By Ostergard P. R.
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Extra resources for A 2-(22, 8, 4) Design Cannot Have a 2-(10, 4, 4) Subdesign
Chern. Senses 27(3), 293-298. 2. Friedberg, I. and Godzik:, A. (2005) Connecting the protein structure universe by using sparse recurring fragments. Structure 13(8), 1213-1224. 3. Hann, M. M. and aprea, T. 1. (2004) Pursuing the lead1ik:eness concept in pharmaceutical research. Curro Opin. Chern. BioI. 8, 255-263. 4. , Ross, D. , et al. (2000) A gene expression database for the molecular pharmacology of cancer. Nature Genet. 24(3),236-244. 5. Ross, D. , Eisen, M. , et al. (2000) Systematic variation in gene expression patterns in human cancer cell lines.
2006) Prediction of anticancer drug potency from expression of genes involved in growth factor signaling. Pharm. Res. 23(2), 336-349. 7. Schneider, G. and Fechner, D. (2005) Computer-based de novo design of drug-like molecules. Nat. Rev. Drug Discov. 4(8), 649-663. 8. Ortiz, A. , et al. (2006) Computational approaches to model ligand selectivity in drug design. Curro Top Med. Chern. 6( 1). 41-55. 4 _ DNA Microarrays in Drug Discovery and Development Neelam Azad, Anand Krishnan V. Iyer, and Yon Rojanasakul Abstract Ever since the completion of the human genome project, there has been great interest in the research community toward addressing the role played by multiple genes to orchestrate complex cellular functions.
As thousands of SNPs and haplotypes (linked genetic variation) are catalogued and, even more importantly, selectively identified as clinically significant, the era of individualized medicine is becoming more of a reality. gov). These polymorphisms, or normal variations in DNA sequences, somehow contribute to our individual uniqueness, not only in outward appearance, but more importantly of whether we are predisposed to certain diseases or drug-related adverse reactions. Determining the clinical relevance of 10 million or so of these single nucleotide variations will indeed be a Herculean task.