dc.creatorde Lima Junior, Mario Maciel
dc.creatorReis, Leonardo Oliveira
dc.creatorGuilhen, Ana Carolina Trindade
dc.creatorGranja, Fabiana
dc.creatorde Lima Oliveira, Mariana Nicolau
dc.creatorFerreira, Ubirajara
dc.creatorCunha, Lucas Leite
dc.creatorWard, Laura Sterian
dc.date2012-Dec
dc.date2015-11-27T13:28:09Z
dc.date2015-11-27T13:28:09Z
dc.date.accessioned2018-03-29T01:14:44Z
dc.date.available2018-03-29T01:14:44Z
dc.identifierMedical Oncology (northwood, London, England). v. 29, n. 4, p. 2889-94, 2012-Dec.
dc.identifier1559-131X
dc.identifier10.1007/s12032-012-0157-4
dc.identifierhttp://www.ncbi.nlm.nih.gov/pubmed/22246524
dc.identifierhttp://repositorio.unicamp.br/jspui/handle/REPOSIP/199845
dc.identifier22246524
dc.identifier.urihttp://repositorioslatinoamericanos.uchile.cl/handle/2250/1300078
dc.descriptionWe investigated the role of N-acetyltransferases (NAT) in prostate cancer (PCa) susceptibility. NAT are polymorphic in the population and metabolize important carcinogenic products directly involved in the tumor initiation process. This prospective case-control study utilized the polymerase chain reaction-based restriction fragment length polymorphism method and comprised a cohort of consecutive 478 individuals: 126 men with prostate cancer; 101 men with benign prostatic hyperplasia (BPH); and a control health population of 177 female and 74 male blood donors from the same region. NAT2 slow or fast acetylators genotypes were determined by the combination of four variant alleles. Lifetime occupational history, dietary patterns, cigarette smoking and other anamnestic data were obtained by interviews. We were not able to find any correlation among smoking, dietary patterns, parameters of tumor aggressiveness or patient outcome and any NAT2 genotypes or phenotypes considered in separate or in different combinations. However, there was an association between NAT2T481C (OR=0.47; 95% CI=0.26-0.84; P=0.01) and NAT2A803G (OR=0.57; 95% CI=0.33-0.97; P=0.04) polymorphisms and PCa protection. Conversely, the presence of NAT2G857A genotype increased the risk of PCa more than 3 times (OR=3.57; 95% CI=1.39-9.15; P=0.005). Slow acetylator NAT2*7A and NAT2*6B genotypes occurred in 10.31% of PCa but in none of BPH patients (P=0.0007). The control health population confirmed the results and allowed the exclusion of possible biases caused by gender influence on genotype inheritance and by the inclusion of not diagnosed prostate diseases patients among the control individuals. We suggest that the investigation of germline polymorphisms of NAT2 gene may be useful in the assessment of Latin American patients at risk of BPH and PCa.
dc.description29
dc.description2889-94
dc.languageeng
dc.relationMedical Oncology (northwood, London, England)
dc.relationMed. Oncol.
dc.rightsfechado
dc.rights
dc.sourcePubMed
dc.subjectAged
dc.subjectArylamine N-acetyltransferase
dc.subjectCase-control Studies
dc.subjectFemale
dc.subjectGenetic Predisposition To Disease
dc.subjectGenotype
dc.subjectHumans
dc.subjectLatin America
dc.subjectMale
dc.subjectMiddle Aged
dc.subjectPolymorphism, Genetic
dc.subjectProspective Studies
dc.subjectProstatic Hyperplasia
dc.subjectProstatic Neoplasms
dc.titleN-acetyltransferase-2 Gene Polymorphisms And Prostate Cancer Susceptibility In Latin American Patients.
dc.typeArtículos de revistas


Este ítem pertenece a la siguiente institución