifier.authorityKhoo, US=rp00362en_HK
dc.identifier.authorityCheung, ANY=rp00542en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1093/carcin/bgl014en_HK
dc.identifier.pmid16574671-
dc.identifier.scopuseid_2-s2.0-33745618981en_HK
dc.identifier.hkuros119653en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-33745618981&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume27en_HK
dc.identifier.issue7en_HK
dc.identifier.spage1502en_HK
dc.identifier.epage1506en_HK
dc.identifier.isiWOS:000238906200025-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridYang, CQ=8390403300en_HK
dc.identifier.scopusauthoridChan, KYK=7406034195en_HK
dc.identifier.scopusauthoridNgan, HYS=34571944100en_HK
dc.identifier.scopusauthoridKhoo, US=7004195799en_HK
dc.identifier.scopusauthoridChiu, PM=7103182596en_HK
dc.identifier.scopusauthoridChan, QKY=8390404100en_HK
dc.identifier.scopusauthoridXue, WC=7103165268en_HK
dc.identifier.scopusauthoridCheung, ANY=54927484100en_HK
dc.identifier.citeulike739404-

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