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Your search keyword '"Teo, Y.Y."' showing total 3 results
Start Over Author "Teo, Y.Y." Topic genetics
3 results on '"Teo, Y.Y."'

1. Identification of new susceptibility loci for type 2 diabetes and shared etiological pathways with coronary heart disease

Author

Zhao, W., Rasheed, A., Tikkanen, E., Lee, J.J., Butterworth, A.S., Howson, J.M.M., Assimes, T.L., Chowdhury, R., Orho-Melander, M., Damrauer, S., Small, A., Asma, S., Imamura, M., Yamauch, T., Chambers, J.C., Chen, P., Sapkota, B.R., Shah, N., Jabeen, S., Surendran, P., Lu, Y.C., Zhang, W.H., Imran, A., Abbas, S., Majeed, F., Trindade, K., Qamar, N., Mallick, N.H., Yaqoob, Z., Saghir, T., Rizvi, S.N.H., Memon, A., Rasheed, S.Z., Memon, F.U.R., Mehmood, K., Ahmed, N., Qureshi, I.H., Tanveer-us-Salam, Iqbal, W., Malik, U., Mehra, N., Kuo, J.Z., Sheu, W.H.H., Guo, X.Q., Hsiung, C.A., Juang, J.M.J., Taylor, K.D., Hung, Y.J., Lee, W.J., Quertermous, T., Lee, I.T., Hsu, C.C., Bottinger, E.P., Ralhan, S., Teo, Y.Y., Wang, T.D., Alam, D.S., Angelantonio, E. di, Epstein, S., Nielsen, S.F., Nordestgaard, B.G., Tybjaerg-Hansen, A., Young, R., Benn, M., Frikke-Schmidt, R., Kamstrup, P.R., Biobank, M., Jukema, J.W., Sattar, N., Smit, R., Chung, R.H., Liang, K.W., Anand, S., Sanghera, D.K., Ripatti, S., Loos, R.J.F., Kooner, J.S., Tai, E.S., Rotter, J.I., Chen, Y.D.I., Frossard, P., Maeda, S., Kadowaki, T., Reilly, M., Pare, G., Melander, O., Salomaa, V., Rader, D.J., Danesh, J., Voight, B.F., Saleheen, D., CHD Exome Consortium, EPIC-CVD Consortium, EPIC-Interact Consortium, Butterworth, Adam [0000-0002-6915-9015], Howson, Joanna [0000-0001-7618-0050], Chowdhury, Rajiv [0000-0003-4881-5690], Surendran, Praveen [0000-0002-4911-6077], Di Angelantonio, Emanuele [0000-0001-8776-6719], Danesh, John [0000-0003-1158-6791], and Apollo - University of Cambridge Repository

Subjects
0301 basic medicine, endocrine system diseases, EPIC-Interact Consortium, Genome-wide association study, Coronary Disease, Type 2 diabetes, ACID-BINDING PROTEIN, Comorbidity, 030204 cardiovascular system & hematology, VARIANTS, Cardiovascular, Bioinformatics, Medical and Health Sciences, 0302 clinical medicine, Risk Factors, 2.1 Biological and endogenous factors, ARTERY-DISEASE, Molecular Targeted Therapy, Aetiology, health care economics and organizations, 11 Medical and Health Sciences, Genetics & Heredity, RISK, Metabolic Syndrome, 0303 health sciences, CHD Exome+ Consortium, Diabetes, Single Nucleotide, Biological Sciences, 3. Good health, Europe, Heart Disease, MENDELIAN RANDOMIZATION, Medical genetics, Life Sciences & Biomedicine, Type 2, Metabolic Networks and Pathways, Asian Continental Ancestry Group, medicine.medical_specialty, endocrine system, Asia, education, European Continental Ancestry Group, Mutation, Missense, Single-nucleotide polymorphism, Biology, Polymorphism, Single Nucleotide, Article, White People, EPIC-CVD Consortium, GENETIC ARCHITECTURE, 03 medical and health sciences, Asian People, Clinical Research, Mendelian randomization, Diabetes Mellitus, Genetics, Genetic predisposition, medicine, Humans, Genetic Predisposition to Disease, Obesity, Genetic variability, cardiovascular diseases, Polymorphism, GENOME-WIDE ASSOCIATION, Heart Disease - Coronary Heart Disease, Metabolic and endocrine, METAANALYSIS, AP2, 030304 developmental biology, Science & Technology, Human Genome, nutritional and metabolic diseases, Odds ratio, 06 Biological Sciences, medicine.disease, HLA-DRB5 Chains, Michigan Biobank, 030104 developmental biology, ATHEROSCLEROSIS, Diabetes Mellitus, Type 2, Genetic Loci, Mutation, Missense, human activities, Biomarkers, Genome-Wide Association Study, Developmental Biology
Abstract

Danish Saleheen, Benjamin Voight and colleagues perform genome-wide analysis of multi-ancestry cohorts to identify genetic associations with type 2 diabetes (T2D) and coronary heart disease (CHD). They find novel loci and show that 24% of T2D loci are also associated with CHD and that greater genetic risk of T2D increases risk of CHD. To evaluate the shared genetic etiology of type 2 diabetes (T2D) and coronary heart disease (CHD), we conducted a genome-wide, multi-ancestry study of genetic variation for both diseases in up to 265,678 subjects for T2D and 260,365 subjects for CHD. We identify 16 previously unreported loci for T2D and 1 locus for CHD, including a new T2D association at a missense variant in HLA-DRB5 (odds ratio (OR) = 1.29). We show that genetically mediated increase in T2D risk also confers higher CHD risk. Joint T2D–CHD analysis identified eight variants—two of which are coding—where T2D and CHD associations appear to colocalize, including a new joint T2D–CHD association at the CCDC92 locus that also replicated for T2D. The variants associated with both outcomes implicate new pathways as well as targets of existing drugs, including icosapent ethyl and adipocyte fatty-acid-binding protein.

