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Breast cancer risk and polymorphisms in genes involved in metabolism of estrogens (CYP17, HSD17β1, COMT and MnSOD)

2006-10Artigo científico Acesso aberto
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dc.contributor.authorSilva, Susana N.
dc.contributor.authorCabral, Marisa N.
dc.contributor.authorDe Castro, Guilherme Bezerra
dc.contributor.authorPires, Marcelo
dc.contributor.authorAzevedo, Ana Paula
dc.contributor.authorManita, Isabel
dc.contributor.authorPina, Julieta Esperança
dc.contributor.authorRueff, José
dc.contributor.authorRueff, Jose
dc.contributor.authorGaspar, Jorge
dc.contributor.institutionNOVA Medical School|Faculdade de Ciências Médicas (NMS|FCM)
dc.contributor.pblSpandidos Publications
dc.date.accessioned2024-03-14T00:01:49Z
dc.date.available2024-03-14T00:01:49Z
dc.date.issued2006-10
dc.description.abstractPolymorphisms in genes encoding enzymes involved in estrogen metabolism are held to be candidates for associations with breast disease, since there is evidence that circulating estrogens are associated with breast cancer risk. In this study, we evaluated the frequency of different polymorphisms related with estrogen metabolism [ COMT Val158Met, CYP17 (5′UTR, T27C); HSD17β1 Gly313Ser and MnSOD Val16Ala] in a breast cancer resistant population, the Xavante Indians, and the frequencies were compared with the ones reported in other populations where breast cancer case-control studies dealing with these polymorphisms have been carried out. The data obtained showed that, apart from the MnSOD Val16Ala polymorphism where the frequency of the variant allele was much higher than that reported in other populations, all the others were within the range reported in other populations. Considering these data we carried out a case-control study in the Portuguese population (241 cases and 457 controls) in order to evaluate the potential role of this polymorphism in breast cancer susceptibility. The results obtained did not reveal a significant association between individual genotypes and breast cancer risk. However, when the population was stratified for breast feeding, it was observed that for the patients that never breast fed the presence of the variant allele (Ala) was marginally associated with a decreased risk for this pathology (adjusted OR: 0.575 (0.327-1.011). These data seem to suggest that individuals who never breast fed with MnSOD Val16Ala variant allele are at a lower risk for breast cancer, but larger studies are required to confirm these results.en
dc.description.versionpublishersversion
dc.description.versionpublished
dc.format.extent8
dc.format.extent96851
dc.identifier.doi10.3892/or.16.4.781
dc.identifier.issn1021-335X
dc.identifier.otherPURE: 85303347
dc.identifier.otherPURE UUID: 5f6a3a95-c6a6-4aed-9374-78dd41dc846f
dc.identifier.otherScopus: 34548771907
dc.identifier.otherPubMed: 16969494
dc.identifier.otherWOS: 000240879000020
dc.identifier.otherORCID: /0000-0002-9122-0732/work/155465706
dc.identifier.urihttp://hdl.handle.net/10362/164900
dc.identifier.urlhttps://www.scopus.com/pages/publications/34548771907
dc.language.isoeng
dc.peerreviewedyes
dc.subjectBreast cancer
dc.subjectBreast feeding
dc.subjectCOMT gene polymorphism
dc.subjectCYP17 gene polymorphism
dc.subjectHSD17β1 gene polymorphism
dc.subjectMnSOD gene polymorphism
dc.subjectOncology
dc.subjectCancer Research
dc.subjectSDG 3 - Good Health and Well-being
dc.titleBreast cancer risk and polymorphisms in genes involved in metabolism of estrogens (CYP17, HSD17β1, COMT and MnSOD)en
dc.title.subtitlePossible protective role of MnSOD gene polymorphism Val/Ala and Ala/Ala in women that never breast feden
dc.typejournal article
degois.publication.firstPage781
degois.publication.issue4
degois.publication.lastPage788
degois.publication.titleOncology Reports
degois.publication.volume16
dspace.entity.typePublication
person.familyNameRueff
person.givenNameJose
person.identifier793666
person.identifier.ciencia-id0E15-908D-EA21
person.identifier.orcid0000-0002-8456-7295
person.identifier.ridE-6426-2013
person.identifier.scopus-author-id7006536439
rcaap.rightsopenAccess
relation.isAuthorOfPublication91a3b5ac-0328-498d-8cb8-08555b202306
relation.isAuthorOfPublication.latestForDiscovery91a3b5ac-0328-498d-8cb8-08555b202306

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