Figure 1
Figure 1. Pie chart illustrating the molecular and genetic aberrations as well as their nonrandom associations in pediatric AML. (A) Total group: Integrative analysis of recurrent cytogenetic aberrations (MLL-rearrangements, t(8;21), inv(16), t(15;17), t(7;12), and t(6;9), CN and other nonspecific cytogenetic subgroups and type I molecular aberrations (in FLT3-ITD, WT1, N-RAS, K-RAS, PTPN11, and c-KIT) based on 237 unselected de novo pediatric AML patients. Each sector indicates the percentage of patients harboring 1 or more of the aforementioned mutations. (B) CN group: Pie chart based on 40 cytogenetically normal de novo pediatric AML patients analyzed for the presence of type II molecular aberrations (in NUP98-NSD1, CEBPA dm, NPM1, MLL-PTD, and other molecular aberrations) and type I molecular aberrations (in FLT3-ITD, WT1, N-RAS, K-RAS, PTPN11, and c-KIT). Each sector indicates the percentage of patients harboring 1 or more of the aforementioned mutations. None indicates patients with only wild-type alleles of genes tested. Adapted from Hollink et al22 and Balgobind et al27 with permission.

Pie chart illustrating the molecular and genetic aberrations as well as their nonrandom associations in pediatric AML. (A) Total group: Integrative analysis of recurrent cytogenetic aberrations (MLL-rearrangements, t(8;21), inv(16), t(15;17), t(7;12), and t(6;9), CN and other nonspecific cytogenetic subgroups and type I molecular aberrations (in FLT3-ITD, WT1, N-RAS, K-RAS, PTPN11, and c-KIT) based on 237 unselected de novo pediatric AML patients. Each sector indicates the percentage of patients harboring 1 or more of the aforementioned mutations. (B) CN group: Pie chart based on 40 cytogenetically normal de novo pediatric AML patients analyzed for the presence of type II molecular aberrations (in NUP98-NSD1, CEBPA dm, NPM1, MLL-PTD, and other molecular aberrations) and type I molecular aberrations (in FLT3-ITD, WT1, N-RAS, K-RAS, PTPN11, and c-KIT). Each sector indicates the percentage of patients harboring 1 or more of the aforementioned mutations. None indicates patients with only wild-type alleles of genes tested. Adapted from Hollink et al22  and Balgobind et al27  with permission.

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