Objective: To explore the influence of FLT3-ITD mutation and ITD mutation length on the prognosis in non-M3 acute myeloid leukemia (AML), overall survival (OS) and relapse free survival (RFS) were followed to evaluate the prognosis in AML patients. Methods: Clinical features and therapeutic effect were retrospectively analyzed in 75 AML patients with FLT3-ITD mutation and 76 AML patients without FLT3-ITD with normal karotype from June 2011 to April 2016. Genomic DNA was amplified by PCR, and FLT3-ITD mutation length was analyzed by DNA sequences. Results: AML patinets with FLT3-ITD mutation had higher WBC and the bone morrow (BM) blast than wild type without FLT3 mutation (WT ) (95.13 vs 10.85, P=0.000; 72% vs 59%, P=0.003). The incidence of complete remission (CR) in AML with FLT3-ITD mutation less than that in WT (70.42% vs 94.7%, P=0.001). OS (P=0.000) and RFS (P=0.000) were significantly longer in FLT3-ITD mutated AML who received allo-HSCT compared with these who received consolidation chemotherapy, and which were similar to patients with WT after allo-HSCT. Patients with maintenance sorafenib after allo-HSCT had longer OS (P=0.038) and RFS (P=0.048) than control group. AML patients with FLT3-ITDs exceeding 60 bp in length were associated with shorter OS compared with these with FLT3-ITDs less than 60 bp (P=0.028). OS and RFS were similar betwen the two groups with diferent ITD lengths which just received consolidation chemotherapy. Besides, AML patients with shorter ITDs who received allo-HSCT had longer OS than these patients with ITDs exceeding 60 bp (P=0.042), and which were also similar to patients with WT after allo-HSCT. Conclusion: AML patients with FLT3-ITD mutation had poor prognosis, even worse in patients with ITD exceeding 60bp. Chemotherapy alone didn't improve the survival of patients with FIT3-ITD mutation. Allo-HSCT is an effective therapeutic strategy for FLT3-ITD mutated AML patients. Sorafenib was approved to be an effective maintenance therapy after allo-HSCT in AML patients with FLT3-ITD mutation.

Disclosures

No relevant conflicts of interest to declare.

Author notes

*

Asterisk with author names denotes non-ASH members.

Sign in via your Institution