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1. Genome-wide association study of pediatric obsessive-compulsive traits: shared genetic risk between traits and disorder

Author

Burton, CL, Lemire, M, Xiao, B, Corfield, EC, Erdman, L, Bralten, J, Poelmans, G, Yu, D, Shaheen, SM, Goodale, T, Sinopoli, VM, Askland, KD, Barlassina, C, Bienvenu, OJ, Black, D, Bloch, M, Brentani, H, Camarena, B, Cappi, C, Cath, D, Cavallini, MC, Ciullo, V, Conti, D, Cook, EH, Coric, V, Cullen, BA, Cusi, D, Davis, LK, Delorme, R, Denys, D, Derks, E, Eapen, V, Edlund, C, Falkai, P, Fyer, AJ, Geller, DA, Goes, FS, Grabe, HJ, Grados, MA, Greenberg, BD, Grünblatt, E, Guo, W, Hounie, AG, Jenike, M, Keenan, CL, Kennedy, JL, Khramtsova, EA, Knowles, JA, Krasnow, J, Lange, C, Lanzagorta, N, Leboyer, M, Liang, KY, Lochner, C, Macciardi, F, Maher, B, Mathews, CA, Mattheisen, M, McCracken, JT, McGregor, N, McLaughlin, NCR, Miguel, EC, Neale, B, Nestadt, G, Nestadt, PS, Nicolini, H, Nurmi, EL, Osiecki, L, Piacentini, J, Pittenger, C, Posthuma, D, Pulver, AE, Rasmussen, SA, Rauch, S, Richter, MA, Riddle, MA, Ripke, S, Ruhrmann, S, Sampaio, AS, Samuels, JF, Scharf, JM, Shugart, YY, Smit, JH, Stein, DJ, Stewart, SE, Turiel, M, Vallada, H, Veenstra-VanderWeele, J, Vulink, N, Wagner, M, Walitza, S, Wang, Y, Wendland, J, Zai, G, Soreni, N, Hanna, GL, Fitzgerald, KD, Rosenberg, D, Paterson, AD, Burton, CL, Lemire, M, Xiao, B, Corfield, EC, Erdman, L, Bralten, J, Poelmans, G, Yu, D, Shaheen, SM, Goodale, T, Sinopoli, VM, Askland, KD, Barlassina, C, Bienvenu, OJ, Black, D, Bloch, M, Brentani, H, Camarena, B, Cappi, C, Cath, D, Cavallini, MC, Ciullo, V, Conti, D, Cook, EH, Coric, V, Cullen, BA, Cusi, D, Davis, LK, Delorme, R, Denys, D, Derks, E, Eapen, V, Edlund, C, Falkai, P, Fyer, AJ, Geller, DA, Goes, FS, Grabe, HJ, Grados, MA, Greenberg, BD, Grünblatt, E, Guo, W, Hounie, AG, Jenike, M, Keenan, CL, Kennedy, JL, Khramtsova, EA, Knowles, JA, Krasnow, J, Lange, C, Lanzagorta, N, Leboyer, M, Liang, KY, Lochner, C, Macciardi, F, Maher, B, Mathews, CA, Mattheisen, M, McCracken, JT, McGregor, N, McLaughlin, NCR, Miguel, EC, Neale, B, Nestadt, G, Nestadt, PS, Nicolini, H, Nurmi, EL, Osiecki, L, Piacentini, J, Pittenger, C, Posthuma, D, Pulver, AE, Rasmussen, SA, Rauch, S, Richter, MA, Riddle, MA, Ripke, S, Ruhrmann, S, Sampaio, AS, Samuels, JF, Scharf, JM, Shugart, YY, Smit, JH, Stein, DJ, Stewart, SE, Turiel, M, Vallada, H, Veenstra-VanderWeele, J, Vulink, N, Wagner, M, Walitza, S, Wang, Y, Wendland, J, Zai, G, Soreni, N, Hanna, GL, Fitzgerald, KD, Rosenberg, D, and Paterson, AD

Abstract

Using a novel trait-based measure, we examined genetic variants associated with obsessive-compulsive (OC) traits and tested whether OC traits and obsessive-compulsive disorder (OCD) shared genetic risk. We conducted a genome-wide association analysis (GWAS) of OC traits using the Toronto Obsessive-Compulsive Scale (TOCS) in 5018 unrelated Caucasian children and adolescents from the community (Spit for Science sample). We tested the hypothesis that genetic variants associated with OC traits from the community would be associated with clinical OCD using a meta-analysis of all currently available OCD cases. Shared genetic risk was examined between OC traits and OCD in the respective samples using polygenic risk score and genetic correlation analyses. A locus tagged by rs7856850 in an intron of PTPRD (protein tyrosine phosphatase δ) was significantly associated with OC traits at the genome-wide significance level (p = 2.48 × 10−8). rs7856850 was also associated with OCD in a meta-analysis of OCD case/control genome-wide datasets (p = 0.0069). The direction of effect was the same as in the community sample. Polygenic risk scores from OC traits were significantly associated with OCD in case/control datasets and vice versa (p’s < 0.01). OC traits were highly, but not significantly, genetically correlated with OCD (rg = 0.71, p = 0.062). We report the first validated genome-wide significant variant for OC traits in PTPRD, downstream of the most significant locus in a previous OCD GWAS. OC traits measured in the community sample shared genetic risk with OCD case/control status. Our results demonstrate the feasibility and power of using trait-based approaches in community samples for genetic discovery.

