dc.creatorNascimento, H
dc.creatorCoy, CSR
dc.creatorTeori, MT
dc.creatorBoin, IFSF
dc.creatorGoes, JRN
dc.creatorCosta, FF
dc.creatorLima, CSP
dc.date2003
dc.dateAPR
dc.date2014-08-01T18:36:23Z
dc.date2015-11-26T18:05:03Z
dc.date2014-08-01T18:36:23Z
dc.date2015-11-26T18:05:03Z
dc.date.accessioned2018-03-29T00:47:18Z
dc.date.available2018-03-29T00:47:18Z
dc.identifierDiseases Of The Colon & Rectum. Lippincott Williams & Wilkins, v. 46, n. 4, n. 510, n. 515, 2003.
dc.identifier0012-3706
dc.identifierWOS:000182179100013
dc.identifier10.1097/01.DCR.0000054665.78762.9B
dc.identifierhttp://www.repositorio.unicamp.br/jspui/handle/REPOSIP/81476
dc.identifierhttp://repositorio.unicamp.br/jspui/handle/REPOSIP/81476
dc.identifier.urihttp://repositorioslatinoamericanos.uchile.cl/handle/2250/1293026
dc.descriptionIntroduction: Glutathione S-transferase enzymes mediate exposure to cytotoxic and genotoxic agents and may be involved in cancer susceptibility. Both glutathione S-transferase mu 1 (GSTM1) and GST theta 1 (GSTT1) genes have a null variant allele in which the entire gene is absent. The association of glutathione S-transferase null genotype and risk of developing colorectal cancer is not yet fully clarified. Methods: We tested whether the null genotypes for GSTM1 and GSTT1 genes altered the risk for sporadic colorectal adenocarcinoma in Brazilian patients. Genomic DNA from 102 sporadic colorectal adenocarcinoma patients and 300 controls was analyzed by polymerase chain reaction. Results: Frequencies of GSTM1, GSTT1, and null combined genotypes were similar in patients and controls (49.9 vs. 44.6 percent, 16.6 vs. 17.3 percent, and 8.8 vs. 8 percent, respectively). We found a 1.03-fold (95 percent confidence interval, 0.96-1.10) and 1.08-fold (95 percent confidence interval, 0.99-1.18) increased risk associated with GSTM1 and GSTT1 null genotypes, respectively (P=0.45 and P=0.08) and a 1.18-fold (95 percent confidence interval, 0.47-2.90) increased risk associated with the combined null genotype (P=0.74). The GSTT1 null genotype was more common in patients who were diagnosed before the age of 60 years than in those who were diagnosed at an older age (28.8 vs. 4 percent, respectively; P=0.0008). Conclusions: The results suggest that inherited absence of this carcinogen detoxification pathway may not be associated with sporadic colorectal adenocarcinoma in the present cases. However, a higher frequency of GSTT1 null genotype in patients diagnosed before the age of 60 years suggests that this genotype could influence the age of disease onset in Brazil.
dc.description46
dc.description4
dc.description510
dc.description515
dc.languageen
dc.publisherLippincott Williams & Wilkins
dc.publisherPhiladelphia
dc.publisherEUA
dc.relationDiseases Of The Colon & Rectum
dc.relationDis. Colon Rectum
dc.rightsfechado
dc.sourceWeb of Science
dc.subjectcolorectal cancer
dc.subjectepidemiology
dc.subjectglutathione S-transferase
dc.subjectGSTM1
dc.subjectGSTT1
dc.subjectColon-cancer
dc.subjectGenetic-polymorphism
dc.subjectMetabolic Genotypes
dc.subjectCigarette-smoking
dc.subjectIncreased Risk
dc.subjectTheta Gstt1
dc.subjectGstm1
dc.subjectSusceptibility
dc.subjectCarcinogenesis
dc.subjectM1
dc.titlePossible influence of glutathione S-transferase GSTT1 null genotype on age of onset of sporadic colorectal adenocarcinoma
dc.typeArtículos de revistas


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