Figure 3. Representative examples of clonal evolution of genetic lesions during CLL transformation to RS and subsequent RS progression. (a and b) Different tumor clones acquire biallelic TP53 disruption in RS and RSII in case 4. (a) Graphs reporting the variants’ adjusted frequencies as identified by WES analysis in the TP53 gene in the CLL, RS, and RSII phases of case 4. (b) Heatmap showing median-smoothed log2 CN ratio of the short arm of chromosome 17 in the CLL, RS, and RSII phases of case 4. (c and d) Progressive accumulation of multiple genetic lesions leading to NOTCH signaling activation in case 5. (c) Graphs reporting the variants’ adjusted frequencies as identified by WES analysis in the NOTCH1 and SPEN genes in the CLL, RS, and RSII phases of case 5. (d) Schematic of mutations affecting NOTCH1 and SPEN in the CLL, RS, and RSII phases of case 5.
Figure 3.

Representative examples of clonal evolution of genetic lesions during CLL transformation to RS and subsequent RS progression. (a and b) Different tumor clones acquire biallelic TP53 disruption in RS and RSII in case 4. (a) Graphs reporting the variants’ adjusted frequencies as identified by WES analysis in the TP53 gene in the CLL, RS, and RSII phases of case 4. (b) Heatmap showing median-smoothed log2 CN ratio of the short arm of chromosome 17 in the CLL, RS, and RSII phases of case 4. (c and d) Progressive accumulation of multiple genetic lesions leading to NOTCH signaling activation in case 5. (c) Graphs reporting the variants’ adjusted frequencies as identified by WES analysis in the NOTCH1 and SPEN genes in the CLL, RS, and RSII phases of case 5. (d) Schematic of mutations affecting NOTCH1 and SPEN in the CLL, RS, and RSII phases of case 5.

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