Published
2021

2. Age at first birth in women is genetically associated with increased risk of schizophrenia

Author

Ni, G, Gratten, J, Wray, NR, Lee, SH, Ripke, S, Neale, BM, Corvin, A, Walters, JTR, Farh, KH, Holmans, PA, Lee, P, Bulik-Sullivan, B, Collier, DA, Huang, H, Pers, TH, Agartz, I, Agerbo, E, Albus, M, Alexander, M, Amin, F, Bacanu, SA, Begemann, M, Belliveau, RA, Bene, J, Bergen, SE, Bevilacqua, E, Bigdeli, TB, Black, DW, Bruggeman, R, Buccola, NG, Buckner, RL, Byerley, W, Cahn, W, Cai, G, Campion, D, Cantor, RM, Carr, VJ, Carrera, N, Catts, SV, Chambert, KD, Chan, RCK, Chen, RYL, Chen, EYH, Cheng, W, Cheung, EFC, Chong, SA, Cloninger, CR, Cohen, D, Cohen, N, Cormican, P, Craddock, N, Crowley, JJ, Curtis, D, Davidson, M, Davis, KL, Degenhardt, F, Del Favero, J, Demontis, D, Dikeos, D, Dinan, T, Djurovic, S, Donohoe, G, Drapeau, E, Duan, J, Dudbridge, F, Durmishi, N, Eichhammer, P, Eriksson, J, Escott-Price, V, Essioux, L, Fanous, AH, Farrell, MS, Frank, J, Franke, L, Freedman, R, Freimer, NB, Friedl, M, Friedman, JI, Fromer, M, Genovese, G, Georgieva, L, Giegling, I, Giusti-Rodríguez, P, Godard, S, Goldstein, JI, Golimbet, V, Gopal, S, Haan, L de, Hammer, C, Hamshere, ML, Hansen, M, Hansen, T, Haroutunian, V, Hartmann, AM, Henskens, FA, Herms, S, Hirschhorn, JN, Hoffmann, P, Hofman, A, Hollegaard, MV, Hougaard, DM, Ikeda, M, Joa, I, Juliá, A, Kahn, RS, Kalaydjieva, L, Karachanak-Yankova, S, Karjalainen, J, Kavanagh, D, Keller, MC, Kennedy, JL, Khrunin, A, Kim, Y, Klovins, J, Knowles, JA, Konte, B, Kucinskas, V, Kucinskiene, ZA, Kuzelova-Ptackova, H, Kähler, AK, Laurent, C, Keong, JLC, Legge, SE, Lerer, B, Li, M, Li, T, Liang, KY, Lieberman, J, Limborska, S, Loughland, CM, Lubinski, J, Lönnqvist, J, Macek, M, Magnusson, PKE, Maher, BS, Maier, W, Mallet, J, Marsal, S, Mattheisen, M, Mattingsdal, M, McCarley, RW, McDonald, C, McIntosh, AM, Meier, S, Meijer, CJ, Melegh, B, Melle, I, Mesholam-Gately, RI, Metspalu, A, Michie, PT, Milani, L, Milanova, V, Mokrab, Y, Morris, DW, Mors, O, Murphy, KC, Murray, RM, Myin-Germeys, I, Müller-Myhsok, B, Nelis, M, Nenadic, I, Nertney, DA, Nestadt, G, Nicodemus, KK, Nikitina-Zake, L, Nisenbaum, L, Nordin, A, O'Callaghan, E, O'Dushlaine, C, O'Neill, FA, Oh, SY, Olincy, A, Olsen, L, van Os, JV, Pantelis, C, Papadimitriou, GN, Papiol, S, Parkhomenko, E, Pato, MT, Paunio, T, Pejovic-Milovancevic, M, Perkins, DO, Pietiläinen, O, Pimm, J, Pocklington, AJ, Powell, J, Price, A, Pulver, AE, Purcell, SM, Quested, D, Rasmussen, HB, Reichenberg, A, Reimers, MA, Richards, AL, Roffman, JL, Roussos, P, Ruderfer, DM, Salomaa, V, Sanders, AR, Schall, U, Schubert, CR, Schulze, TG, Schwab, SG, Scolnick, EM, Scott, RJ, Seidman, LJ, Shi, J, Sigurdsson, E, Silagadze, T, Silverman, JM, Sim, K, Slominsky, P, Smoller, JW, So, HC, Spencer, CCA, Stahl, EA, Stefansson, H, Steinberg, S, Stogmann, E, Straub, RE, Strengman, E, Strohmaier, J, Stroup, TS, Subramaniam, M, Suvisaari, J, Svrakic, DM, Szatkiewicz, JP, Söderman, E, Thirumalai, S, Toncheva, D, Tosato, S, Veijola, J, Waddington, J, Walsh, D, Wang, D, Wang, Q, Webb, BT, Weiser, M, Wildenauer, DB, Williams, NM, Williams, S, Witt, SH, Wolen, AR, Wong, EHM, Wormley, BK, Xi, HS, Zai, CC, Zheng, Xuebin, Zimprich, F, Stefansson, K, Visscher, PM, Adolfsson, R, Andreassen, OA, Blackwood, DHR, Bramon, E, Buxbaum, JD, Børglum, AD, Cichon, S, Darvasi, A, Domenici, E, Ehrenreich, H, Esko, T, Gejman, PV, Gill, M, Gurling, H, Hultman, CM, Iwata, N, Jablensky, AV, Jönsson, EG, Kendler, KS, Kirov, G, Knight, J, Lencz, T, Levinson, DF, Li, QS, Liu, J, Malhotra, AK, McCarroll, SA, McQuillin, A, Moran, JL, Mortensen, PB, Mowry, BJ, Nöthen, MM, Ophoff, RA, Owen, MJ, Palotie, A, Pato, CN, Petryshen, TL, Posthuma, Daniëlle, Rietschel, M, Riley, BP, Rujescu, D, Sham, PC, Clair, DS, Weinberger, DR, Wendland