Search Results
You are looking at 1 - 2 of 2 items for
- Author: Gila Neta x
- Refine by access: All content x
Occupational and Environmental Epidemiology Branch, Department of Health Studies, Radiation Epidemiology Branch, Core Genotype Facility, Biostatistics Branch, Department of Head and Neck Surgery, Information Management Services, Division of Cancer Epidemiology and Genetics, Department of Health and Human Services, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892, USA
Search for other papers by Briseis Aschebrook-Kilfoy in
Google Scholar
PubMed
Search for other papers by Gila Neta in
Google Scholar
PubMed
Search for other papers by Alina V Brenner in
Google Scholar
PubMed
Search for other papers by Amy Hutchinson in
Google Scholar
PubMed
Search for other papers by Ruth M Pfeiffer in
Google Scholar
PubMed
Search for other papers by Erich M Sturgis in
Google Scholar
PubMed
Search for other papers by Li Xu in
Google Scholar
PubMed
Search for other papers by William Wheeler in
Google Scholar
PubMed
Search for other papers by Michele M Doody in
Google Scholar
PubMed
Search for other papers by Stephen J Chanock in
Google Scholar
PubMed
Search for other papers by Alice J Sigurdson in
Google Scholar
PubMed
Relationships are unclear between polymorphisms in genes involved in metabolism and detoxification of various chemicals and papillary thyroid cancer (PTC) risk as well as their potential modification by alcohol or tobacco intake. We evaluated associations between 1647 tagging single nucleotide polymorphisms (SNPs) in 132 candidate genes/regions involved in metabolism of exogenous and endogenous compounds (Phase I/II, oxidative stress, and metal binding pathways) and PTC risk in 344 PTC cases and 452 controls. For 15 selected regions and their respective SNPs, we also assessed interaction with alcohol and tobacco use. Logistic regression models were used to evaluate the main effect of SNPs (P trend) and interaction with alcohol/tobacco intake. Gene- and pathway-level associations and interactions (P gene interaction) were evaluated by combining P trend values using the adaptive rank-truncated product method. While we found associations between PTC risk and nine SNPs (P trend≤0.01) and seven genes/regions (P region<0.05), none remained significant after correction for the false discovery rate. We found a significant interaction between UGT2B7 and NAT1 genes and alcohol intake (P gene interaction=0.01 and 0.02 respectively) and between the CYP26B1 gene and tobacco intake (P gene interaction=0.02). Our results are suggestive of interaction between the genetic polymorphisms in several detoxification genes and alcohol or tobacco intake on risk of PTC. Larger studies with improved exposure assessment should address potential modification of PTC risk by alcohol and tobacco intake to confirm or refute our findings.
Search for other papers by Ruta Sahasrabudhe in
Google Scholar
PubMed
Search for other papers by Ana Estrada in
Google Scholar
PubMed
Search for other papers by Paul Lott in
Google Scholar
PubMed
Search for other papers by Lynn Martin in
Google Scholar
PubMed
Department of Biochemistry and Molecular Medicine, Grupo de Citogenética, Wellcome Trust Centre for Human Genetics, Hospital Pablo Tobón Uribe, Division of Cancer Control and Population Sciences, Center for the Promotion of Interdisciplinary Education and Research, Graduate School of Medicine, Departments of Molecular Epidemiology, Radiation Medical Sciences, Nagasaki University Research Centre for Genomic Instability and Carcinogenesis, Fundación de Genómica y Genética Molecular, School of Medicine, UC Davis Genome Center, University of California, Davis, 451 Health Sciences Drive, Davis, California 95616, USA
Search for other papers by Guadalupe Polanco Echeverry in
Google Scholar
PubMed
Search for other papers by Alejandro Velez in
Google Scholar
PubMed
Search for other papers by Gila Neta in
Google Scholar
PubMed
Department of Biochemistry and Molecular Medicine, Grupo de Citogenética, Wellcome Trust Centre for Human Genetics, Hospital Pablo Tobón Uribe, Division of Cancer Control and Population Sciences, Center for the Promotion of Interdisciplinary Education and Research, Graduate School of Medicine, Departments of Molecular Epidemiology, Radiation Medical Sciences, Nagasaki University Research Centre for Genomic Instability and Carcinogenesis, Fundación de Genómica y Genética Molecular, School of Medicine, UC Davis Genome Center, University of California, Davis, 451 Health Sciences Drive, Davis, California 95616, USA
