A genomewide scan for early-onset coronary artery disease in 438 families: the GENECARD Study

Elizabeth R. Hauser; David C. Crossman; Christopher B. Granger; Jonathan L. Haines; Christopher J. H. Jones; Vincent Mooser; Brendan McAdam; Bernhard R. Winkelmann; Alan H. Wiseman; J. Brent Muhlestein; Alan G. Bartel; Charles A. Dennis; Elaine Dowdy; Susan Estabrooks; Karen Eggleston; Sheila Francis; Kath Roche; Paula W. Clevenger; Liling Huang; Bonnie Pedersen; Svati Shah; Silke Schmidt; Carol Haynes; Sandra West; Donny Asper; Michael Booze; Sanjay Sharma; Scott Sundseth; Lefkos Middleton; Allen D. Roses; Michael A. Hauser; Jeffery M. Vance; Margaret A. Pericak-Vance; William E. Kraus

doi:10.1086/423900

A genomewide scan for early-onset coronary artery disease in 438 families: the GENECARD Study

Elizabeth R. Hauser, David C. Crossman, Christopher B. Granger, Jonathan L. Haines, Christopher J. H. Jones, Vincent Mooser, Brendan McAdam, Bernhard R. Winkelmann, Alan H. Wiseman, J. Brent Muhlestein, Alan G. Bartel, Charles A. Dennis, Elaine Dowdy, Susan Estabrooks, Karen Eggleston, Sheila Francis, Kath Roche, Paula W. Clevenger, Liling Huang, Bonnie PedersenSvati Shah, Silke Schmidt, Carol Haynes, Sandra West, Donny Asper, Michael Booze, Sanjay Sharma, Scott Sundseth, Lefkos Middleton, Allen D. Roses, Michael A. Hauser, Jeffery M. Vance, Margaret A. Pericak-Vance, William E. Kraus

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Abstract

A family history of coronary artery disease (CAD), especially when the disease occurs at a young age, is a potent risk factor for CAD. DNA collection in families in which two or more siblings are affected at an early age allows identification of genetic factors for CAD by linkage analysis. We performed a genomewide scan in 1,168 individuals from 438 families, including 493 affected sibling pairs with documented onset of CAD before 51 years of age in men and before 56 years of age in women. We prospectively defined three phenotypic subsets of families: (1) acute coronary syndrome in two or more siblings; (2) absence of type 2 diabetes in all affected siblings; and (3) atherogenic dyslipidemia in any one sibling. Genotypes were analyzed for 395 microsatellite markers. Regions were defined as providing evidence for linkage if they provided parametric two-point LOD scores >1.5, together with nonparametric multipoint LOD scores >1.0. Regions on chromosomes 3q13 (multipoint LOD = 3.3; empirical P value

Original language	English
Pages (from-to)	436-447
Number of pages	12
Journal	American Journal of Human Genetics
Volume	75
Issue number	3
DOIs	https://doi.org/10.1086/423900
Publication status	Published - Sep 2004

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Hauser, E. R., Crossman, D. C., Granger, C. B., Haines, J. L., Jones, C. J. H., Mooser, V., McAdam, B., Winkelmann, B. R., Wiseman, A. H., Muhlestein, J. B., Bartel, A. G., Dennis, C. A., Dowdy, E., Estabrooks, S., Eggleston, K., Francis, S., Roche, K., Clevenger, P. W., Huang, L., ... Kraus, W. E. (2004). A genomewide scan for early-onset coronary artery disease in 438 families: the GENECARD Study. American Journal of Human Genetics, 75(3), 436-447. https://doi.org/10.1086/423900

@article{f40876f5d071465694e779f987af28c7,

title = "A genomewide scan for early-onset coronary artery disease in 438 families: the GENECARD Study",

abstract = "A family history of coronary artery disease (CAD), especially when the disease occurs at a young age, is a potent risk factor for CAD. DNA collection in families in which two or more siblings are affected at an early age allows identification of genetic factors for CAD by linkage analysis. We performed a genomewide scan in 1,168 individuals from 438 families, including 493 affected sibling pairs with documented onset of CAD before 51 years of age in men and before 56 years of age in women. We prospectively defined three phenotypic subsets of families: (1) acute coronary syndrome in two or more siblings; (2) absence of type 2 diabetes in all affected siblings; and (3) atherogenic dyslipidemia in any one sibling. Genotypes were analyzed for 395 microsatellite markers. Regions were defined as providing evidence for linkage if they provided parametric two-point LOD scores >1.5, together with nonparametric multipoint LOD scores >1.0. Regions on chromosomes 3q13 (multipoint LOD = 3.3; empirical P value ",