, JR, Werge, T, Daly, MJ, Sullivan, PF, O'Donovan, MC, Ni, G, Gratten, J, Wray, NR, Lee, SH, Ripke, S, Neale, BM, Corvin, A, Walters, JTR, Farh, KH, Holmans, PA, Lee, P, Bulik-Sullivan, B, Collier, DA, Huang, H, Pers, TH, Agartz, I, Agerbo, E, Albus, M, Alexander, M, Amin, F, Bacanu, SA, Begemann, M, Belliveau, RA, Bene, J, Bergen, SE, Bevilacqua, E, Bigdeli, TB, Black, DW, Bruggeman, R, Buccola, NG, Buckner, RL, Byerley, W, Cahn, W, Cai, G, Campion, D, Cantor, RM, Carr, VJ, Carrera, N, Catts, SV, Chambert, KD, Chan, RCK, Chen, RYL, Chen, EYH, Cheng, W, Cheung, EFC, Chong, SA, Cloninger, CR, Cohen, D, Cohen, N, Cormican, P, Craddock, N, Crowley, JJ, Curtis, D, Davidson, M, Davis, KL, Degenhardt, F, Del Favero, J, Demontis, D, Dikeos, D, Dinan, T, Djurovic, S, Donohoe, G, Drapeau, E, Duan, J, Dudbridge, F, Durmishi, N, Eichhammer, P, Eriksson, J, Escott-Price, V, Essioux, L, Fanous, AH, Farrell, MS, Frank, J, Franke, L, Freedman, R, Freimer, NB, Friedl, M, Friedman, JI, Fromer, M, Genovese, G, Georgieva, L, Giegling, I, Giusti-Rodríguez, P, Godard, S, Goldstein, JI, Golimbet, V, Gopal, S, Haan, L de, Hammer, C, Hamshere, ML, Hansen, M, Hansen, T, Haroutunian, V, Hartmann, AM, Henskens, FA, Herms, S, Hirschhorn, JN, Hoffmann, P, Hofman, A, Hollegaard, MV, Hougaard, DM, Ikeda, M, Joa, I, Juliá, A, Kahn, RS, Kalaydjieva, L, Karachanak-Yankova, S, Karjalainen, J, Kavanagh, D, Keller, MC, Kennedy, JL, Khrunin, A, Kim, Y, Klovins, J, Knowles, JA, Konte, B, Kucinskas, V, Kucinskiene, ZA, Kuzelova-Ptackova, H, Kähler, AK, Laurent, C, Keong, JLC, Legge, SE, Lerer, B, Li, M, Li, T, Liang, KY, Lieberman, J, Limborska, S, Loughland, CM, Lubinski, J, Lönnqvist, J, Macek, M, Magnusson, PKE, Maher, BS, Maier, W, Mallet, J, Marsal, S, Mattheisen, M, Mattingsdal, M, McCarley, RW, McDonald, C, McIntosh, AM, Meier, S, Meijer, CJ, Melegh, B, Melle, I, Mesholam-Gately, RI, Metspalu, A, Michie, PT, Milani, L, Milanova, V, Mokrab, Y, Morris, DW, Mors, O, Murphy, KC, Murray, RM, Myin-Germeys, I, Müller-Myhsok, B, Nelis, M, Nenadic, I, Nertney, DA, Nestadt, G, Nicodemus, KK, Nikitina-Zake, L, Nisenbaum, L, Nordin, A, O'Callaghan, E, O'Dushlaine, C, O'Neill, FA, Oh, SY, Olincy, A, Olsen, L, van Os, JV, Pantelis, C, Papadimitriou, GN, Papiol, S, Parkhomenko, E, Pato, MT, Paunio, T, Pejovic-Milovancevic, M, Perkins, DO, Pietiläinen, O, Pimm, J, Pocklington, AJ, Powell, J, Price, A, Pulver, AE, Purcell, SM, Quested, D, Rasmussen, HB, Reichenberg, A, Reimers, MA, Richards, AL, Roffman, JL, Roussos, P, Ruderfer, DM, Salomaa, V, Sanders, AR, Schall, U, Schubert, CR, Schulze, TG, Schwab, SG, Scolnick, EM, Scott, RJ, Seidman, LJ, Shi, J, Sigurdsson, E, Silagadze, T, Silverman, JM, Sim, K, Slominsky, P, Smoller, JW, So, HC, Spencer, CCA, Stahl, EA, Stefansson, H, Steinberg, S, Stogmann, E, Straub, RE, Strengman, E, Strohmaier, J, Stroup, TS, Subramaniam, M, Suvisaari, J, Svrakic, DM, Szatkiewicz, JP, Söderman, E, Thirumalai, S, Toncheva, D, Tosato, S, Veijola, J, Waddington, J, Walsh, D, Wang, D, Wang, Q, Webb, BT, Weiser, M, Wildenauer, DB, Williams, NM, Williams, S, Witt, SH, Wolen, AR, Wong, EHM, Wormley, BK, Xi, HS, Zai, CC, Zheng, Xuebin, Zimprich, F, Stefansson, K, Visscher, PM, Adolfsson, R, Andreassen, OA, Blackwood, DHR, Bramon, E, Buxbaum, JD, Børglum, AD, Cichon, S, Darvasi, A, Domenici, E, Ehrenreich, H, Esko, T, Gejman, PV, Gill, M, Gurling, H, Hultman, CM, Iwata, N, Jablensky, AV, Jönsson, EG, Kendler, KS, Kirov, G, Knight, J, Lencz, T, Levinson, DF, Li, QS, Liu, J, Malhotra, AK, McCarroll, SA, McQuillin, A, Moran, JL, Mortensen, PB, Mowry, BJ, Nöthen, MM, Ophoff, RA, Owen, MJ, Palotie, A, Pato, CN, Petryshen, TL, Posthuma, Daniëlle, Rietschel, M, Riley, BP, Rujescu, D, Sham, PC, Clair, DS, Weinberger, DR, Wendland, JR, Werge, T, Daly, MJ, Sullivan, PF, and O'Donovan, MC

