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Blood, Vol. 112, Issue 10, 4178-4183, November 15, 2008
Genome-wide copy number profiling reveals molecular evolution from diagnosis to relapse in childhood acute lymphoblastic leukemia
Blood Yang et al.
112: 4178
Supplemental materials for: Yang et al
Files in this Data Supplement:
- Document 1. Supplemental materials and methods (PDF, 6.28 MB)
- Table S1. Sample analysis by Affymetrix SNP array (GeneChip® Human Mapping 500K set) and Affymetrix Gene Expression array (U133A microarray) (PDF, 207 KB)
- Table S2. Primers and probes used for genomic real-time PCR (PDF, 241 KB)
- Table S3. Genomic real-time PCR results (PDF, 121 KB)
- Figure S1. Time to relapse differed significantly by CDKN2A status at diagnosis (JPG, 35.6 KB)
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Boxes include data between the 25th and 75th percentiles, and whiskers indicate the minimal and maximal values excluding the outliers.
- Figure S2. Unsupervised hierarchical clustering of patient samples based on CNAs at diagnosis (JPG, 84.2 KB)
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Top Panel: 20 cases clustered into 3 groups showing distinct CNA pattern. Bottom Panel: average time to relapse (in months) differed significantly among groups.
- Figure S3. Copy number profiles at 6 antigen receptor gene rearrangement loci (JPG, 111 KB)
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Copy number changes in leukemic blasts involving T cell receptor and Immunoglobulin gene rearrangements are shown by patient (orange: diagnosis, green: relapse) at 2p11.2 (IGKL), 7p14.1 (TRGV), 7q34 (TRBV), 14q11.2 (TRAV, TRDV, TRDJ, TRDC, and TRAJ), 14q32.33 (IGHV), and 22q11.22 (IGLL).
- Figure S4. Correlation between copy number change and gene expression change from diagnosis to relapse (JPG, 51 KB)
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For each diagnosis/relapse pair and each gene, relative copy number change represents log2 ratio of relapse - log2 ratio of diagnosis. Relative gene expression represents the ratio of expression at diagnosis to relapse (shown as log2). Red: relative copy number gains, blue: relative copy number losses, and black: no change in copy number. The overrepresentation of data in the upper right and lower left quadrants indicates concordant correlation between copy number change and gene expression from diagnosis to relapse (P = 5.6 × 10−49). Global correlation between relative copy number change and gene expression from diagnosis to relapse also reached statistical significance (P = 2.2 × 10−16).
- Figure S5. The correlation of gene expression levels in matched diagnosis and relapse samples was inversely associated with time to relapse (JPG, 19.3 KB)
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Correlation coefficient was estimated by comparing expression of 14,500 genes between diagnosis and relapse. Each dot represents a patient.
- Figure S6. Identification and classification of somatically acquired copy number alterations (CNA) (JPG, 46.4 KB)
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CNV: germline copy number variations (inherited); Sg: average signal intensity of the region of interest (log ratio) in the germline sample. Pd/g: P value for difference in signal intensity distribution between diagnosis and germline samples, as estimated by paired Wilcoxon test. Pr/g: P value for difference between relapse and germline samples. Pd/r: P value for difference between diagnosis and relapse samples.
- Figure S7. Distribution of LC50 of mercaptopurine (A, n=121) and prednisone (B, n=114) in primary ALL samples (JPG, 25 KB)
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- Figure S8. Relationship between MSH6 gene expression and prednisolone sensitivity in primary ALL samples based on data from Holleman et al. New England Journal of Medicine 351:533-542 (JPG, 45.1 KB)
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Statistical significance was assessed using the Kruskal-Wallis test. Boxes include data between the 25th and 75th percentiles, and whiskers indicate the minimal and maximal values excluding the outliers.
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