Figure 4.
TET2 mutations as background mutations. Thanks to TET2 mutations as background mutations, the disease will occur and develop by the accumulation of additional mutations. In the first example (42), TET2-D1384V in HSCs, then in NPM1 and FLT3 mutation, induced an AML. In the second example (31, 44), TET2 mutation with JAK2V617F-positive generated thrombocythemia, which can transform into secondary myelofibrosis due to an additional ASXL1 mutation. In the third example (23), mutations in SRSF2, then in KRAS mutation developed a chronic myelomonocytic leukemia (CMML).
