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3. International Lung Cancer Consortium: Coordinated association study of 10 potential lung cancer susceptibility variants

Author

Behnaz Pezeshki Naeim, Heike Bickeböller, James McKay, Vladimir Janout, Chikako Kiyohara, Shanbeh Zienolddiny, Aage Haugen, Eric J. Duell, Angeline S. Andrew, Joshua E. Muscat, Neonilia Szeszenia-Dabrowska, Ying Wang, Hendrik Dienemann, Michael J. Thun, Rayjean J. Hung, Jolanta Lissowska, Vladimir Bencko, Maria Teresa Landi, Keitaro Matsuo, Marcin Lener, Hongbing Shen, Angela Risch, Thomas Illig, Joanna Trubicka, Daniel P.K. Ng, Neil E. Caporaso, Margaret R. Spitz, H. Dean Hosgood, Paul Brennan, Jin Hee Kim, Philip Lazarus, Qing Lan, Adeline Seow, Eleonora Fabianova, Yun Chul Hong, Demetrius Albanes, Paolo Boffetta, Loic Le Marchand, Jan Lubinski, H.-Erich Wichmann, Takeshi Suzuki, Ping Yang, Zuo-Feng Zhang, Vali Constantinescu, Amelie Chabrier, Christopher I. Amos, Peter Rudnai, Lenka Foretova, Wiebke Sauter, Thérèse Truong, Carla J. Gallagher, David Zaridze, Truong, T., Sauter, W., McKay, J.D., Hosgood III, D.H., Gallagher, C., Amos, C.I., Spitz, M., Muscat, J., Lazarus, P., Illig, T., Wichmann, H.E., Bickeböller, H., Risch, A., Dienemann, H., Zhang, Z.-F., Naeim, B.P., Yang, P., Zienolddiny, S., Haugen, A., Marchand, L.L., Hong, Y.-C., Kim, J.H., Duell, E.J., Andrew, A.S., Kiyohara, C., Shen, H., Matsuo, K., Suzuki, T., Seow, A., Ng, D.P., Lan, Q., Zaridze, D., Szeszenia-Dabrowska, N., Lissowska, J., Rudnai, P., Fabianova, E., Constantinescu, V., Bencko, V., Foretova, L., Janout, V., Caporaso, N.E., Albanes, D., Thun, M., Landi, M.T., Trubicka, J., Lener, M., Lubinski, J., Wang, Y., Chabrier, A., Boffetta, P., Brennan, P., and Hung, R.J.

Subjects
Adult, Male, Oncology, Cancer Research, medicine.medical_specialty, Candidate gene, Lung Neoplasms, Genotype, Genome-wide association study, 03 medical and health sciences, 0302 clinical medicine, Internal medicine, Odds Ratio, medicine, Humans, Genetic Predisposition to Disease, Lung cancer, Methylenetetrahydrofolate Reductase (NADPH2), Aged, 030304 developmental biology, Molecular Epidemiology, 0303 health sciences, biology, Lung Cancer, Intracellular Signaling Peptides and Proteins, Cancer, General Medicine, Odds ratio, Middle Aged, medicine.disease, susceptibility variant, Lung cancer susceptibility, 3. Good health, 030220 oncology & carcinogenesis, Methylenetetrahydrofolate reductase, Immunology, biology.protein, Female, Tumor Suppressor p53-Binding Protein 1, Consortium, Genome-Wide Association Study, Molecular Chaperones
Abstract