Published
2018

3. Evidence of Gene-Environment Interaction for Two Genes on Chromosome 4 and Environmental Tobacco Smoke in Controlling the Risk of Nonsyndromic Cleft Palate

Author

Pajewski, NM, Wu, T, Schwender, H, Ruczinski, I, Murray, JC, Marazita, ML, Munger, RG, Hetmanski, JB, Parker, MM, Wang, P, Murray, T, Taub, M, Li, S, Redett, RJ, Fallin, MD, Liang, KY, Wu-Chou, YH, Chong, SS, Yeow, V, Ye, X, Wang, H, Huang, S, Jabs, EW, Shi, B, Wilcox, AJ, Jee, SH, Scott, AF, Beaty, TH, Pajewski, NM, Wu, T, Schwender, H, Ruczinski, I, Murray, JC, Marazita, ML, Munger, RG, Hetmanski, JB, Parker, MM, Wang, P, Murray, T, Taub, M, Li, S, Redett, RJ, Fallin, MD, Liang, KY, Wu-Chou, YH, Chong, SS, Yeow, V, Ye, X, Wang, H, Huang, S, Jabs, EW, Shi, B, Wilcox, AJ, Jee, SH, Scott, AF, and Beaty, TH

Abstract

Nonsyndromic cleft palate (CP) is one of the most common human birth defects and both genetic and environmental risk factors contribute to its etiology. We conducted a genome-wide association study (GWAS) using 550 CP case-parent trios ascertained in an international consortium. Stratified analysis among trios with different ancestries was performed to test for GxE interactions with common maternal exposures using conditional logistic regression models. While no single nucleotide polymorphism (SNP) achieved genome-wide significance when considered alone, markers in SLC2A9 and the neighboring WDR1 on chromosome 4p16.1 gave suggestive evidence of gene-environment interaction with environmental tobacco smoke (ETS) among 259 Asian trios when the models included a term for GxE interaction. Multiple SNPs in these two genes were associated with increased risk of nonsyndromic CP if the mother was exposed to ETS during the peri-conceptual period (3 months prior to conception through the first trimester). When maternal ETS was considered, fifteen of 135 SNPs mapping to SLC2A9 and 9 of 59 SNPs in WDR1 gave P values approaching genome-wide significance (10(-6)

