Disease Markers: Cancer Genomics by Robert L. Strausberg

By Robert L. Strausberg

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We are left with a long list of gene-drug (or gene-gene) correlations, each of which must be assessed for its biological sense. N. Weinstein et al. / Searching for pharmacogenomic markers: The synergy between omic and hypothesis-driven research 83 7. Organizing the literature on gene-gene and gene-drug correlations: MedMiner and EDGAR Fig. 4. Illustration of the principle of the clustered image map (CIM) for compact representation of high-dimensional data. Red in this case indicates high gene expression; blue indicates low expression.

But for most purposes, including the search for molecular markers, spot identity proved crucial. For the identification, we developed our own version of a rapid MALDI-TOF mass spectrometric technique based on peptide mapping [31]. The essential steps in the method included in-gei digestion of the proteins with combinations of proteases, purification of the peptides, analysis by MALDI-TOF mass spectrometry, and peptide fingerprinting. N. Weinstein et al. / Searching for pharmacogenomic markers: The synergy between omic and hypothesis-driven research job of a small academic laboratory to identify hundreds of proteins in that way.

However, the precise physiological and functional significance of this regulation is still unknown. The most frequent splice variants include the additional 17 aminoacids inserted Nterminal to the first zinc finger through the inclusion of exon 5 Insertion of the KTS tripeptide has a profound effect on both the DNA-binding affinity and the specificity of WT1. The WT1-KTS isoform binds to a 9-bp early growth response protein (EGR-1) consensus site with high affinity whereas the + KTS splice variant binds to the same site 10- to 20-fold more weakly [33].

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