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Conference Paper: Single nucleotide polymorphisms (SNPs) in the coding sequence of follicle stimulating hormone receptor (FSHR) are associated with ovarian cancer susceptibility

TitleSingle nucleotide polymorphisms (SNPs) in the coding sequence of follicle stimulating hormone receptor (FSHR) are associated with ovarian cancer susceptibility
Authors
Issue Date2004
PublisherAmerican Association for Cancer Research
Citation
AACR 95th Annual Meeting, Orlando FL, 27–31 March 2004. In Cancer Research, 2004, v. 64 n. 7S, p. 1041 Abstract no. 4510 How to Cite?
AbstractBackground: Follicle stimulating hormone (FSH) and its receptor (FSHR) are important in ovarian functions and may implicate in ovarian carcinogenesis. Single nucleotide polymorphism (SNP) of the FSHR gene has previously been found to affect FSH efficacy. The objective of this study was to investigate possible association between two SNPs of FSHR gene, Ala307Thr and Ser680Asn, and susceptibility to ovarian cancer. Methods: After histological review, genomic DNA was extracted from non-cancer tissue of 203 ovarian-cancer patients and 267 age-matched control subjects who had surgery for benign gynecological lesions. The genotypes at Ala307Thr and Ser680Asn were assessed by restriction fragment length polymorphism (RFLP) assay. Results: Genotype frequencies were as listed in the table. The genotypes were in Hardy-Weinburg equilibrium for the control group. Homozygous Thr/Thr for SNP Ala307Thr and Asn/Asn for SNP Ser680Asn seem to carry lower risk of ovarian cancer (OR=0.66; 95%CI=0.45-0.96; p=0.030 and OR=0.60; 95%CI=0.41-0.86; p=0.007 respectively). The protective effect was more pronounced for ovarian cancer of serous (OR=0.43; 95%CI=0.24-0.77; p=0.004 for SNP Ala307Thr; OR=0.43; 95%CI=0.24-0.76; p=0.004 for SNP Ser680Asn) and mucinous (OR=0.40; 95%CI=0.18-0.89; p=0.030 for SNPAla307Thr; OR=0.24; 95%CI=0.10-0.56; p<0.001 for SNP Ser680Asn) types. Interestingly, no association was found between these two SNPs with ovarian cancer of endometrioid and clear cell types. Preliminary analysis of FSHR mRNA and protein expression on different histological types of ovarian cancers by reverse transcription (RT)-PCR and immunohistochemistry showed that expression was found in serous and mucinous types of ovarian cancers but not the endometrioid and clear cell carcinomas. Conclusions: Our results suggest that SNPs at these two sites may affect FSHR function and the susceptibility of the women to ovarian cancer. Serous and mucinous ovarian cancer may adopt different carcinogenetic pathways when compared with endometrioid and clear cell carcinomas known to be associated with endometriosis. The possibility of linkage disequilibrium of these two SNPs in Chinese and their effect in combination are being assessed.
Persistent Identifierhttp://hdl.handle.net/10722/113725
ISSN
2015 Impact Factor: 8.556
2015 SCImago Journal Rankings: 5.372

 

DC FieldValueLanguage
dc.contributor.authorYang, Cen_HK
dc.contributor.authorNgan, HYSen_HK
dc.contributor.authorKhoo, USen_HK
dc.contributor.authorChan, YKen_HK
dc.contributor.authorChiu, PMen_HK
dc.contributor.authorChan, QKYen_HK
dc.contributor.authorXue, Wen_HK
dc.contributor.authorCheung, ANYen_HK
dc.date.accessioned2010-09-26T04:28:28Z-
dc.date.available2010-09-26T04:28:28Z-
dc.date.issued2004en_HK
dc.identifier.citationAACR 95th Annual Meeting, Orlando FL, 27–31 March 2004. In Cancer Research, 2004, v. 64 n. 7S, p. 1041 Abstract no. 4510-
dc.identifier.issn0008-5472-
dc.identifier.urihttp://hdl.handle.net/10722/113725-
dc.description.abstractBackground: Follicle stimulating hormone (FSH) and its receptor (FSHR) are important in ovarian functions and may implicate in ovarian carcinogenesis. Single nucleotide polymorphism (SNP) of the FSHR gene has previously been found to affect FSH efficacy. The objective of this study was to investigate possible association between two SNPs of FSHR gene, Ala307Thr and Ser680Asn, and susceptibility to ovarian cancer. Methods: After histological review, genomic DNA was extracted from non-cancer tissue of 203 ovarian-cancer patients and 267 age-matched control subjects who had surgery for benign gynecological lesions. The genotypes at Ala307Thr and Ser680Asn were assessed by restriction fragment length polymorphism (RFLP) assay. Results: Genotype frequencies were as listed in the table. The genotypes were in Hardy-Weinburg equilibrium for the control group. Homozygous Thr/Thr for SNP Ala307Thr and Asn/Asn for SNP Ser680Asn seem to carry lower risk of ovarian cancer (OR=0.66; 95%CI=0.45-0.96; p=0.030 and OR=0.60; 95%CI=0.41-0.86; p=0.007 respectively). The protective effect was more pronounced for ovarian cancer of serous (OR=0.43; 95%CI=0.24-0.77; p=0.004 for SNP Ala307Thr; OR=0.43; 95%CI=0.24-0.76; p=0.004 for SNP Ser680Asn) and mucinous (OR=0.40; 95%CI=0.18-0.89; p=0.030 for SNPAla307Thr; OR=0.24; 95%CI=0.10-0.56; p<0.001 for SNP Ser680Asn) types. Interestingly, no association was found between these two SNPs with ovarian cancer of endometrioid and clear cell types. Preliminary analysis of FSHR mRNA and protein expression on different histological types of ovarian cancers by reverse transcription (RT)-PCR and immunohistochemistry showed that expression was found in serous and mucinous types of ovarian cancers but not the endometrioid and clear cell carcinomas. Conclusions: Our results suggest that SNPs at these two sites may affect FSHR function and the susceptibility of the women to ovarian cancer. Serous and mucinous ovarian cancer may adopt different carcinogenetic pathways when compared with endometrioid and clear cell carcinomas known to be associated with endometriosis. The possibility of linkage disequilibrium of these two SNPs in Chinese and their effect in combination are being assessed.-
dc.languageengen_HK
dc.publisherAmerican Association for Cancer Research-
dc.relation.ispartofCancer Researchen_HK
dc.titleSingle nucleotide polymorphisms (SNPs) in the coding sequence of follicle stimulating hormone receptor (FSHR) are associated with ovarian cancer susceptibilityen_HK
dc.typeConference_Paperen_HK
dc.identifier.emailNgan, HYS: hysngan@hkucc.hku.hken_HK
dc.identifier.emailKhoo, US: uskhoo@pathology.hku.hken_HK
dc.identifier.emailChan, YK: kelvinc@pathology.hku.hken_HK
dc.identifier.emailChiu, PM: h9994065@hkusua.hku.hken_HK
dc.identifier.emailChan, QKY: h9841511@graduate.hku.hken_HK
dc.identifier.emailCheung, ANY: anycheun@hkucc.hku.hken_HK
dc.identifier.authorityNgan, HYS=rp00346en_HK
dc.identifier.authorityKhoo, US=rp00362en_HK
dc.identifier.authorityChan, YK=rp00453en_HK
dc.identifier.authorityCheung, ANY=rp00542en_HK
dc.identifier.hkuros87369en_HK

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