Published
2014

4. Evidence of gene-environment interaction for two genes on chromosome 4 and environmental tobacco smoke in controlling the risk of nonsyndromic cleft palate

Author

Wu, T, Schwender, H, Ruczinski, I, Murray, JC, Marazita, ML, Munger, RG, Hetmanski, JB, Parker, MM, Wang, P, Murray, T, Taub, M, Li, S, Redett, RJ, Fallin, MD, Liang, KY, Wu-Chou, YH, Chong, SS, Yeow, V, Ye, X, Wang, H, Huang, S, Jabs, EW, Shi, B, Wilcox, AJ, Jee, SH, Scott, AF, Beaty, TH, Wu, T, Schwender, H, Ruczinski, I, Murray, JC, Marazita, ML, Munger, RG, Hetmanski, JB, Parker, MM, Wang, P, Murray, T, Taub, M, Li, S, Redett, RJ, Fallin, MD, Liang, KY, Wu-Chou, YH, Chong, SS, Yeow, V, Ye, X, Wang, H, Huang, S, Jabs, EW, Shi, B, Wilcox, AJ, Jee, SH, Scott, AF, and Beaty, TH

Abstract

Nonsyndromic cleft palate (CP) is one of the most common human birth defects and both genetic and environmental risk factors contribute to its etiology. We conducted a genome-wide association study (GWAS) using 550 CP case-parent trios ascertained in an international consortium. Stratified analysis among trios with different ancestries was performed to test for GxE interactions with common maternal exposures using conditional logistic regression models. While no single nucleotide polymorphism (SNP) achieved genome-wide significance when considered alone, markers in SLC2A9 and the neighboring WDR1 on chromosome 4p16.1 gave suggestive evidence of gene-environment interaction with environmental tobacco smoke (ETS) among 259 Asian trios when the models included a term for GxE interaction. Multiple SNPs in these two genes were associated with increased risk of nonsyndromic CP if the mother was exposed to ETS during the peri-conceptual period (3 months prior to conception through the first trimester). When maternal ETS was considered, fifteen of 135 SNPs mapping to SLC2A9 and 9 of 59 SNPs in WDR1 gave P values approaching genome-wide significance (10-6

Published
2014

5. Evidence of gene-environment interaction for two genes on chromosome 4 and environmental tobacco smoke in controlling the risk of nonsyndromic cleft palate

Author

Wu, T, Schwender, H, Ruczinski, I, Murray, JC, Marazita, ML, Munger, RG, Hetmanski, JB, Parker, MM, Wang, P, Murray, T, Taub, M, Li, S, Redett, RJ, Fallin, MD, Liang, KY, Wu-Chou, YH, Chong, SS, Yeow, V, Ye, X, Wang, H, Huang, S, Jabs, EW, Shi, B, Wilcox, AJ, Jee, SH, Scott, AF, Beaty, TH, Wu, T, Schwender, H, Ruczinski, I, Murray, JC, Marazita, ML, Munger, RG, Hetmanski, JB, Parker, MM, Wang, P, Murray, T, Taub, M, Li, S, Redett, RJ, Fallin, MD, Liang, KY, Wu-Chou, YH, Chong, SS, Yeow, V, Ye, X, Wang, H, Huang, S, Jabs, EW, Shi, B, Wilcox, AJ, Jee, SH, Scott, AF, and Beaty, TH

Abstract

Nonsyndromic cleft palate (CP) is one of the most common human birth defects and both genetic and environmental risk factors contribute to its etiology. We conducted a genome-wide association study (GWAS) using 550 CP case-parent trios ascertained in an international consortium. Stratified analysis among trios with different ancestries was performed to test for GxE interactions with common maternal exposures using conditional logistic regression models. While no single nucleotide polymorphism (SNP) achieved genome-wide significance when considered alone, markers in SLC2A9 and the neighboring WDR1 on chromosome 4p16.1 gave suggestive evidence of gene-environment interaction with environmental tobacco smoke (ETS) among 259 Asian trios when the models included a term for GxE interaction. Multiple SNPs in these two genes were associated with increased risk of nonsyndromic CP if the mother was exposed to ETS during the peri-conceptual period (3 months prior to conception through the first trimester). When maternal ETS was considered, fifteen of 135 SNPs mapping to SLC2A9 and 9 of 59 SNPs in WDR1 gave P values approaching genome-wide significance (10-6

Published
2014

6. Evidence of gene-environment interaction for two genes on chromosome 4 and environmental tobacco smoke in controlling the risk of nonsyndromic cleft palate

