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Your search keyword '"Wei, Qingyi"' showing total 49 results
Start Over Author "Wei, Qingyi" Journal molecular carcinogenesis
49 results on '"Wei, Qingyi"'

3. Novel genetic variants in the P38MAPK pathway gene ZAK and susceptibility to lung cancer

Author

Feng, Yun, Wang, Yanru, Liu, Hongliang, Liu, Zhensheng, Mills, Coleman, Owzar, Kouros, Xie, Jichun, Han, Younghun, Qian, David C., Hung RJ, Rayjean J., Brhane, Yonathan, McLaughlin, John, Brennan, Paul, Bickeböller, Heike, Rosenberger, Albert, Houlston, Richard S., Caporaso, Neil, Landi, Maria Teresa, Brüske, Irene, Risch, Angela, Ye, Yuanqing, Wu, Xifeng, Christiani, David C., Amos, Christopher I., and Wei, Qingyi

Published
2018
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22. Novel genetic variants inHDAC2andPPARGC1Aof the CREB‐binding protein pathway predict survival of non‐small‐cell lung cancer

Author

Tang, Dongfang, primary, Zhao, Yu Chen, additional, Qian, Danwen, additional, Liu, Hongliang, additional, Luo, Sheng, additional, Patz, Edward F., additional, Moorman, Patricia G., additional, Su, Li, additional, Shen, Sipeng, additional, Christiani, David C., additional, Glass, Carolyn, additional, Gao, Wen, additional, and Wei, Qingyi, additional

Published
2019
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30. Novel genetic variants in the P38MAPK pathway geneZAKand susceptibility to lung cancer

Author

Feng, Yun, primary, Wang, Yanru, additional, Liu, Hongliang, additional, Liu, Zhensheng, additional, Mills, Coleman, additional, Owzar, Kouros, additional, Xie, Jichun, additional, Han, Younghun, additional, Qian, David C., additional, Hung RJ, Rayjean J., additional, Brhane, Yonathan, additional, McLaughlin, John, additional, Brennan, Paul, additional, Bickeböller, Heike, additional, Rosenberger, Albert, additional, Houlston, Richard S., additional, Caporaso, Neil, additional, Landi, Maria Teresa, additional, Brüske, Irene, additional, Risch, Angela, additional, Ye, Yuanqing, additional, Wu, Xifeng, additional, Christiani, David C., additional, Amos, Christopher I., additional, and Wei, Qingyi, additional

Published
2017
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32. Pathway-analysis of published genome-wide association studies of lung cancer: A potential role for theCYP4F3locus

Author

Yin, Jieyun, primary, Liu, Hongliang, additional, Liu, Zhensheng, additional, Owzar, Kouros, additional, Han, Younghun, additional, Su, Li, additional, Wei, Yongyue, additional, Hung, Rayjean J., additional, Brhane, Yonathan, additional, McLaughlin, John, additional, Brennan, Paul, additional, Bickeboeller, Heike, additional, Rosenberger, Albert, additional, Houlston, Richard S., additional, Caporaso, Neil, additional, Landi, Maria Teresa, additional, Heinrich, Joachim, additional, Risch, Angela, additional, Christiani, David C., additional, Amos, Christopher I., additional, and Wei, Qingyi, additional

Published
2017
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39. Genetic variant rs16430 6bp > 0bp at the microRNA-binding site inTYMSand risk of sporadic breast cancer risk in non-hispanic white women aged ≤55 years

Author

Guan, Xiaoxiang, primary, Liu, Hongliang, additional, Ju, Jingfang, additional, Li, Yangkai, additional, Li, Peng, additional, Wang, Li-E, additional, Brewster, Abenaa M., additional, Buchholz, Thomas A., additional, Arun, Banu K., additional, Wei, Qingyi, additional, and Liu, Zhensheng, additional

Published
2013
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43. Association between polymorphisms in the GSTA4 gene and risk of lung cancer: A case-control study in a Southeastern Chinese population

Author

Qian, Ji, primary, Jing, Jianying, additional, Jin, Guangfu, additional, Wang, Haifeng, additional, Wang, Yi, additional, Liu, Hongliang, additional, Wang, Haijian, additional, Li, Rui, additional, Fan, Weiwei, additional, An, Yu, additional, Sun, Weiwei, additional, Ma, Hongxia, additional, Miao, Ruifeng, additional, Hu, Zhibin, additional, Jin, Li, additional, Wei, Qingyi, additional, Shen, Hongbing, additional, Huang, Wei, additional, and Lu, Daru, additional

Published
2008
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48. Susceptibility loci of CNOT6 in the general mRNA degradation pathway and lung cancer risk-A re-analysis of eight GWASs.

