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Protein posttranslational modifications, and the biological pathways assembled based on various chemical genomics approaches. For instance, global study of genetic interactions can unravel the genetic basis for drug sensitivity. It is well known that some cancer cells are more resistant or prone to certain anti-cancer drugs. One of the determining factors of drug sensitivity is genetic variation in genes in the same biological pathway s ; as the drug target. Some mutations can increase or decrease rapamycin sensitivity by as much as 10, 000-fold Chan et al. 2000 ; . Mutations in yeast DNA repair and checkpoint pathways have also significant altered sensitivity to 23 different anti-cancer compounds Simon et al. 2000 ; . Drug sensitivity profiles of different types of cancers can be developed based on relative expression of genes involved in biological pathway s ; the drug interferes with. They should be valuable to devise customized protocols for effective treatment of individual cancers. In addition, many hypersensitive genes, genes with significant altered expression or proteins with different modification may be used as direct or secondary drug targets. Inhibition of the secondary targets can sensitize cells to the original drug, thereby significantly decreasing the dosages of the drugs to minimize side effects while achieving maximal therapeutic values. We foresee that chemical ligands should become available for any given protein, which allows chemical modulation of the protein's activity, both positively or negatively, and completely or selectively. These chemical ligands can equip us with the ultimate power to examine every molecular detail of cellular and organismic physiology, which, in turn, can also facilitate the understanding of disease mechanisms, the discovery of highly specific drugs and the devising of customized clinical protocols to treat individual disease conditions. Acknowledgement We thank J. Carvalho for reading the manuscript. This work was supported by grants from National Cancer Institute and American Diabetes Association. References Alaimo, P.J., M.A. Shogren Knaak, and K.M. Shokat. 2001. Chemical genetic approaches for the elucidation of signaling pathways. Curr Opin Chem Biol 5: 360-7. Alberts, A.W., J. Chen, G. Kuron, V. Hunt, J. Huff, C. Hoffman, J. Rothrock, M. Lopez, H. Joshua, E. Harris, A. Patchett, R. Monaghan, S. Currie, E. Stapley, G. AlbersSchonberg, O. Hensens, J. Hirshfield, K. Hoogsteen, J. Liesch, and J. Springer. 1980. Mevinolin: a highly potent competitive inhibitor of hydroxymethylglutaryl-coenzyme A reductase and a cholesterol-lowering agent. Proc Natl Acad Sci U S A 77: 3957-61. Amara, J.F., T. Clackson, V.M. Rivera, T. Guo, T. Keenan, S. Natesan, R. Pollock, W. Yang, N.L. Courage, D.A. Holt, and M. Gilman. 1997. A versatile synthetic dimerizer for the regulation of protein-protein interactions. Proc Natl Acad Sci U S A 94: 10618-23. Aravind, L., V.M. Dixit, and E.V. Koonin. 2001. Apoptotic molecular machinery: vastly increased complexity in and xenical.
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