By William J. LaRochelle, Richard A. Shimkets
An built-in evaluation of melanoma drug discovery and improvement from the bench to the health center, displaying with huge strokes and consultant examples the drug improvement method as a community of associated parts prime from the found goal to the last word healing product. Following a structures biology procedure, the authors clarify genomic databases and the way to find oncological ambitions from them, how then to develop from the gene and transcript to the extent of protein biochemistry, how subsequent to maneuver from the chemical realm to that of the dwelling phone and, finally, pursue animal modeling and medical improvement. rising melanoma therapeutics together with Ritux an, Erbitux, Gleevec Herceptin, Avastin, ABX-EGF, Velcade, Kepivance, Iressa, Tarceva, and Zevalin are addressed. Highlights contain melanoma genomics, pharmacogenomics, transcriptomics, gene expression research, proteomic and enzymatic melanoma profiling applied sciences, and mobile and animal techniques to melanoma aim validation.
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LaRochelle and R. A. , Totowa, NJ 19 20 Hermeking 1. ALTERATIONS IN ONCOGENES AND TUMOR SUPPRESSOR GENES CAUSE CANCER Cancer is a disease primarily caused by the genetic activation of oncogenes and inactivation of tumor suppressor genes (1–4). In addition, epigenetic inactivation of tumor suppressors by CpG methylation of promoter sequences seems to occur at a substantial frequency (5). In the last 20 yr, numerous oncogenes and tumor suppressor genes have been identified. Oncogenes were initially identified via analysis of retroviruses that cause cancer in mice and chicken (1).
Science 1995; 270:484–487. 31. Hermeking H. Serial analysis of gene expression and cancer. Curr Opin Oncol 2003; 15:44–49. 32. Hermeking H, Lengauer C, Polyak K, et al. 14-3-3 Sigma is a p53-regulated inhibitor of G2/M progression. Mol Cell 1997; 1:3–11. 33. He TC, Sparks AB, Rago C, et al. Identification of c-MYC as a target of the APC pathway. Science 1998; 281:1509–1512. 34. Polyak K, Xia Y, Zweier JL, Kinzler KW, Vogelstein B. A model for p53-induced apoptosis. Nature 1997; 389:300–305. 35.
1. Schematics showing ESTs and EST clusters. (A) Schematic description of ESTs from different tissue libraries and their corresponding clusters. Similar color lines represent ESTs from the same transcript, letters (P, prostate; H, heart; L, liver) represent the tissue from which the EST was generated. (B) Schematics of the EST cluster for GDEP. Each line represents one EST. The cluster consists of 19 ESTs, and the composite cluster is about 510 nucleotides in length. (See Color Plate 1 following p.