Figure 1
Figure 1. Somatic mutation frequencies in CLL relapsing after FCR treatment. (A) Average number of nonsynonymous mutations in both the pretreatment and relapse samples and the number of shared mutations in the 28 samples with matched constitutional DNA. (B) Frequency of the 6 mutation classes for pretreatment and relapse-specific mutations in the 28 samples with matched constitutional DNA. Statistical significance was assessed using 796 pretreatment mutations and 425 relapse-specific mutations. (C) Recurrently mutated genes. Columns represent patients (n = 41) and rows genes or genetic lesions. Color-coding indicates the type of mutation or genomic alteration. Case names in gray were analyzed without matched normal DNA. The majority of cases with TP53 aberrations harbored a mutation without coexisting del(17p); this is explained by the fact that the TP53 mutation status was not known in most cases before the start of the FCR regime in contrast to fluorescence in situ hybridization detection of del(17p), which had been performed in all cases. All TP53 mutations were deemed damaging and have been reported previously. CNA, copy-number aberration; PR, partial relapse; UPD, uniparental disomy.

Somatic mutation frequencies in CLL relapsing after FCR treatment. (A) Average number of nonsynonymous mutations in both the pretreatment and relapse samples and the number of shared mutations in the 28 samples with matched constitutional DNA. (B) Frequency of the 6 mutation classes for pretreatment and relapse-specific mutations in the 28 samples with matched constitutional DNA. Statistical significance was assessed using 796 pretreatment mutations and 425 relapse-specific mutations. (C) Recurrently mutated genes. Columns represent patients (n = 41) and rows genes or genetic lesions. Color-coding indicates the type of mutation or genomic alteration. Case names in gray were analyzed without matched normal DNA. The majority of cases with TP53 aberrations harbored a mutation without coexisting del(17p); this is explained by the fact that the TP53 mutation status was not known in most cases before the start of the FCR regime in contrast to fluorescence in situ hybridization detection of del(17p), which had been performed in all cases. All TP53 mutations were deemed damaging and have been reported previously. CNA, copy-number aberration; PR, partial relapse; UPD, uniparental disomy.

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