Author

Zhou F, Wang Y, Liu H, Ready N, Han Y, Hung RJ, Brhane Y, McLaughlin J, Brennan P, Bickeböller H, Rosenberger A, Houlston RS, Caporaso N, Landi MT, Brüske I, Risch A, Ye Y, Wu X, Christiani DC, Goodman G, Chen C, Amos CI, and Wei Q

Subjects
Gene Expression Regulation, Neoplastic, Genetic Predisposition to Disease, Genome-Wide Association Study, Humans, Linkage Disequilibrium, Lung pathology, Lung Neoplasms epidemiology, Lung Neoplasms pathology, Quantitative Trait Loci, RNA, Messenger chemistry, Exoribonucleases genetics, Lung Neoplasms genetics, Polymorphism, Single Nucleotide, RNA Stability, RNA, Messenger genetics
Abstract

Purpose: mRNA degradation is an important regulatory step for controlling gene expression and cell functions. Genetic abnormalities involved in mRNA degradation genes were found to be associated with cancer risks. Therefore, we systematically investigated the roles of genetic variants in the general mRNA degradation pathway in lung cancer risk., Experimental Design: Meta-analyses were conducted using summary data from six lung cancer genome-wide association studies (GWASs) from the Transdisciplinary Research in Cancer of the Lung and additional two GWASs from Harvard University and deCODE in the International Lung Cancer Consortium. Expression quantitative trait loci analysis (eQTL) was used for in silico functional validation of the identified significant susceptibility loci., Results: This pathway-based analysis included 6816 single nucleotide polymorphisms (SNP) in 68 genes in 14 463 lung cancer cases and 44 188 controls. In the single-locus analysis, we found that 20 SNPs were associated with lung cancer risk with a false discovery rate threshold of <0.05. Among the 11 newly identified SNPs in CNOT6, which were in high linkage disequilibrium, the rs2453176 with a RegulomDB score "1f" was chosen as the tagSNP for further analysis. We found that the rs2453176 T allele was significantly associated with lung cancer risk (odds ratio = 1.11, 95% confidence interval = 1.04-1.18) in the eight GWASs. In the eQTL analysis, we found that levels of CNOT6 mRNA expression were significantly correlated with the rs2453176 T allele, which provided additional biological basis for the observed positive association., Conclusion: The CNOT6 rs2453176 SNP may be a new functional susceptible locus for lung cancer risk. © 2016 Wiley Periodicals, Inc., (© 2016 Wiley Periodicals, Inc.)

Published
2017
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49. Genetic variant rs16430 6bp > 0bp at the microRNA-binding site in TYMS and risk of sporadic breast cancer risk in non-Hispanic white women aged ≤ 55 years.

Author

Guan X, Liu H, Ju J, Li Y, Li P, Wang LE, Brewster AM, Buchholz TA, Arun BK, Wei Q, and Liu Z

Subjects
3' Untranslated Regions, Base Sequence, Binding Sites, Breast metabolism, Breast Neoplasms epidemiology, Female, Genetic Predisposition to Disease, Genetic Variation, Humans, Linkage Disequilibrium, MicroRNAs chemistry, MicroRNAs genetics, Middle Aged, Risk Factors, Sequence Alignment, Thymidylate Synthase metabolism, Breast Neoplasms genetics, MicroRNAs metabolism, Polymorphism, Single Nucleotide, Thymidylate Synthase genetics, White People genetics
Abstract

Thymidylate synthase (TYMS) is involved in the folate metabolism and provision of nucleotides needed for DNA synthesis and repair. Thus, functional genetic variants in TYMS may alter cancer risk. In the study, we evaluated associations of three germline variants (rs2790 A > G, rs16430 6 bp > 0 bp, and rs1059394 C > T) in the predicted miRNA-binding sites of TYMS with risk of sporadic breast cancer in non-Hispanic white women aged ≤ 55. We found that carriers of the rs16430 0 bp variant allele had an increased risk of breast cancer [adjusted odd ratio (OR) = 1.37, 95% confidence interval (CI): 1.08-1.73; P = 0.010], compared with carriers of the 6 bp/6 bp genotype. This increased risk was more evident in older subjects (OR = 1.47, 95% CI = 1.06-2.03, P = 0.022), never smokers (OR = 1.67, 95% CI = 1.23-2.25, P < 0.001), never drinkers (OR = 1.44, 95% CI = 1.01-2.05, P = 0.043), and estrogen receptor-positive patients (OR = 1.46, 95% CI = 1.11-1.92, P = 0.006), regardless of tumor stages. The results are consistent with the functional analyses of rs16430 as previously reported, which showed that the 0 bp allele had a decrease in both luciferase activity by ∼ 70% and mRNA levels by ∼ 50% compared with the 6bp allele. Additionally, the rs16430 variant was predicted to influence the binding activity of miR-561. Taken together, these findings indicate that the TYMS rs16430 may contribute to the etiology of sporadic breast cancer in non-Hispanic white women aged ≤ 55 yr. Further validation in large population-based or cohort studies is needed., (© 2013 Wiley Periodicals, Inc.)

Published
2015
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