Cbf Aml and additional mutations

Neither RUNX1-CBFA2T1 nor CBFB-MYH11 alone are capable of inducing overt AML. These fusion genes dictate the phenotype of the disease, but additional abnormalities are required for the leukemic transformation. Recent studies have demonstrated that 40% of AML patients with inv(16) acquire either KIT exon 8, KIT Asp816, FLT3 ITD, or FLT3 Asp835 mutations.63 64

Mutations of the KIT gene were less common in t(8;21) AML, with a frequency of about 13% and were absent in non-CBF AML.64 Mutations of the FLT3 and KIT gene were mutually exclusive.

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