Search for other papers by Meiko Takahasi in
Google Scholar
PubMed
Search for other papers by Vladimir Saenko in
Google Scholar
PubMed
Department of Biochemistry and Molecular Medicine, Grupo de Citogenética, Wellcome Trust Centre for Human Genetics, Hospital Pablo Tobón Uribe, Division of Cancer Control and Population Sciences, Center for the Promotion of Interdisciplinary Education and Research, Graduate School of Medicine, Departments of Molecular Epidemiology, Radiation Medical Sciences, Nagasaki University Research Centre for Genomic Instability and Carcinogenesis, Fundación de Genómica y Genética Molecular, School of Medicine, UC Davis Genome Center, University of California, Davis, 451 Health Sciences Drive, Davis, California 95616, USA
Search for other papers by Norisato Mitsutake in
Google Scholar
PubMed
Search for other papers by Emma Jaeguer in
Google Scholar
PubMed
Search for other papers by Carlos Simon Duque in
Google Scholar
PubMed
Search for other papers by Alejandro Rios in
Google Scholar
PubMed
Search for other papers by Mabel Bohorquez in
Google Scholar
PubMed
Search for other papers by Rodrigo Prieto in
Google Scholar
PubMed
Search for other papers by Angel Criollo in
Google Scholar
PubMed
Search for other papers by Magdalena Echeverry in
Google Scholar
PubMed
Search for other papers by Ian Tomlinson in
Google Scholar
PubMed
Search for other papers by on behalf of the TCUKIN and CORGI Consortiums in
Google Scholar
PubMed
Department of Biochemistry and Molecular Medicine, Grupo de Citogenética, Wellcome Trust Centre for Human Genetics, Hospital Pablo Tobón Uribe, Division of Cancer Control and Population Sciences, Center for the Promotion of Interdisciplinary Education and Research, Graduate School of Medicine, Departments of Molecular Epidemiology, Radiation Medical Sciences, Nagasaki University Research Centre for Genomic Instability and Carcinogenesis, Fundación de Genómica y Genética Molecular, School of Medicine, UC Davis Genome Center, University of California, Davis, 451 Health Sciences Drive, Davis, California 95616, USA
Department of Biochemistry and Molecular Medicine, Grupo de Citogenética, Wellcome Trust Centre for Human Genetics, Hospital Pablo Tobón Uribe, Division of Cancer Control and Population Sciences, Center for the Promotion of Interdisciplinary Education and Research, Graduate School of Medicine, Departments of Molecular Epidemiology, Radiation Medical Sciences, Nagasaki University Research Centre for Genomic Instability and Carcinogenesis, Fundación de Genómica y Genética Molecular, School of Medicine, UC Davis Genome Center, University of California, Davis, 451 Health Sciences Drive, Davis, California 95616, USA
Search for other papers by Luis G Carvajal Carmona in
Google Scholar
PubMed
The G allele of the rs6983267 single-nucleotide polymorphism, located on chromosome 8q24, has been associated with increased risk of several cancer types. The association between rs6983267G and thyroid cancer (TC) has been tested in different populations, mostly of European ancestry, and has led to inconclusive results. While significant associations have been reported in the British and Polish populations, no association has been detected in populations from Spain, Italy and the USA. To further investigate the role of rs6983267G in TC susceptibility, we evaluated rs6983267 genotypes in three populations of different continental ancestry (British Isles, Colombia and Japan), providing a total of 3067 cases and 8575 controls. We detected significant associations between rs6983267G and TC in the British Isles (odds ratio (OR)=1.19, 95% CI: 1.11–1.27, P=4.03×10−7), Japan (OR=1.20, 95% CI: 1.03–1.41, P=0.022) and a borderline significant association of similar effect direction and size in Colombia (OR=1.19, 95% CI: 0.99–1.44, P=0.069). A meta-analysis of our multi-ethnic study and previously published non-overlapping datasets, which included a total of 5484 cases and 12 594 controls, confirmed the association between rs6983267G and TC (P=1.23×10−7, OR=1.13, 95% CI: 1.08–1.18). Our results therefore support the notion that rs6983267G is a bona fide TC risk variant that increases the risk of disease by ∼13%.