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

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TitleSingle nucleotide polymorphisms of follicle-stimulating hormone receptor are associated with ovarian cancer susceptibility
AuthorsYang, CQ1
Chan, KYK1
Ngan, HYS1
Khoo, US1
Chiu, PM1
Chan, QKY1
Xue, WC1
Cheung, ANY1
Issue Date2006
PublisherOxford University Press. The Journal's web site is located at http://carcin.oxfordjournals.org/
CitationCarcinogenesis, 2006, v. 27 n. 7, p. 1502-1506 [How to Cite?]
DOI: http://dx.doi.org/10.1093/carcin/bgl014
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.
ISSN0143-3334
2011 Impact Factor: 5.702
2011 SCImago Journal Rankings: 0.692
DOIhttp://dx.doi.org/10.1093/carcin/bgl014
ReferencesReferences in Scopus
DC Field
Value
dc.contributor.authorYang, CQ
dc.contributor.authorChan, KYK
dc.contributor.authorNgan, HYS
dc.contributor.authorKhoo, US
dc.contributor.authorChiu, PM
dc.contributor.authorChan, QKY
dc.contributor.authorXue, WC
dc.contributor.authorCheung, ANY
dc.date.accessioned2010-09-06T09:27:20Z
dc.date.available2010-09-06T09:27:20Z
dc.date.issued2006
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.
dc.description.natureLink_to_subscribed_fulltext
dc.identifier.citationCarcinogenesis, 2006, v. 27 n. 7, p. 1502-1506 [How to Cite?]
DOI: http://dx.doi.org/10.1093/carcin/bgl014
dc.identifier.citeulike739404
dc.identifier.doihttp://dx.doi.org/10.1093/carcin/bgl014
dc.identifier.epage1506
dc.identifier.hkuros119653
dc.identifier.isiWOS:000238906200025
dc.identifier.issn0143-3334
2011 Impact Factor: 5.702
2011 SCImago Journal Rankings: 0.692
dc.identifier.issue7
dc.identifier.openurl
dc.identifier.pmid16574671
dc.identifier.scopuseid_2-s2.0-33745618981
dc.identifier.spage1502
dc.identifier.urihttp://hdl.handle.net/10722/87255
dc.identifier.volume27
dc.languageeng
dc.publisherOxford University Press. The Journal's web site is located at http://carcin.oxfordjournals.org/
dc.publisher.placeUnited Kingdom
dc.relation.ispartofCarcinogenesis
dc.relation.referencesReferences in Scopus
dc.rightsCarcinogenesis. Copyright © Oxford University Press.
dc.subject.meshBase Sequence
dc.subject.meshCase-Control Studies
dc.subject.meshFemale
dc.subject.meshGenetic Predisposition to Disease
dc.subject.meshHumans
dc.subject.meshOvarian Neoplasms - genetics
dc.subject.meshPolymerase Chain Reaction
dc.subject.meshPolymorphism, Restriction Fragment Length
dc.subject.meshPolymorphism, Single Nucleotide - genetics
dc.subject.meshReceptors, FSH - genetics
dc.subject.meshRisk Factors
dc.titleSingle nucleotide polymorphisms of follicle-stimulating hormone receptor are associated with ovarian cancer susceptibility
dc.typeArticle
Author Affiliations
  1. The University of Hong Kong