(Circulation. 2002;106:768.)
© 2002 American Heart Association, Inc.
Editorial |
From the Section of Cardiology Baylor College of Medicine, Department of Medicine, (A.J.M.), and Human Genetics Center and Institute of Molecular Medicine (E.B.), University of Texas Health Science Center at Houston.
Correspondence to A.J. Marian, MD, Associate Professor of Medicine, Section of Cardiology, One Baylor Plaza, 519D Houston, TX 77030. E-mail amarian@bcm.tmc.edu
Key Words: Editorials genetics hypoxia edema hypertension, pulmonary
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
Even after detailed analyses of past events, future events are difficult, if not impossible, to predict. Few are those who could have predicted that a long and monotonous DNA molecule would potentially revolutionize the future of science and medicine. Even after the acceptance of DNA as the basic hereditary material, few predicted either the rapid rate of discovery of genes and mutations that cause the simply inherited mendelian diseases or the speed at which international public and private efforts made it possible to read the complete sequence of the human genome. Today, genes are implicated in all aspects of the human condition, ranging from susceptibility to common diseases to differences in clinical outcomes. Further analysis of the human genome sequence has led to the identification of millions of single-nucleotide variations (single-nucleotide polymorphisms [SNPs]), which form the backbone of interindividual variations in disease susceptibility, clinical outcome, and response to therapy (pharmacogenetics). Massive efforts are currently underway to unleash the potential usefulness of SNPs in clinical medicine. The ultimate goal is to develop "personalized medicine" by creating SNP profiles for identification of those at increased risk in a preclinical setting, providing information about the pathology of disease in subgroups of patients, and targeting drugs and other treatments to those patients who are most likely to respond.
See p 826
We have witnessed (and sometimes participated in) a plethora of association studies exploring susceptibility genes for a diverse array of human diseases and other traits. In this issue of Circulation, Droma et
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