Background: Analysis of candidate genes in individual studies has had only limited success in identifying particular gene variants that are conclusively associated with lung cancer risk. In the International Lung Cancer Consortium (ILCCO), we conducted a coordinated genotyping study of 10 common variants selected because of their prior evidence of an association with lung cancer. These variants belonged to candidate genes from different cancerrelated pathways including inflammation (IL1B), folate metabolism (MTHFR), regulatory function (AKAP9 and CAMKK1), cell adhesion (SEZL6) and apoptosis (FAS, FASL, TP53, TP53BP1 and BAT3). Methods: Genotype data from 15 ILCCO case-control studies were available for a total of 8431 lung cancer cases and 11 072 controls of European descent and Asian ethnic groups. Unconditional logistic regression was used to model the association between each variant and lung cancer risk. Results: Only the association between a non-synonymous variant of TP53BP1 (rs560191) and lung cancer risk was significant (OR = 0.91, P = 0.002). This association was more striking for squamous cell carcinoma (OR = 0.86, P = 6 × 10-4). No heterogeneity by center, ethnicity, smoking status, age group or sex was observed. In order to confirm this association, we included results for this variant from a set of independent studies (9966 cases/11 722 controls) and we reported similar results. When combining all these studies together, we reported an overall OR = 0.93 (0.89-0.97) (P = 0.001). This association was significant only for squamous cell carcinoma [OR = 0.89 (0.85-0.95), P = 1 × 10-4]. Conclusion: This study suggests that rs560191 is associated to lung cancer risk and further highlights the value of consortia in replicating or refuting published genetic associations. © The Author 2010. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org.

Published
2010

4. Renal cell carcinoma, occupational pesticide exposure and modification by glutathione S-transferase polymorphisms

Author

Ivana Holcatova, Wong-Ho Chow, Jan P. Gromiec, M. Navritalova, H. Kollarova, Vladimir Janout, Sara Karami, Nathanial Rothman, T. Stewart, Rayjean J. Hung, Dana Mates, S. J. Chanock, Neonilia Szeszenia-Dabrowska, Paul Brennan, Paolo Boffetta, David Zaridze, Anush Mukeria, Vladimir Bencko, Lee E. Moore, Karami, S., Boffetta, P., Rothman, N., Hung, R.J., Stewart, T., Zaridze, D., Navritalova, M., Mates, D., Janout, V., Kollarova, H., Bencko, V., Szeszenia-Dabrowska, N., Holcatova, I., Mukeria, A., Gromiec, J., Chanock, S.J., Brennan, P., Chow, W.-H., and Moore, L.E.

Subjects
Adult, Male, Cancer Research, medicine.medical_specialty, Physiology, Risk Assessment, GST, glutathione S-transferase, Interviews as Topic, Occupational medicine, Risk Factors, Occupational Exposure, Internal medicine, Genotype, medicine, Humans, Pesticides, Allele, Carcinoma, Renal Cell, neoplasms, Aged, Glutathione Transferase, Aged, 80 and over, Molecular Epidemiology, Polymorphism, Genetic, biology, Case-control study, General Medicine, Odds ratio, Middle Aged, Kidney Neoplasms, United States, Confidence interval, OR, odds ratio, Europe, Glutathione S-transferase, Endocrinology, confidence interval, Case-Control Studies, biology.protein, RCC, renal cell carcinoma, Female, Risk assessment
Abstract

This study investigated associations between occupational pesticide exposure and renal cell carcinoma (RCC) risk. To follow-up on a previous report by Buzio et al., we also considered whether this association could be modified by glutathione S-transferase M1 and T1 (GSTM1 and GSTT1) genotypes. About 1097 RCC cases and 1476 controls from Central and Eastern Europe were interviewed to collect data on lifetime occupational histories. Occupational information for jobs held for at least 12 months duration was coded for pesticide exposures and assessed for frequency and intensity of exposure. GSTM1 and GSTT1 gene deletions were analyzed using TaqMan® assays. A significant increase in RCC risk was observed among subjects ever exposed to pesticides [odds ratio (OR): 1.60; 95% confidence interval (CI): 1.00-2.55]. After stratification by genotypes, increased risk was observed among exposed subjects with at least one GSTM1 active allele (OR: 4.00; 95% CI: 1.55-10.33) but not among exposed subjects with two GSTM1 inactive alleles compared with unexposed subjects with two inactive alleles (P-interaction: 0.04). Risk was highest among exposed subjects with both GSTM1 and GSTT1 active genotypes (OR: 6.47; 95% CI: 1.82-23.00; P-interaction: 0.02) compared with unexposed subjects with at least one GSTM1 or T1 inactive genotype. In the largest RCC case-control study with genotype information conducted to date, we observed that risk associated with pesticide exposure was exclusive to individuals with active GSTM1/T1 genotypes. These findings further support the hypothesis that glutathione S-transferase polymorphisms can modify RCC risk associated with occupational pesticide exposure. © The Author 2008. Published by Oxford University Press. All rights reserved.

