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dc.contributor.CRUESPUNIVERSIDADE ESTADUAL DE CAMPINASpt_BR
dc.contributor.authorunicampBarbieri, Raquel Bueno-
dc.contributor.authorunicampBúfalo, Natássia Elena-
dc.contributor.authorunicampSecolin, Rodrigo-
dc.typeArtigopt_BR
dc.titleEvidence that polymorphisms in detoxification genes modulate the susceptibility for sporadic medullary thyroid carcinomapt_BR
dc.contributor.authorBarbieri, R. B.-
dc.contributor.authorBufalo, N. E.-
dc.contributor.authorSecolin, R.-
dc.contributor.authorSilva, A. C. N.-
dc.contributor.authorAssumpcao, L. V. M.-
dc.contributor.authorMaciel, R. M. B.-
dc.contributor.authorCerutti, J. M.-
dc.contributor.authorWard, L. S.-
dc.subjectPolimorfismo (Genética)pt_BR
dc.subjectGlândula tireóidept_BR
dc.subject.otherlanguageGenetic polymorphismspt_BR
dc.subject.otherlanguageThyroid glandpt_BR
dc.description.abstractPolymorphic low-penetrance genes have been consistently associated with the susceptibility to a series of human tumors, including differentiated thyroid cancer. To determine their role in medullary thyroid cancer (MTC), we used TaqMan SNP method to genotype 47 sporadic MTC (s-MTC) and a control group of 578 healthy individuals for CYP1A2* F, CYP1A1m1, GSTP1, NAT2 and 72TP53. A logistic regression analysis showed that NAT2C/C (OR=3.87; 95% CI=2.11-7.10; P=2.2 x 10(-5)) and TP53C/C genotypes (OR=3.87; 95% CI=1.78-6.10; P=2.8 x 10(-4)) inheritance increased the risk of s-MTC. A stepwise regression analysis indicated that TP53C/C genotype contributes with 8.07% of the s-MTC risk. We were unable to identify any relationship between NAT2 and TP53 polymorphisms suggesting they are independent factors of risk to s-MTC. In addition, there was no association between the investigated genes and clinical or pathological features of aggressiveness of the tumors or the outcome of MTC patients. In conclusion, we demonstrated that detoxification genes and apoptotic and cell cycle control genes are involved in the susceptibility of s-MTC and may modulate the susceptibility to the diseasept_BR
dc.relation.ispartofEuropean journal of endocrinologypt_BR
dc.relation.ispartofabbreviationEur j endocrinolpt_BR
dc.publisher.cityBristolpt_BR
dc.publisher.countryReino Unidopt_BR
dc.publisherBioScientificapt_BR
dc.date.issued2012-
dc.date.monthofcirculationFeb.pt_BR
dc.language.isoengpt_BR
dc.description.volume166pt_BR
dc.description.issuenumber2pt_BR
dc.description.firstpage241pt_BR
dc.description.lastpage245pt_BR
dc.rightsFechadopt_BR
dc.sourceWOSpt_BR
dc.identifier.issn0804-4643pt_BR
dc.identifier.eissn1479-683Xpt_BR
dc.identifier.doi10.1530/EJE-11-0843pt_BR
dc.identifier.urlhttps://eje.bioscientifica.com/view/journals/eje/166/2/241.xmlpt_BR
dc.description.sponsorshipFUNDAÇÃO DE AMPARO À PESQUISA DO ESTADO DE SÃO PAULO - FAPESPpt_BR
dc.description.sponsordocumentnumber07067-5pt_BR
dc.date.available2020-08-31T15:10:05Z-
dc.date.accessioned2020-08-31T15:10:05Z-
dc.description.provenanceSubmitted by Cintia Oliveira de Moura (cintiaom@unicamp.br) on 2020-08-31T15:10:05Z No. of bitstreams: 0. Added 1 bitstream(s) on 2021-01-04T15:14:42Z : No. of bitstreams: 1 000300295000012.pdf: 214657 bytes, checksum: faf62db9fea14d604d5bd3dcf5acc705 (MD5)en
dc.description.provenanceMade available in DSpace on 2020-08-31T15:10:05Z (GMT). No. of bitstreams: 0 Previous issue date: 2012en
dc.identifier.urihttp://repositorio.unicamp.br/jspui/handle/REPOSIP/348355-
dc.contributor.departmentsem informaçãopt_BR
dc.contributor.departmentsem informaçãopt_BR
dc.contributor.departmentsem informaçãopt_BR
dc.contributor.unidadeFaculdade de Ciências Médicaspt_BR
dc.contributor.unidadeFaculdade de Ciências Médicaspt_BR
dc.contributor.unidadeFaculdade de Ciências Médicaspt_BR
dc.identifier.source000300295000012pt_BR
dc.creator.orcidsem informaçãopt_BR
dc.creator.orcidsem informaçãopt_BR
dc.creator.orcid0000-0002-2485-9560pt_BR
dc.type.formArtigopt_BR
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