Priorities and standards in pharmacogenetic research

被引:81
作者
Need, AC
Motulsky, AG
Goldstein, DB
机构
[1] Duke Univ, Ctr Populat Genom & Pharmacogenet, Inst Genome Sci & Policy, Durham, NC 27710 USA
[2] Univ Washington, Dept Med Med Genet, Seattle, WA 98195 USA
[3] Univ Washington, Dept Genome Sci, Seattle, WA 98195 USA
关键词
D O I
10.1038/ng1593
中图分类号
Q3 [遗传学];
学科分类号
071007 ; 090102 ;
摘要
The current enthusiasm for pharmacogenetics draws much of its inspiration from the relatively few examples of polymorphisms that have marked and seemingly clinically relevant effects on drug response. In this regard, pharmacogenetic research has paralleled the study of human disease, which has enjoyed success in identifying mutations underlying mendelian conditions. Progress in deciphering the genetics of complex diseases, involving the interaction of multiple genes with each other and with the environment has been considerably less successful. In most instances, drug responses will probably also prove to be complex, influenced by both the environment and multiple genetic factors. For pharmacogenetics to deliver on its potential, this complexity will need to be recognized and accommodated, both in basic research and in clinical application of pharmacogenetics. As the attention of researchers begins to shift toward more systematic pharmacogenetic investigations, we suggest some priorities and standards for pharmacogenetic research.
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收藏
页码:671 / 681
页数:11
相关论文
共 76 条
[1]   Pharmacogenetic analysis of adverse drug effect reveals genetic variant for susceptibility to liver toxicity [J].
Acuña G. ;
Foernzler D. ;
Leong D. ;
Rabbia M. ;
Smit R. ;
Dorflinger E. ;
Gasser R. ;
Hoh J. ;
Ott J. ;
Borroni E. ;
To Z. ;
Thompson A. ;
Li J. ;
Hashimoto L. ;
Lindpaintner K. .
The Pharmacogenomics Journal, 2002, 2 (5) :327-334
[2]   A single-nucleotide polymorphism tagging set for human drug metabolism and transport [J].
Ahmadi, KR ;
Weale, ME ;
Xue, ZYY ;
Soranzo, N ;
Yarnall, DP ;
Briley, JD ;
Maruyama, Y ;
Kobayashi, M ;
Wood, NW ;
Spurr, NK ;
Burns, DK ;
Roses, AD ;
Saunders, AM ;
Goldstein, DB .
NATURE GENETICS, 2005, 37 (01) :84-89
[3]  
[Anonymous], TREATMENT EPILEPSY
[4]   Association studies for quantitative traits in structured populations [J].
Bacanu, SA ;
Devlin, B ;
Roeder, K .
GENETIC EPIDEMIOLOGY, 2002, 22 (01) :78-93
[5]   Fenfluramine-induced pulmonary vasoconstriction:: role of serotonin receptors and potassium channels [J].
Belohlávková, S ;
Simák, J ;
Kokesová, A ;
Hnilicková, O ;
Hampl, V .
JOURNAL OF APPLIED PHYSIOLOGY, 2001, 91 (02) :755-761
[6]  
Berson A, 2001, J PHARMACOL EXP THER, V299, P793
[7]   Serotonin 5-HT2B receptor loss of function mutation in a patient with fenfluramine-associated primary pulmonary hypertension [J].
Blanpain, C ;
Le Poul, E ;
Parma, J ;
Knoop, C ;
Detheux, M ;
Parmentier, M ;
Vassart, G ;
Abramowicz, MJ .
CARDIOVASCULAR RESEARCH, 2003, 60 (03) :518-528
[8]   Phylogenetic shadowing of primate sequences to find functional regions of the human genome [J].
Boffelli, D ;
McAuliffe, J ;
Ovcharenko, D ;
Lewis, KD ;
Ovcharenko, I ;
Pachter, L ;
Rubin, EM .
SCIENCE, 2003, 299 (5611) :1391-1394
[9]   Discovering genotypes underlying human phenotypes: past successes for mendelian disease, future approaches for complex disease [J].
Botstein, D ;
Risch, N .
NATURE GENETICS, 2003, 33 (Suppl 3) :228-237
[10]   Serotonin-transporter polymorphism pharmacogenetics in diarrhea-predominant irritable bowel syndrome [J].
Camilleri, M ;
Atanasova, E ;
Carlson, PJ ;
Ahmad, U ;
Kim, HJ ;
Viramontes, BE ;
McKinzie, S ;
Urrutia, R .
GASTROENTEROLOGY, 2002, 123 (02) :425-432