Published
2008

5. Development of lung cancer before the age of 50: the role of xenobiotic metabolizing genes

Author

Ilaria Bellini, Lenka Foretova, Stefano Landi, Jolanta Lissowska, Federica Gemignani, Vladimir Bencko, Valerie Gaborieau, David Zaridze, Rayjean J. Hung, Janet Hall, Dana Mates, Neonilia Szeszenia-Dabrowska, Federico Canzian, Peter Rudnai, Roberto Barale, Vladimir Janout, Paul Brennan, Lydie Gioia-Patricola, Eleonora Fabianova, Paolo Boffetta, Gemignani, F., Landi, S., Szeszenia-Dabrowska, N., Zaridze, D., Lissowska, J., Rudnai, P., Fabianova, E., Mates, D., Foretova, L., Janout, V., Bencko, V., Gaborieau, V., Gioia-Patricola, L., Bellini, I., Barale, R., Canzian, F., Hall, J., Boffetta, P., Hung, R.J., and Brennan, P.

Subjects
Adult, Male, Cancer Research, Lung Neoplasms, Development lung cancer before age of 50 role xenobiotic metabolizing gene, Single-nucleotide polymorphism, EPHX1, Biology, medicine.disease_cause, Polymorphism, Single Nucleotide, Xenobiotics, medicine, Humans, Age of Onset, Lung cancer, CYP2A6, Oligonucleotide Array Sequence Analysis, Genetics, Haplotype, Heterozygote advantage, General Medicine, Middle Aged, medicine.disease, Metabolic Detoxication, Phase II, Phenotype, Haplotypes, Case-Control Studies, Methylenetetrahydrofolate reductase, biology.protein, Female, Metabolic Detoxication, Phase I, Carcinogenesis
Abstract

The role of genes coding for xenobiotic metabolizing enzymes (XMEs) and the risk of lung cancer is unclear. Under the assumption that these genes may be more important among people having a diagnosis of lung cancer at younger ages, we have investigated the role of single-nucleotide polymorphisms (SNPs) within phase I and phase II XME genes, and also genes involved in the metabolism of nucleic acids in a series of young onset patients and matched controls. We genotyped 299 lung cancer cases diagnosed before the age of 50 and 317 controls, from six countries of Central and Eastern Europe, by use of an oligonucleotide microarray and arrayed primer extension technique for 45 SNPs in 15 phase I XME genes, 46 SNPs in 17 phase II genes and 9 SNPs in 4 genes related to metabolism of nucleic acids. Heterozygote carriers of SNPs in CYP1A2 1545T>C, -164C>A and -740T>G; CYP2A6 -47A>C; MDR1 3435T>C; NAT1 1088T>A and 1095A>C; GSTA2 S112T; GSTM3 V224I and MTHFR A222V had altered risk of developing lung cancer. Phenotypes reconstructed after haplotype analyses showed that the carriers of the combined NAT1 fast+ NAT2 fast phenotypes were at lower risk when compared with those with the combined NAT1 slow + NAT2 slow acetylator phenotypes. Finally, extensive EPHX1 metabolizers showed an increased risk as compared with the poor metabolizers. © The Author 2007. Published by Oxford University Press. All rights reserved.