Author

Wu, T, Schwender, H, Ruczinski, I, Murray, JC, Marazita, ML, Munger, RG, Hetmanski, JB, Parker, MM, Wang, P, Murray, T, Taub, M, Li, S, Redett, RJ, Fallin, MD, Liang, KY, Wu-Chou, YH, Chong, SS, Yeow, V, Ye, X, Wang, H, Huang, S, Jabs, EW, Shi, B, Wilcox, AJ, Jee, SH, Scott, AF, Beaty, TH, Wu, T, Schwender, H, Ruczinski, I, Murray, JC, Marazita, ML, Munger, RG, Hetmanski, JB, Parker, MM, Wang, P, Murray, T, Taub, M, Li, S, Redett, RJ, Fallin, MD, Liang, KY, Wu-Chou, YH, Chong, SS, Yeow, V, Ye, X, Wang, H, Huang, S, Jabs, EW, Shi, B, Wilcox, AJ, Jee, SH, Scott, AF, and Beaty, TH

Abstract

Nonsyndromic cleft palate (CP) is one of the most common human birth defects and both genetic and environmental risk factors contribute to its etiology. We conducted a genome-wide association study (GWAS) using 550 CP case-parent trios ascertained in an international consortium. Stratified analysis among trios with different ancestries was performed to test for GxE interactions with common maternal exposures using conditional logistic regression models. While no single nucleotide polymorphism (SNP) achieved genome-wide significance when considered alone, markers in SLC2A9 and the neighboring WDR1 on chromosome 4p16.1 gave suggestive evidence of gene-environment interaction with environmental tobacco smoke (ETS) among 259 Asian trios when the models included a term for GxE interaction. Multiple SNPs in these two genes were associated with increased risk of nonsyndromic CP if the mother was exposed to ETS during the peri-conceptual period (3 months prior to conception through the first trimester). When maternal ETS was considered, fifteen of 135 SNPs mapping to SLC2A9 and 9 of 59 SNPs in WDR1 gave P values approaching genome-wide significance (10-6

Published
2014

7. A genome-wide association study of cleft lip with and without cleft palate identifies risk variants near MAFB and ABCA4

Author

Beaty, TH, Murray, JC, Marazita, ML, Munger, RG, Ruczinski, I, Hetmanski, JB, Liang, KY, Wu, T, Murray, T, Fallin, MD, Redett, RA, Raymond, G, Schwender, H, Jin, SC, Cooper, ME, Dunnwald, M, Mansilla, MA, Leslie, E, Bullard, S, Lidral, AC, Moreno, LM, Menezes, R, Vieira, AR, Petrin, A, Wilcox, AJ, Lie, RT, Jabs, EW, Wu-Chou, YH, Chen, PK, Wang, H, Ye, X, Huang, S, Yeow, V, Chong, SS, Jee, SH, Shi, B, Christensen, K, Melbye, M, Doheny, KF, Pugh, EW, Ling, H, Castilla, EE, Czeizel, AE, Ma, L, Field, LL, Brody, L, Pangilinan, F, Mills, JL, Molloy, AM, Kirke, PN, Scott, JM, Arcos-Burgos, M, Scott, AF, Beaty, TH, Murray, JC, Marazita, ML, Munger, RG, Ruczinski, I, Hetmanski, JB, Liang, KY, Wu, T, Murray, T, Fallin, MD, Redett, RA, Raymond, G, Schwender, H, Jin, SC, Cooper, ME, Dunnwald, M, Mansilla, MA, Leslie, E, Bullard, S, Lidral, AC, Moreno, LM, Menezes, R, Vieira, AR, Petrin, A, Wilcox, AJ, Lie, RT, Jabs, EW, Wu-Chou, YH, Chen, PK, Wang, H, Ye, X, Huang, S, Yeow, V, Chong, SS, Jee, SH, Shi, B, Christensen, K, Melbye, M, Doheny, KF, Pugh, EW, Ling, H, Castilla, EE, Czeizel, AE, Ma, L, Field, LL, Brody, L, Pangilinan, F, Mills, JL, Molloy, AM, Kirke, PN, Scott, JM, Arcos-Burgos, M, and Scott, AF

Abstract

Case-parent trios were used in a genome-wide association study of cleft lip with and without cleft palate. SNPs near two genes not previously associated with cleft lip with and without cleft palate (MAFB, most significant SNP rs13041247, with odds ratio (OR) per minor allele = 0.704, 95% CI 0.635-0.778, P = 1.44 × 10-11; and ABCA4, most significant SNP rs560426, with OR = 1.432, 95% CI 1.292-1.587, P = 5.01 × 10-12) and two previously identified regions (at chromosome 8q24 and IRF6) attained genome-wide significance. Stratifying trios into European and Asian ancestry groups revealed differences in statistical significance, although estimated effect sizes remained similar. Replication studies from several populations showed confirming evidence, with families of European ancestry giving stronger evidence for markers in 8q24, whereas Asian families showed stronger evidence for association with MAFB and ABCA4. Expression studies support a role for MAFB in palatal development. © 2010 Nature America, Inc. All rights reserved.