Published
2017

2. Genome-wide association study identifies three novel loci for type 2 diabetes

Author

Hara, K., Fujita, H., Johnson, T.A., Yamauchi, T., Yasuda, K., Horikoshi, M., Peng, C., Hu, C., Ma, R.C., Imamura, M., Iwata, M., Tsunoda, T., Morizono, T., Shojima, N., So, W.Y., Leung, T.F., Kwan, P., Zhang, R., Wang, J., Yu, W., Maegawa, H., Hirose, H., DIAGRAM Consortium (Huth, C., Gieger, C., Klopp, N., Meitinger, T., Illig, T., Grallert, H., Thorand, B., Wichmann, H.-E., Petersen, A.-K.), Kaku, K., Ito, C., Watada, H., Tanaka, Y., Tobe, K., Kashiwagi, A., Kawamori, R., Jia, W., Chan, J.C., Teo, Y.Y., Shyong, T.E., Kamatani, N., Kubo, M., Maeda, S., Kadowaki, T., and Internal Medicine

Subjects
Leptin, Monocarboxylic Acid Transporters, Single-nucleotide polymorphism, Genome-wide association study, Biology, Polymorphism, Single Nucleotide, SDG 3 - Good Health and Well-being, Genotype, Genetics, Humans, Genetic Predisposition to Disease, 1000 Genomes Project, Allele, Molecular Biology, Genetics (clinical), Guanine Nucleotide Dissociation Inhibitors, Genome, Human, Haplotype, Genetic Variation, General Medicine, Odds ratio, MicroRNAs, Diabetes Mellitus, Type 2, Haplotypes, Genetic Loci, Imputation (genetics), Genome-Wide Association Study
Abstract

Although over 60 loci for type 2 diabetes (T2D) have been identified, there still remains a large genetic component to be clarified. To explore unidentified loci for T2D, we performed a genome-wide association study (GWAS) of 6 209 637 single-nucleotide polymorphisms (SNPs), which were directly genotyped or imputed using East Asian references from the 1000 Genomes Project (June 2011 release) in 5976 Japanese patients with T2D and 20 829 nondiabetic individuals. Nineteen unreported loci were selected and taken forward to follow-up analyses. Combined discovery and follow-up analyses (30 392 cases and 34 814 controls) identified three new loci with genome-wide significance, which were MIR129-LEP [rs791595; risk allele = A; risk allele frequency (RAF) = 0.080; P = 2.55 × 10(-13); odds ratio (OR) = 1.17], GPSM1 [rs11787792; risk allele = A; RAF = 0.874; P = 1.74 × 10(-10); OR = 1.15] and SLC16A13 (rs312457; risk allele = G; RAF = 0.078; P = 7.69 × 10(-13); OR = 1.20). This study demonstrates that GWASs based on the imputation of genotypes using modern reference haplotypes such as that from the 1000 Genomes Project data can assist in identification of new loci for common diseases.

Published
2014
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3. Analysis of MDR1 haplotypes in Parkinson's disease in a white population

Author

Tan, Eng-King, Drozdzik, Marek, Bialecka, Monika, Honczarenko, Krystyna, Klodowska-Duda, Gabriela, Teo, Y.Y., Tang, Kun, Wong, Li-Peng, Chong, Samuel S., Tan, Chris, Yew, Kenneth, Zhao, Yi, and Lee, Caroline GL

Subjects
*PARKINSON'S disease, *PATIENTS, *BIOCHEMISTRY, *GENETICS, *ALGORITHMS
Abstract

Abstract: The MDR1 multidrug transporter is important in regulating environmental xenobiotics and hence may play a causative role in Parkinson''s disease (PD). MDR1 haplotype comprising 2677 G>T/A and 3435 C>T may be protective against PD. Using a case control methodology, we investigated the association of MDR1 haplotypes (single nucleotide polymorphisms (SNPs) 2677 G>T/A and 3435 C>T) in a Polish PD population. Seven SNPs, extending from the promoter to exon 28 of the MDR1 gene in 158 PD patients and 139 healthy controls were evaluated. Specifically we examined the association of haplotypes containing SNPs 2677 G>T/A and 3435 C>T and risk of PD. The multivariate logistic regression model was used to evaluate the effects of the covariates on the phenotypes. Haplotypes’ frequencies were estimated using the Expectation–Maximization algorithm. The frequency of each individual SNPs; -41 A>G (intron –1), -145 C>G (exon 1), -129 T>C (exon 1), 1236 T>C (exon 12), 2677 G>T/A (exon 21), 3435 C>T (exon 26), and 4036 A>G (exon 28) did not differ between PD and controls. However, there was a trend towards significance in PD patients having the haplotype 2677G-3435C (p<0.09, chi-square 2.85, odds ratio 0.25, 95% CI 0.06–1.08). Haplotype constructs of the other loci did not differ significantly between the two groups. There was a weak protective effect of the haplotype 2677G-3435C in our white population. However, the MDR1 haplotypes did not generally modulate the risk of PD. [Copyright &y& Elsevier]

Published
2004
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