Figure 2.

TEL/AML1 gene expression signature of Set-A patients. (A) Two-class SAM was applied to Set-A data. The data were filtered on the basis of a difference greater than 1.7 fold and a Q value less than 2%, leaving 103 clones (1000 permutations, median false positive = 4) associated with a TEL/AML1 signature. Clustering analysis of Set-A patients segregates TEL/AML1-positive patients together, except for patient 17 who clusters with patient 11 in a distinct branch and for patient 9 who does not present a TEL/AML1 fusion transcript, and segregates with TEL/AML1-positive ALL. Gene expression is visualized, with green and red representing down and up-regulated genes, respectively. Gray corresponds to missing data (absence of signal) as described in "Patients, Materials and Methods". The color scale above the dendrogram extends from 0.125 to 8.0 times the mean (-3 to +3 in log2 space). Two gene clusters (indicated by black arrows), consisting of either up-regulated genes or down-regulated genes, differentiate TEL/AML1-positive and -negative ALL. Gray arrows indicate the branches, which were unable on their own to segregate TEL/AML1 positive patients. (B) Support tree of Set-A and Set-B patients using the 55 clones (44 distinct genes) identified by the clustering analysis. Resampling with replacement was conducted on experiments and genes for 100 iterations. The branches of the resulted tree are colorized to denote the percentage of times a given node was supported over the resampling trials. Two branches still distinguished TEL/AML1-positive ALL from TEL/AML1-negative ALL with 100% reproducibility when Set-B samples have been added to Set-A. Two stable clusters of genes (up- and down-regulated genes) were identified and further explored by functional analysis.

Gandemer et al. BMC Genomics 2007 8:385   doi:10.1186/1471-2164-8-385
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