Figure 1.
Study overview. (A) TARGET data used for copy number variants assessment in the 13q12.2 region in either T-ALL or AML patients. (B) Schematic figure of the region where FLT3 (light green rectangle) and PAN3 (light blue rectangle) genes are located. (Upper) Wild-type scenario. (Middle) Largest 13p12.2 deletion found by Yang et al. (Lower) Location of 13q12.2 deletion found in the AML patient (highlighted rectangle). DS1 (FLT3 promoter, chr13:28 674,500-28 675,000; dark green rectangle), DS2 (chr13:28 710,000-28 715,000; dark blue rectangle) and DS3 (PAN3 intron 8; chr13:28 843,000-28 843,500; red rectangle). (C) Dispersion of FLT3 expression among AML patients demonstrated by boxplot. The dot plot shows the FLT3 expression of each AML patient (green circle), highlighting the diagnostic (blue square) and relapse samples (red triangle) from the female patient who presented a 13q12.2 deletion. These expression data were obtained according to the availability of RNA-sequencing data from patients assessed for copy-number abnormality (n = 203).

Study overview. (A) TARGET data used for copy number variants assessment in the 13q12.2 region in either T-ALL or AML patients. (B) Schematic figure of the region where FLT3 (light green rectangle) and PAN3 (light blue rectangle) genes are located. (Upper) Wild-type scenario. (Middle) Largest 13p12.2 deletion found by Yang et al. (Lower) Location of 13q12.2 deletion found in the AML patient (highlighted rectangle). DS1 (FLT3 promoter, chr13:28 674,500-28 675,000; dark green rectangle), DS2 (chr13:28 710,000-28 715,000; dark blue rectangle) and DS3 (PAN3 intron 8; chr13:28 843,000-28 843,500; red rectangle). (C) Dispersion of FLT3 expression among AML patients demonstrated by boxplot. The dot plot shows the FLT3 expression of each AML patient (green circle), highlighting the diagnostic (blue square) and relapse samples (red triangle) from the female patient who presented a 13q12.2 deletion. These expression data were obtained according to the availability of RNA-sequencing data from patients assessed for copy-number abnormality (n = 203).

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