Published
2010

8. A genome-wide association study of cleft lip with and without cleft palate identifies risk variants near MAFB and ABCA4

Author

Beaty, TH, Murray, JC, Marazita, ML, Munger, RG, Ruczinski, I, Hetmanski, JB, Liang, KY, Wu, T, Murray, T, Fallin, MD, Redett, RA, Raymond, G, Schwender, H, Jin, SC, Cooper, ME, Dunnwald, M, Mansilla, MA, Leslie, E, Bullard, S, Lidral, AC, Moreno, LM, Menezes, R, Vieira, AR, Petrin, A, Wilcox, AJ, Lie, RT, Jabs, EW, Wu-Chou, YH, Chen, PK, Wang, H, Ye, X, Huang, S, Yeow, V, Chong, SS, Jee, SH, Shi, B, Christensen, K, Melbye, M, Doheny, KF, Pugh, EW, Ling, H, Castilla, EE, Czeizel, AE, Ma, L, Field, LL, Brody, L, Pangilinan, F, Mills, JL, Molloy, AM, Kirke, PN, Scott, JM, Arcos-Burgos, M, Scott, AF, Beaty, TH, Murray, JC, Marazita, ML, Munger, RG, Ruczinski, I, Hetmanski, JB, Liang, KY, Wu, T, Murray, T, Fallin, MD, Redett, RA, Raymond, G, Schwender, H, Jin, SC, Cooper, ME, Dunnwald, M, Mansilla, MA, Leslie, E, Bullard, S, Lidral, AC, Moreno, LM, Menezes, R, Vieira, AR, Petrin, A, Wilcox, AJ, Lie, RT, Jabs, EW, Wu-Chou, YH, Chen, PK, Wang, H, Ye, X, Huang, S, Yeow, V, Chong, SS, Jee, SH, Shi, B, Christensen, K, Melbye, M, Doheny, KF, Pugh, EW, Ling, H, Castilla, EE, Czeizel, AE, Ma, L, Field, LL, Brody, L, Pangilinan, F, Mills, JL, Molloy, AM, Kirke, PN, Scott, JM, Arcos-Burgos, M, and Scott, AF

Abstract

Case-parent trios were used in a genome-wide association study of cleft lip with and without cleft palate. SNPs near two genes not previously associated with cleft lip with and without cleft palate (MAFB, most significant SNP rs13041247, with odds ratio (OR) per minor allele = 0.704, 95% CI 0.635-0.778, P = 1.44 × 10-11; and ABCA4, most significant SNP rs560426, with OR = 1.432, 95% CI 1.292-1.587, P = 5.01 × 10-12) and two previously identified regions (at chromosome 8q24 and IRF6) attained genome-wide significance. Stratifying trios into European and Asian ancestry groups revealed differences in statistical significance, although estimated effect sizes remained similar. Replication studies from several populations showed confirming evidence, with families of European ancestry giving stronger evidence for markers in 8q24, whereas Asian families showed stronger evidence for association with MAFB and ABCA4. Expression studies support a role for MAFB in palatal development. © 2010 Nature America, Inc. All rights reserved.

Published
2010

9. The prediction of midlife coronary heart disease and hypertension in young adults: the Johns Hopkins multiple risk equations.

Author

Pearson, TA, Pearson, TA, LaCroix, AZ, Mead, LA, Liang, KY, Pearson, TA, Pearson, TA, LaCroix, AZ, Mead, LA, and Liang, KY

Abstract

Educating medical students about the identification of risk factors for coronary disease and hypertension should be enhanced by exercises in which medical students identify their own risk factors and visualize the impact of current risk status on future risk of disease. A cohort of 1,130 former Johns Hopkins medical students were examined in medical school and followed annually from 1948 to 1964 to identify youthful factors associated with the development of coronary heart disease and hypertension in midlife. In the ensuing years through 1984, 51 cases of coronary heart disease and 114 cases of hypertension developed. Multiple risk equations using Cox proportional hazards regression were developed to predict these endpoints. Incidence of coronary heart disease was predicted best by an equation containing age, serum cholesterol at baseline, cigarette smoking at baseline, and paternal history of coronary disease. Hypertension was predicted best by an equation containing age, systolic blood pressure at baseline, paternal history of hypertension, and Quetelet index. These equations were applied to a class of present-day medical students to demonstrate the considerable variability in 30-year risk of coronary disease or hypertension. Thus, coronary heart disease and hypertension in midlife can be predicted by factors identified in youth. The Johns Hopkins multiple risk equations may be valuable as tools in preventive cardiology education to illustrate risk assessment and the importance of risk factor interventions.

