Figure 1
Figure 1. Distribution of breakpoints on CRLF2. (A) Each denotes an individual CRLF2 breakpoint sequenced from a B-ALL with a CRLF2-IGH translocation. The ■ denotes the position of the CRLF2 breakpoints sequenced from B-ALL with CRLF2-P2RY8 intrachromosomal deletions. The arrow labeled “CRLF2” indicates the position and transcriptional direction of the CRLF2 gene. Numbering is per the March 2006 (hg18) build from the UCSC Genome Browser (http://genome.ucsc.edu/). (B) Overall frequency of CRLF2 breakpoints at various distance intervals from CpG. (C) Overall frequency of CRLF2 breakpoints at various distance intervals from CAC. Proportions of CRLF2 breakpoints at distances of 0 bp, 1-2 bp, 3-4 bp, 5-8 bp, and > 8 bp from CpG (B) or CAC (C) are graphed for the CRLF2 region. The distribution for actual leukemia breakpoints is shown in black, and that for a random distribution between the farthest breakpoints is shown in gray. If the black and gray bars parallel one another, then the patient breakpoints appear random in their distribution relative to the specified motif. However, when they follow opposite trends (ie, the gray bars rise with increasing distance from the specified motif while the black bars fall), then the breakage process appears to concentrate around the motif.

Distribution of breakpoints on CRLF2. (A) Each denotes an individual CRLF2 breakpoint sequenced from a B-ALL with a CRLF2-IGH translocation. The ■ denotes the position of the CRLF2 breakpoints sequenced from B-ALL with CRLF2-P2RY8 intrachromosomal deletions. The arrow labeled “CRLF2” indicates the position and transcriptional direction of the CRLF2 gene. Numbering is per the March 2006 (hg18) build from the UCSC Genome Browser (http://genome.ucsc.edu/). (B) Overall frequency of CRLF2 breakpoints at various distance intervals from CpG. (C) Overall frequency of CRLF2 breakpoints at various distance intervals from CAC. Proportions of CRLF2 breakpoints at distances of 0 bp, 1-2 bp, 3-4 bp, 5-8 bp, and > 8 bp from CpG (B) or CAC (C) are graphed for the CRLF2 region. The distribution for actual leukemia breakpoints is shown in black, and that for a random distribution between the farthest breakpoints is shown in gray. If the black and gray bars parallel one another, then the patient breakpoints appear random in their distribution relative to the specified motif. However, when they follow opposite trends (ie, the gray bars rise with increasing distance from the specified motif while the black bars fall), then the breakage process appears to concentrate around the motif.

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