Table 3.
Somatic mutations producing clonal hematopoiesis of oncogenic potential (CHOP).
Effects of the Mutant on Clonal Cells | Affected | |||
---|---|---|---|---|
Mutation | Differentiation | Proliferation | Oncogenesis | Myeloid Neoplasm |
BCR-ABL1p210 | + | + | + * | Ph+ CML |
JAK2 V617F | + | +/- | - | MPN |
CALR mutations | + | +/- | - | MPN |
MPL mutations | ++ | +/- | - | |
KIT D816V | ++ | +/- | - | ISM and AdvSM |
FIP1L1-PDGFRA | + | +/- | - | CEL, MPN-eo |
RUNX1- RUNX1T1 | +/- | ++ | + | AML |
CBFβ-MYH11 | +/- | ++ | + | AML |
FLT3 ITD mutations | +/- | + | +/- | AML |
NPM1 mutations | - | ++ | +/- | AML |
KRAS, HRAS mutations | - | ++ | + | AML |
TP53 mutations | - | + | + | MPN, CMML, AML |
* The oncogenic potential of BCR-ABL1 is well documented and correlates with the invariable transition of (untreated) chronic phase CML into accelerated and blast phase CML. Abbreviations: Ph+ CML, Philadelphia chromosome-positive chronic myeloid leukemia; MPN, myeloproliferative neoplasms; ISM, indolent systemic mastocytosis; AdvSM, advanced systemic mastocytosis; CEL, chronic eosinophilic leukemia; MPN-eo, MPN with eosinophilia; AML, acute myeloid leukemia; CMML, chronic myelomonocytic leukemia.