Published
2007

6. Identification of lung cancer histology-specific variants applying Bayesian framework variant prioritization approaches within the TRICL and ILCCO consortia

Author

Keitaro Matsuo, Neil E. Caporaso, John R. Gosney, Juncheng Dai, Maiken Elvestad Gabrielsen, Margaret R. Spitz, Frank Skorpen, Tõnu Vooder, Neonila Szeszenia-Dabrowska, Paul Brennan, Brian E. Henderson, Shelley S. Tworoger, Vladimir Bencko, Xuchen Zong, Younghun Han, Olaide Y. Raji, Yufei Wang, Andres Metspalu, Hidemi Ito, Irene Orlow, Michael W. Marcus, Eleonora Fabianova, Chu Chen, James McKay, Ping Yang, Gary E. Goodman, Hans E. Krokan, Demetrius Albanes, Timothy Eisen, Geoffrey Liu, Ying Chen, Triantafillos Liloglou, Jolanta Lissowska, Lynne R. Wilkens, Mari Nelis, Mark Lathrop, John K. Field, Fumihiko Matsuda, Di Zhang, Yongyue Wei, Dana Mates, Peter Rudnai, Yonathan Brhane, Jun She, Victoria L. Stevens, Inger Njølstad, Hongbing Shen, Darren R. Brenner, Maria Teresa Landi, Susan M. Gapstur, Li Su, Michael P.A. Davies, David Zaridze, Loic Le Marchand, John R. McLaughlin, Dong Xie, Paolo Boffetta, Rayjean J. Hung, Peter Broderick, Albert Rosenberger, Hendrik Dienemann, Lenka Foretova, Thomas Muley, Christopher I. Amos, Vladimi Janout, David C. Christiani, Joachim Heinrich, Yafang Li, Lars J. Vatten, Mattias Johansson, Richard S. Houlston, Xifeng Wu, Kristjan Välk, Wei V. Chen, Heike Bickeböller, Angela Risch, Maria Timofeeva, Brenner, D.R., Amos, C.I., Brhane, Y., Timofeeva, M.N., Caporaso, N., Wang, Y., Christiani, D.C., Bickeböller, H., Yang, P., Albanes, D., Stevens, V.L., Gapstur, S., McKay, J., Boffetta, P., Zaridze, D., Szeszenia-Dabrowska, N., Lissowska, J., Rudnai, P., Fabianova, E., Mates, D., Bencko, V., Foretova, L., Janout, V., Krokan, H.E., Skorpen, F., Gabrielsen, M.E., Vatten, L., Njølstad, I., Chen, C., Goodman, G., Lathrop, M., Vooder, T., Välk, K., Nelis, M., Metspalu, A., Broderick, P., Eisen, T., Wu, X., Zhang, D., Chen, W., Spitz, M.R., Wei, Y., Su, L., Xie, D., She, J., Matsuo, K., Matsuda, F., Ito, H., Risch, A., Heinrich, J., Rosenberger, A., Muley, T., Dienemann, H., Field, J.K., Raji, O., Chen, Y., Gosney, J., Liloglou, T., Davies, M.P.A., Marcus, M., McLaughlin, J., Orlow, I., Han, Y., Li, Y., Zong, X., Johansson, M., Liu, G., Tworoger, S.S., Le Marchand, L., Henderson, B.E., Wilkens, L.R., Dai, J., Shen, H., Houlston, R.S., Landi, M.T., Brennan, P., and Hung, R.J.

Subjects
Cancer Research, Lung Neoplasms, Bayesian probability, Genome-wide association study, Original Manuscript, Computational biology, Adenocarcinoma, Bioinformatics, 03 medical and health sciences, Bayes' theorem, 0302 clinical medicine, medicine, Humans, Genetic Predisposition to Disease, Lung cancer, 030304 developmental biology, Genetic association, 0303 health sciences, business.industry, Case-control study, Bayes Theorem, General Medicine, medicine.disease, 3. Good health, ComputingMethodologies_PATTERNRECOGNITION, 030220 oncology & carcinogenesis, Meta-analysis, Case-Control Studies, Carcinoma, Squamous Cell, business, Genome-Wide Association Study
Abstract

