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R. Tracy (2008)
‘Deep phenotyping’: characterizing populations in the era of genomics and systems biologyCurrent Opinion in Lipidology, 19
P. Wilson, E. Schaefer, M. Larson, J. Ordovás (1996)
Apolipoprotein E alleles and risk of coronary disease. A meta-analysis.Arteriosclerosis, thrombosis, and vascular biology, 16 10
S. Boekholdt, F. Sacks, J. Jukema, J. Shepherd, D. Freeman, A. McMahon, F. Cambien, V. Nicaud, G. Grooth, P. Talmud, S. Humphries, G. Miller, G. Eiriksdottir, V. Gudnason, H. Kauma, S. Kakko, M. Savolainen, M. Arca, A. Montali, S. Liu, H. Lanz, A. Zwinderman, J. Kuivenhoven, J. Kastelein (2005)
Cholesteryl Ester Transfer Protein TaqIB Variant, High-Density Lipoprotein Cholesterol Levels, Cardiovascular Risk, and Efficacy of Pravastatin Treatment: Individual Patient Meta-Analysis of 13 677 SubjectsCirculation, 111
G. Grooth, A. Klerkx, E. Stroes, A. Stalenhoef, J. Kastelein, J. Kuivenhoven (2004)
A review of CETP and its relation to atherosclerosis Published, JLR Papers in Press, September 1, 2004. DOI 10.1194/jlr.R400007-JLR200Journal of Lipid Research, 45
GJ de Grooth, AH Klerkx, ES Stroes, AF Stalenhoef, JJ Kastelein, JA Kuivenhoven (2004)
A review of CETP and its relation to atherosclerosis., 45
D. Rader, Jonathan Cohen, H. Hobbs (2003)
Monogenic hypercholesterolemia: new insights in pathogenesis and treatment.The Journal of clinical investigation, 111 12
A. Lusis, R. Mar, P. Pajukanta (2004)
Genetics of atherosclerosis.Annual review of genomics and human genetics, 5
P. Wilson, R. Myers, M. Larson, J. Ordovás, P. Wolf, E. Schaefer (1994)
Apolipoprotein E alleles, dyslipidemia, and coronary heart disease. The Framingham Offspring Study.JAMA, 272 21
I. Kullo, K. Ding (2007)
Mechanisms of Disease: the genetic basis of coronary heart diseaseNature Clinical Practice Cardiovascular Medicine, 4
G. Smith, S. Ebrahim (2003)
'Mendelian randomization': can genetic epidemiology contribute to understanding environmental determinants of disease?International journal of epidemiology, 32 1
A. Bennet, E. Angelantonio, Z. Ye, F. Wensley, A. Dahlin, A. Ahlbom, B. Keavney, R. Collins, B. Wiman, U. Faire, J. Danesh (2007)
Association of apolipoprotein E genotypes with lipid levels and coronary risk.JAMA, 298 11
A. Thompson, E. Angelantonio, N. Sarwar, S. Erqou, D. Saleheen, R. Dullaart, B. Keavney, Z. Ye, J. Danesh (2008)
Association of cholesteryl ester transfer protein genotypes with CETP mass and activity, lipid levels, and coronary risk.JAMA, 299 23
J. Ordovás, E. Tai (2008)
Why study gene–environment interactions?Current Opinion in Lipidology, 19
John Thompson, Maruja Lira, L. Durham, Ronald Clark, Mark Bamberger, PatriceM. Milos (2003)
Polymorphisms in the CETP gene and association with CETP mass and HDL levels.Atherosclerosis, 167 2
A Daugherty, DL Rateri (2008)
Atherosclerosis: cell biology and lipoproteins., 19
Editorials represent the opinions EDITORIAL of the authors and JAMA and not those of the American Medical Association. CETP Genes, Metabolic Effects, and Coronary Disease Risk chemical phenotypes related to CETP metabolism, HDL- Peter W. F. Wilson, MD cholesterol (HDL-C) level (a traditional risk factor for which the blood level is partly determined by CETP activity), and HE BURDEN OF ATHEROSCLEROTIC CORONARY HEART CHD risk estimates. disease (CHD) is tremendous—both genes and The CETP genotype relationship to CHD risk reported environment contribute to this problem. From a by Thompson et al is similar to that reported in a meta- Tclinical perspective, physicians are well aware of analysis that focused on the CETP TaqIB variants. The study the importance of genetic lipid abnormalities in the causa- 1 by Thompson et al answers the call for a comprehensive tion of CHD. The best studied genetic lipid abnormality analysis of the gene effects related to CETP, its metabo- is familial hypercholesterolemia (FH), which can cause lites, and CHD risk, and differs from previous analyses by clinical findings such as xanthomas, early atherosclerosis, including much more data, especially concerning the in- and premature CHD. Approximately 1 out of 500 of the termediate biomarkers
JAMA – American Medical Association
Published: Jun 18, 2008
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