Figure 3
Figure 3. multiple genetic abnormalities at LT found with comprehensive sequencing. Comprehensive sequencing of paired MPN samples that later transformed to AML found multiple genetic abnormalities at transformation as shown by (A) paired MPN/AML mutational diagram as well as (B-D) 3 illustrative cases. For instance, gain of TET2 and KRas mutations (B), loss of JAK2 mutation and acquisition of IDH2 and TP53 mutations (C), and loss of the JAK2 mutation but acquisition of activating mutation in FLT3 could all be observed by comparing chronic MPN and leukemic states. SRSF2 mutations when present in the AML state were always present in the paired antecedent MPN sample. Mutations in c-kit, EZH2, WT1, KRas, HRas, IDH1, U2AF1, SF3B1, ZRSR2, PTEN, RUNX1, and DNMT3a were not seen in either state in this set of patients and hence are not displayed here.

multiple genetic abnormalities at LT found with comprehensive sequencing. Comprehensive sequencing of paired MPN samples that later transformed to AML found multiple genetic abnormalities at transformation as shown by (A) paired MPN/AML mutational diagram as well as (B-D) 3 illustrative cases. For instance, gain of TET2 and KRas mutations (B), loss of JAK2 mutation and acquisition of IDH2 and TP53 mutations (C), and loss of the JAK2 mutation but acquisition of activating mutation in FLT3 could all be observed by comparing chronic MPN and leukemic states. SRSF2 mutations when present in the AML state were always present in the paired antecedent MPN sample. Mutations in c-kit, EZH2, WT1, KRas, HRas, IDH1, U2AF1, SF3B1, ZRSR2, PTEN, RUNX1, and DNMT3a were not seen in either state in this set of patients and hence are not displayed here.

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