author = "Hauser, {Elizabeth R.} and Crossman, {David C.} and Granger, {Christopher B.} and Haines, {Jonathan L.} and Jones, {Christopher J. H.} and Vincent Mooser and Brendan McAdam and Winkelmann, {Bernhard R.} and Wiseman, {Alan H.} and Muhlestein, {J. Brent} and Bartel, {Alan G.} and Dennis, {Charles A.} and Elaine Dowdy and Susan Estabrooks and Karen Eggleston and Sheila Francis and Kath Roche and Clevenger, {Paula W.} and Liling Huang and Bonnie Pedersen and Svati Shah and Silke Schmidt and Carol Haynes and Sandra West and Donny Asper and Michael Booze and Sanjay Sharma and Scott Sundseth and Lefkos Middleton and Roses, {Allen D.} and Hauser, {Michael A.} and Vance, {Jeffery M.} and Pericak-Vance, {Margaret A.} and Kraus, {William E.}",

year = "2004",

month = sep,

doi = "10.1086/423900",

language = "English",

volume = "75",

pages = "436--447",

journal = "American Journal of Human Genetics",

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Hauser, ER, Crossman, DC, Granger, CB, Haines, JL, Jones, CJH, Mooser, V, McAdam, B, Winkelmann, BR, Wiseman, AH, Muhlestein, JB, Bartel, AG, Dennis, CA, Dowdy, E, Estabrooks, S, Eggleston, K, Francis, S, Roche, K, Clevenger, PW, Huang, L, Pedersen, B, Shah, S, Schmidt, S, Haynes, C, West, S, Asper, D, Booze, M, Sharma, S, Sundseth, S, Middleton, L, Roses, AD, Hauser, MA, Vance, JM, Pericak-Vance, MA & Kraus, WE 2004, 'A genomewide scan for early-onset coronary artery disease in 438 families: the GENECARD Study', American Journal of Human Genetics, vol. 75, no. 3, pp. 436-447. https://doi.org/10.1086/423900

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T1 - A genomewide scan for early-onset coronary artery disease in 438 families: the GENECARD Study

AU - Hauser, Elizabeth R.

AU - Crossman, David C.

AU - Granger, Christopher B.

AU - Haines, Jonathan L.

AU - Jones, Christopher J. H.

AU - Mooser, Vincent

AU - McAdam, Brendan

AU - Winkelmann, Bernhard R.

AU - Wiseman, Alan H.

AU - Muhlestein, J. Brent

AU - Bartel, Alan G.

AU - Dennis, Charles A.

AU - Dowdy, Elaine

AU - Estabrooks, Susan

AU - Eggleston, Karen

AU - Francis, Sheila

AU - Roche, Kath

AU - Clevenger, Paula W.

AU - Huang, Liling

AU - Pedersen, Bonnie

AU - Shah, Svati

AU - Schmidt, Silke

AU - Haynes, Carol

AU - West, Sandra

AU - Asper, Donny

AU - Booze, Michael

AU - Sharma, Sanjay

AU - Sundseth, Scott

AU - Middleton, Lefkos

AU - Roses, Allen D.

AU - Hauser, Michael A.

AU - Vance, Jeffery M.

AU - Pericak-Vance, Margaret A.

AU - Kraus, William E.

PY - 2004/9

Y1 - 2004/9

N2 - A family history of coronary artery disease (CAD), especially when the disease occurs at a young age, is a potent risk factor for CAD. DNA collection in families in which two or more siblings are affected at an early age allows identification of genetic factors for CAD by linkage analysis. We performed a genomewide scan in 1,168 individuals from 438 families, including 493 affected sibling pairs with documented onset of CAD before 51 years of age in men and before 56 years of age in women. We prospectively defined three phenotypic subsets of families: (1) acute coronary syndrome in two or more siblings; (2) absence of type 2 diabetes in all affected siblings; and (3) atherogenic dyslipidemia in any one sibling. Genotypes were analyzed for 395 microsatellite markers. Regions were defined as providing evidence for linkage if they provided parametric two-point LOD scores >1.5, together with nonparametric multipoint LOD scores >1.0. Regions on chromosomes 3q13 (multipoint LOD = 3.3; empirical P value

AB - A family history of coronary artery disease (CAD), especially when the disease occurs at a young age, is a potent risk factor for CAD. DNA collection in families in which two or more siblings are affected at an early age allows identification of genetic factors for CAD by linkage analysis. We performed a genomewide scan in 1,168 individuals from 438 families, including 493 affected sibling pairs with documented onset of CAD before 51 years of age in men and before 56 years of age in women. We prospectively defined three phenotypic subsets of families: (1) acute coronary syndrome in two or more siblings; (2) absence of type 2 diabetes in all affected siblings; and (3) atherogenic dyslipidemia in any one sibling. Genotypes were analyzed for 395 microsatellite markers. Regions were defined as providing evidence for linkage if they provided parametric two-point LOD scores >1.5, together with nonparametric multipoint LOD scores >1.0. Regions on chromosomes 3q13 (multipoint LOD = 3.3; empirical P value

U2 - 10.1086/423900

DO - 10.1086/423900

M3 - Article

VL - 75

SP - 436

EP - 447

JO - American Journal of Human Genetics

JF - American Journal of Human Genetics

SN - 0002-9297

IS - 3

ER -