Large-scale genome-wide association studies (GWAS) have likely uncovered all common variants at the GWAS significance level. Additional variants within the suggestive range (0.0001> P > 5×10(-8)) are, however, still of interest for identifying causal associations. This analysis aimed to apply novel variant prioritization approaches to identify additional lung cancer variants that may not reach the GWAS level. Effects were combined across studies with a total of 33456 controls and 6756 adenocarcinoma (AC; 13 studies), 5061 squamous cell carcinoma (SCC; 12 studies) and 2216 small cell lung cancer cases (9 studies). Based on prior information such as variant physical properties and functional significance, we applied stratified false discovery rates, hierarchical modeling and Bayesian false discovery probabilities for variant prioritization. We conducted a fine mapping analysis as validation of our methods by examining top-ranking novel variants in six independent populations with a total of 3128 cases and 2966 controls. Three novel loci in the suggestive range were identified based on our Bayesian framework analyses: KCNIP4 at 4p15.2 (rs6448050, P = 4.6×10(-7)) and MTMR2 at 11q21 (rs10501831, P = 3.1×10(-6)) with SCC, as well as GAREM at 18q12.1 (rs11662168, P = 3.4×10(-7)) with AC. Use of our prioritization methods validated two of the top three loci associated with SCC (P = 1.05×10(-4) for KCNIP4, represented by rs9799795) and AC (P = 2.16×10(-4) for GAREM, represented by rs3786309) in the independent fine mapping populations. This study highlights the utility of using prior functional data for sequence variants in prioritization analyses to search for robust signals in the suggestive range.

Published
2015

7. Genetic polymorphisms of MPO, COMT, MnSOD, NQO1, interactions with environmental exposures and bladder cancer risk

Author

Umberto Gelatti, Agnès Hautefeuille, Rayjean J. Hung, Paul Brennan, Donatella Placidi, Stefano Porru, Christian Malaveille, Paolo Boffetta, Angela Carta, Hung, R.J., Boffetta, P., Brennan, P., Malaveille, C., Gelatti, U., Placidi, D., Carta, A., Hautefeuille, A., and Porru, S.

Subjects
Adult, Male, Cancer Research, Manganese Superoxide Dismutase, Catechol O-Methyltransferase, medicine.disease_cause, Tobacco smoke, Glutathione Peroxidase GPX1, NAD(P)H Dehydrogenase (Quinone), Humans, Medicine, Genetic polymorphism, environmental exposures, bladder cancer, Carcinogen, Aged, Peroxidase, Aged, 80 and over, Cocarcinogenesis, Polymorphism, Genetic, Catechol-O-methyl transferase, Bladder cancer, biology, Superoxide Dismutase, business.industry, Glutathione Peroxidase GPX1, Manganese Superoxide Dismutase, Catalase, Environmental Exposure, General Medicine, Environmental exposure, Middle Aged, Catalase, medicine.disease, Urinary Bladder Neoplasms, Biochemistry, Myeloperoxidase, biology.protein, Cancer research, business, Carcinogenesis, Oxidative stress
Abstract

Tobacco smoking and occupational exposure are major risk factors of bladder cancer via exposure to polycyclic aromatic hydrocarbons (PAHs) and aromatic amines, which lead to oxidative stress and DNA damage. Several enzymes, which play key roles in oxidative stress are polymorphic in humans. Myeloperoxidase (MPO) produces a strong oxidant for microbicidal activity, and activates carcinogens in tobacco smoke. Catechol-O-methyltransferase (COMT) catalyzes the methylation of endo- and xenobiotics and prevents redox cycling. NAD(P)H:quinone oxidoreductase (NQO1) catalyzes the two-electron reduction of quinoid compounds, which also protects cells from redox cycling. Manganese superoxide dismutase (MnSOD) protects cells from free radical injury. To test the hypothesis that the risk of bladder cancer can be influenced by polymorphisms in the genes that modulate oxidative stress, in particular by interacting with environmental carcinogens, we conducted a hospital-based case-control study among men in Brescia, Northern Italy. We recruited and interviewed 201 incident cases and 214 controls from 1997 to 2000. Occupational exposures to PAHs and aromatic amines were coded blindly by occupational physicians. Unconditional multivariate logistic regression was applied to model the association between genetic polymorphisms and bladder cancer risk and the effect of modifications of smoking and occupational exposures were evaluated. MPO G-463A homozygous variant was associated with a reduced risk of bladder cancer with an OR of 0.31 (95% CI = 0.12-0.80). MnSOD Val/Val genotype increased the risk of bladder cancer with OR of 1.91 (95% CI = 1.20-3.04), and there was a combined effect with smoking (OR = 7.20, 95% CI = 3.23-16.1) and PAH (OR = 3.02,95% CI = 1.35-6.74). We did not observe an effect of COMT Val108Met polymorphism. These findings suggest that individual susceptibility of bladder cancer may be modulated by MPO and MnSOD polymorphisms, and that the combination of genetic factors involved in oxidative stress response with environmental carcinogens may play an important role in bladder carcinogenesis. © Oxford University Press 2004; all rights reserved.

