Figure 1.
Molecular classes of AML and concurrent gene mutations in adult patients up to the age of ∼65 years. Class definition is based on the study by Papaemmanuil et al.37 For each AML class denoted in the pie chart, frequent co-occurring mutations are shown in the respective boxes. Data on the frequency of genetic lesions are compiled from the databases of the British Medical Research Council (MRC), the German-Austrian AML Study Group (AMLSG), and from selected studies.37,87,88,299a indicates cohesin genes including RAD21 (∼10%), SMC1A (∼5%), and SMC3 (∼5%); b, inv(16)(p13.1q22) or t(16;16)(p13.1;q22); CBFB-MYH11; c, inv(3)(q21.3q26.2) or t(3;3)(q21.3;q26.2); GATA2,MECOM(EVI1); and d, TP53 mutations are found in ∼45%, and complex karyotypes in ∼70% of this class. The structure of the pie chart is adapted from Grimwade et al,50 generated by Adam Ivey (King’s College London, London, United Kingdom).

Molecular classes of AML and concurrent gene mutations in adult patients up to the age of ∼65 years. Class definition is based on the study by Papaemmanuil et al.37  For each AML class denoted in the pie chart, frequent co-occurring mutations are shown in the respective boxes. Data on the frequency of genetic lesions are compiled from the databases of the British Medical Research Council (MRC), the German-Austrian AML Study Group (AMLSG), and from selected studies.37,87,88,299 a indicates cohesin genes including RAD21 (∼10%), SMC1A (∼5%), and SMC3 (∼5%); b, inv(16)(p13.1q22) or t(16;16)(p13.1;q22); CBFB-MYH11; c, inv(3)(q21.3q26.2) or t(3;3)(q21.3;q26.2); GATA2,MECOM(EVI1); and d, TP53 mutations are found in ∼45%, and complex karyotypes in ∼70% of this class. The structure of the pie chart is adapted from Grimwade et al,50  generated by Adam Ivey (King’s College London, London, United Kingdom).

Close Modal

or Create an Account

Close Modal
Close Modal