Sickle cell disease and hyperreactive malarial splenomegaly (HMS) in young immigrants from Africa.

patient 2112 is in continued complete remission (CCR; 61 ). Interestingly, patient 1179 showed no FLT3/ITD mutation at relapse (Figure 1C), possibly due to loss of the mutated allele during therapy, or, alternatively, the FLT3/ITD-positive clone was eliminated during chemotherapy with a subsequent relapse from a non–FLT3-mutated parental clone. In conclusion, we confirm the presence of FLT3 mutations in pediatric T-ALL (2/72; 2.7%). Although both immature, the immunophenotypes of the FLT3-mutated pediatric and adult2 T-ALL cases differed. In addition, a link between mRNA expression of cKIT/CD117 and FLT3 mutations could not be demonstrated. Since patient 2112 is in CCR and relapse material of patient 1179 did not show evidence for FLT3 mutation, the FLT3-mutated T-ALL subclone seems to be effectively eradicated by current chemotherapy. This suggests that the application of FLT3 inhibitors for FLT3-mutated T-ALL, as suggested by Paietta et al,2 may not further improve treatment outcome in pediatric T-ALL.