Published
2004

8. Folate-related genes and the risk of tobacco-related cancers in Central Europe

Author

Rayjean J. Hung, Ioan Nicolae Mates, Neonila Szeszenia-Dabrowska, Jolanta Lissowska, Lenka Foretova, Mia Hashibe, David Zaridze, Valerie Gaborieau, Peter Rudnai, Federico Canzian, Vladimir Janout, Vladimir Bencko, Janet Hall, James McKay, Paolo Boffetta, Norman Moullan, Paul Brennan, Eleonora Fabianova, Amelie Chabrier, Hung, R.J., Hashibe, M., McKay, J., Gaborieau, V., Szeszenia-Dabrowska, N., Zaridze, D., Lissowska, J., Rudnai, P., Fabianova, E., Mates, I., Foretova, L., Janout, V., Bencko, V., Chabrier, A., Moullan, N., Canzian, F., Hall, J., Boffetta, P., and Brennan, P.

Subjects
Oncology, Cancer Research, Linkage disequilibrium, medicine.medical_specialty, Pathology, 5-Methyltetrahydrofolate-Homocysteine S-Methyltransferase, Polymorphism, Single Nucleotide, MTR, methionine synthase, Folic Acid, Risk Factors, Internal medicine, Neoplasms, Genotype, Tobacco, medicine, Humans, Genetic Predisposition to Disease, Risk factor, Lung cancer, OR, odds ratio, Methylenetetrahydrofolate Reductase (NADPH2), biology, business.industry, Confounding, Cancer, General Medicine, Odds ratio, medicine.disease, CI, confidence interval, Europe, Methylenetetrahydrofolate reductase, Case-Control Studies, biology.protein, business, MTHFR, methylenetetrahydrofolate reductase
Abstract

Folate has been hypothesized to protect against aero-digestive cancers although the evidence is not yet conclusive due to possible confounding by other dietary factors. Sequence variants in folate pathway were suggested to be associated with plasma folate levels and are unlikely to be confounded by other lifestyle factors. We therefore investigated the effects of key folate genetic variants on the risk of aero-digestive cancers and their potential effect modification by folate intake in a multicenter study in Central Europe. A total of 2250 lung cases, 811 upper aero-digestive tract cases and 2899 controls were recruited with blood samples. The methylenetetrahydrofolate reductase (MTHFR) C677T variant was associated with an increased risk of lung cancer with an odds ratio (OR) for homozygote variant of 1.37 [95% confidence interval (CI) =1.10-;1.71]. The two MTHFR variants were in strong linkage disequilibrium, and 677T-1298A appeared to be the primary haplotype associated with cancer risk. The risk estimates for MTHFR 677T/677T genotype was more prominent among lung cancer patients with young onset (OR=1.92,95% CI =1.12-3.29). When stratified by dietary intake of folate, the effect of the MTHFR 677T variant was more prominent among subjects with low intake of folate: the ORs for 677T/677T genotype among subjects with the lowest decile were 2.60 (95% CI =1.39-4.88) and 4.14 (95% CI =1.47-11.7) for lung and upper aero-digestive tract cancer, respectively. In conclusion, we identified a moderate effect of MTHFR C677T on lung cancer risk and a possible effect modification by folate intake that is consistent with the functional data. These results support an important role of folate in protecting against tobacco-related cancers. © The Author 2007. Published by Oxford University Press. All rights reserved.

Published
2007

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