Published
1990

10. The prediction of midlife coronary heart disease and hypertension in young adults: the Johns Hopkins multiple risk equations.

Author

Pearson, TA, Pearson, TA, LaCroix, AZ, Mead, LA, Liang, KY, Pearson, TA, Pearson, TA, LaCroix, AZ, Mead, LA, and Liang, KY

Abstract

Educating medical students about the identification of risk factors for coronary disease and hypertension should be enhanced by exercises in which medical students identify their own risk factors and visualize the impact of current risk status on future risk of disease. A cohort of 1,130 former Johns Hopkins medical students were examined in medical school and followed annually from 1948 to 1964 to identify youthful factors associated with the development of coronary heart disease and hypertension in midlife. In the ensuing years through 1984, 51 cases of coronary heart disease and 114 cases of hypertension developed. Multiple risk equations using Cox proportional hazards regression were developed to predict these endpoints. Incidence of coronary heart disease was predicted best by an equation containing age, serum cholesterol at baseline, cigarette smoking at baseline, and paternal history of coronary disease. Hypertension was predicted best by an equation containing age, systolic blood pressure at baseline, paternal history of hypertension, and Quetelet index. These equations were applied to a class of present-day medical students to demonstrate the considerable variability in 30-year risk of coronary disease or hypertension. Thus, coronary heart disease and hypertension in midlife can be predicted by factors identified in youth. The Johns Hopkins multiple risk equations may be valuable as tools in preventive cardiology education to illustrate risk assessment and the importance of risk factor interventions.

Published
1990

11. Coffee consumption and the incidence of coronary heart disease.

Author

LaCroix, AZ, LaCroix, AZ, Mead, LA, Liang, KY, Thomas, CB, Pearson, TA, LaCroix, AZ, LaCroix, AZ, Mead, LA, Liang, KY, Thomas, CB, and Pearson, TA

Abstract

We conducted a prospective investigation of the effect of coffee consumption on coronary heart disease in 1130 male medical students who were followed for 19 to 35 years. Changes in coffee consumption and cigarette smoking during follow-up were examined in relation to the incidence of clinically evident coronary disease in comparisons of three measures of coffee intake--base-line intake, average intake, and most recent intake reported before the manifestation of coronary disease. Clinical evidence of coronary disease included myocardial infarction, angina, and sudden cardiac death. In separate analyses for each measure of coffee intake, the relative risks for men drinking five or more cups of coffee per day, as compared with nondrinkers, were approximately 2.80 for all three measures in the univariate analyses (maximum width of 95 percent confidence intervals, 1.27 to 6.51). After adjustment for age, current smoking, hypertension status, and base-line level of serum cholesterol, the estimated relative risk for men drinking five or more cups of coffee per day (using the most recent coffee intake measure), as compared with those drinking none, was 2.49 (maximum width of 95 percent confidence interval, 1.08 to 5.77). The association between coffee and coronary disease was strongest when the time between the reports of coffee intake and the coronary event was shortest. These findings support an independent, dose-responsive association of coffee consumption with clinically evident coronary heart disease, which is consistent with a twofold to threefold elevation in risk among heavy coffee drinkers.

Published
1986

12. Coffee consumption and the incidence of coronary heart disease.

Author

LaCroix, AZ, LaCroix, AZ, Mead, LA, Liang, KY, Thomas, CB, Pearson, TA, LaCroix, AZ, LaCroix, AZ, Mead, LA, Liang, KY, Thomas, CB, and Pearson, TA

Abstract

We conducted a prospective investigation of the effect of coffee consumption on coronary heart disease in 1130 male medical students who were followed for 19 to 35 years. Changes in coffee consumption and cigarette smoking during follow-up were examined in relation to the incidence of clinically evident coronary disease in comparisons of three measures of coffee intake--base-line intake, average intake, and most recent intake reported before the manifestation of coronary disease. Clinical evidence of coronary disease included myocardial infarction, angina, and sudden cardiac death. In separate analyses for each measure of coffee intake, the relative risks for men drinking five or more cups of coffee per day, as compared with nondrinkers, were approximately 2.80 for all three measures in the univariate analyses (maximum width of 95 percent confidence intervals, 1.27 to 6.51). After adjustment for age, current smoking, hypertension status, and base-line level of serum cholesterol, the estimated relative risk for men drinking five or more cups of coffee per day (using the most recent coffee intake measure), as compared with those drinking none, was 2.49 (maximum width of 95 percent confidence interval, 1.08 to 5.77). The association between coffee and coronary disease was strongest when the time between the reports of coffee intake and the coronary event was shortest. These findings support an independent, dose-responsive association of coffee consumption with clinically evident coronary heart disease, which is consistent with a twofold to threefold elevation in risk among heavy coffee drinkers.

Published
1986

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