Literature DB >> 16847185

Glutathione S-transferase polymorphisms and risk of differentiated thyroid carcinomas: a case-control analysis.

Tang Ho1, Chong Zhao, Rong Zheng, Zhensheng Liu, Qingyi Wei, Erich M Sturgis.   

Abstract

OBJECTIVE: To determine the association between glutathione S-transferase (GST) polymorphisms and the risk of differentiated thyroid carcinoma (DTC) and benign thyroid tumors.
DESIGN: Case-control study.
SETTING: Tertiary care cancer center. PATIENTS: Two hundred one patients with DTC, 103 patients with benign thyroid tumors, and 680 cancer-free control subjects. MAIN OUTCOME MEASURES: Results of a polymerase chain reaction-based assay for genotyping. A multivariate logistic regression analysis was performed with adjustment for age, sex, ethnicity, tobacco use, and alcohol use.
RESULTS: The patients with DTC were younger, more likely to be female and nonwhite, and less likely to smoke or consume alcohol than the controls. Overall, 55.2% of the DTC cases and 52.6% of the controls were null for the gene for GST-mu1 (GSTM1) (P = .52), and 25.4% of the DTC subjects and 20.6% of the controls were null for the GST-theta1 gene (GSTT1) (P = .15). However, 15.9% of the DTC cases but only 9.4% of the controls were null for both genes (P = .009). In addition, the results of the adjusted multivariate regression analysis suggested that having both null genotypes was associated with an increased risk for DTC (odds ratio [OR], 2.1 [95% confidence interval, 1.3-3.5; P = .003]). This was particularly true for women (OR, 2.5), current smokers (OR, 3.6), and nonwhites (OR, 5.6). A similar analysis demonstrated a nonsignificant association between these genotypes and benign thyroid tumors (OR, 1.5 [95% confidence interval, 0.7-3.0; P=.30).
CONCLUSIONS: Our results suggest that the simultaneous presence of the GSTM1- and GSTT1-null genotypes is a susceptibility factor for DTC. Such knowledge may ultimately help refine cancer prevention efforts; however, larger studies are needed to verify these findings.

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Year:  2006        PMID: 16847185     DOI: 10.1001/archotol.132.7.756

Source DB:  PubMed          Journal:  Arch Otolaryngol Head Neck Surg        ISSN: 0886-4470


  6 in total

1.  Family history of cancer and risk of sporadic differentiated thyroid carcinoma.

Authors:  Li Xu; Guojun Li; Qingyi Wei; Adel K El-Naggar; Erich M Sturgis
Journal:  Cancer       Date:  2011-07-28       Impact factor: 6.860

2.  Combined GSTM1 and GSTT1 null genotypes are associated with a lower risk of papillary thyroid cancer.

Authors:  M C Lemos; E Coutinho; L Gomes; F Carrilho; F Rodrigues; F J Regateiro; M Carvalheiro
Journal:  J Endocrinol Invest       Date:  2008-06       Impact factor: 4.256

3.  GSTM1 and GSTT1 null polymorphisms and risk of salivary gland carcinoma.

Authors:  Sayaka Kondo; Erich M Sturgis; Fanglin Li; Qingyi Wei; Guojun Li
Journal:  Int J Clin Exp Med       Date:  2009-02-25

4.  Polymorphisms of selected xenobiotic genes contribute to the development of papillary thyroid cancer susceptibility in Middle Eastern population.

Authors:  Abdul K Siraj; Muna Ibrahim; Maha Al-Rasheed; Jehad Abubaker; Rong Bu; Shakaib U Siddiqui; Fouad Al-Dayel; Osama Al-Sanea; Abdulrahman Al-Nuaim; Shahab Uddin; Khawla Al-Kuraya
Journal:  BMC Med Genet       Date:  2008-07-05       Impact factor: 2.103

5.  Antioxidant defence-related genetic variants are not associated with higher risk of secondary thyroid cancer after treatment of malignancy in childhood or adolescence.

Authors:  Ana Lina Vodusek; Katja Goricar; Barbara Gazic; Vita Dolzan; Janez Jazbec
Journal:  Radiol Oncol       Date:  2016-02-16       Impact factor: 2.991

6.  Functional polymorphisms in antioxidant genes in Hurthle cell thyroid neoplasm - an association of GPX1 polymorphism and recurrent Hurthle cell thyroid carcinoma.

Authors:  Blaz Krhin; Katja Goricar; Barbara Gazic; Vita Dolzan; Nikola Besic
Journal:  Radiol Oncol       Date:  2016-07-19       Impact factor: 2.991

  6 in total

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