American Society of Hematology

Figure 2

$Clonal evolution of TP53 mutation and 17p deletion in patients with CLL. Sequential analyses of TP53 mutation status and 17p deletion in patients with CLL. Treatment is indicated by arrows. Cbl indicates chlorambucil; F, fludarabine; Dauno, daunorubicin. (Blue) TP53 mutation in percent of total DNA as quantified by sequencing including the sequencing of clones. (Red) Percentage of cells with single signal for TP53 (cases with no evidence of 17p deletion were quantified as 0%). (A) Evolution of monoallelic TP53 mutation in the absence of 17p deletion. Clinically, the patient had chemorefractory disease with the emergence of the TP53 mutation and poor survival despite multiple different substances supporting the relevance of the monoallelic TP53 mutation. At the last mutation analysis, the patient had 2 TP53 mutations (*) on different alleles (p.Cys176Phe, p.Lys139Asn). (B) Evolution of biallelic TP53 inactivation. The mutation preceded the detection of a 17p deletion and was only detectable by cloning (month 14). The deletion was constant at 2 time points and increased (was selected for) after treatment with chlorambucil. (C) Evolution of 17p deletion and TP53 mutation in a patient with CLL after therapy with chlorambucil and fludarabine.$

Clonal evolution of TP53 mutation and 17p deletion in patients with CLL. Sequential analyses of TP53 mutation status and 17p deletion in patients with CLL. Treatment is indicated by arrows. Cbl indicates chlorambucil; F, fludarabine; Dauno, daunorubicin. (Blue) TP53 mutation in percent of total DNA as quantified by sequencing including the sequencing of clones. (Red) Percentage of cells with single signal for TP53 (cases with no evidence of 17p deletion were quantified as 0%). (A) Evolution of monoallelic TP53 mutation in the absence of 17p deletion. Clinically, the patient had chemorefractory disease with the emergence of the TP53 mutation and poor survival despite multiple different substances supporting the relevance of the monoallelic TP53 mutation. At the last mutation analysis, the patient had 2 TP53 mutations (*) on different alleles (p.Cys176Phe, p.Lys139Asn). (B) Evolution of biallelic TP53 inactivation. The mutation preceded the detection of a 17p deletion and was only detectable by cloning (month 14). The deletion was constant at 2 time points and increased (was selected for) after treatment with chlorambucil. (C) Evolution of 17p deletion and TP53 mutation in a patient with CLL after therapy with chlorambucil and fludarabine.

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