ArticleJournal of cancer research and clinical oncology2017
Outcome of FLT3-ITD-positive acute myeloid leukemia: impact of allogeneic stem cell transplantation and tyrosine kinase inhibitor treatment.
Article in Journal of cancer research and clinical oncology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 1 of them a synthesis that pooled it.
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Who cites it
14 citing papers in PubMed, 1 synthesis or guideline pooled it.
- E-26 Transformation-specific Related Gene Expression and Outcomes in Cytogenetically Normal Acute Myeloid Leukemia: A Meta-analysis.Chinese medical journal · 2017Pooled it
- Olutasidenib for mutated IDH1 acute myeloid leukemia: final five-year results from the phase 2 pivotal cohort.Journal of hematology & oncology · 2025Trial
- Pre-transplant FLT3/ITD status predicts outcome in FLT3-mutated acute myeloid leukemia following allogeneic stem cell transplantation.Annals of hematology · 2020Trial
- Observational
- Enhancing Therapeutic Efficacy of FLT3 Inhibitors with Combination Therapy for Treatment of Acute Myeloid Leukemia.International journal of molecular sciences · 2024Review
- Assessment of 2022 European LeukemiaNet risk classification system in real-world cohort from China.Cancer medicine · 2023Article
- Mixed phenotype acute leukemia with PML-RARα positive: a case report and literature review.Molecular cytogenetics · 2021Article
- Review
- High IFITM3 expression predicts adverse prognosis in acute myeloid leukemia.Cancer gene therapy · 2020Article
- Advances in targeted therapy for acute myeloid leukemia.Biomarker research · 2020Review
- Association between increased mutation rates in DNMT3A and FLT3-ITD and poor prognosis of patients with acute myeloid leukemia.Experimental and therapeutic medicine · 2019Article
- The Impact ofCancers · 2019Review
- Quizartinib (AC220): a promising option for acute myeloid leukemia.Drug design, development and therapy · 2019Review
- The novel three-way variant t(6;17;15)(p21;q21;q22) in acute promyelocytic leukemia with an FLT3-ITD mutation: A case report.Oncology letters · 2018Article
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8 authors.
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Abstract
backgroundActivating mutations of the receptor tyrosine kinase FLT3 (fms-related tyrosine kinase 3) reflect the most frequent molecular aberration in acute myeloid leukemia (AML). In particular, FLT3 internal tandem duplications (FLT3-ITD) are characterized by an unfavorable prognosis and allogeneic stem cell transplantation (allogeneic SCT) in first complete remission is recommended. In case of imminent or frank relapse following allogeneic SCT, treatment with FLT3 tyrosine kinase inhibitors (TKI) constitutes a promising clinical approach to induce hematologic remission without conventional chemotherapy. PATIENTS AND
methodsWe retrospectively analyzed the response to induction chemotherapy and the outcome of 76 patients with FLT3-ITD-positive AML including 50 patients who underwent allogeneic SCT. Furthermore, efficacy of TKI treatment was evaluated in 18 patients (median age 54 years, range 21-74) with relapsed or refractory FLT3-ITD-positive AML.
resultsResponse to induction chemotherapy in 76 FLT3-ITD-positive AML patients was characterized by a complete remission (CR) rate of 68%. In total, 50 of 76 patients (66%) underwent allogeneic SCT including 40 patients (80%) in CR. Relapse of AML was observed in 21 of 47 patients (45%) after allogeneic SCT with a median relapse-free survival (RFS) of 13 months (range 3-224) for patients with CR prior to or at day +30 after SCT. Myeloablative conditioning resulted in an improved median RFS of 29 months (4-217) as compared to a reduced intensity conditioning protocol prior to allogeneic SCT with a RFS of 8 months (1-197, P = 0.048), respectively. Median OS of FLT3-ITD-positive AML was 17 months (5-225) for patients who received an allogeneic SCT as compared to 9 months (1-184) for patients who did not undergo SCT. Response of FLT3-ITD-positive AML to sorafenib was characterized by only 3 of 18 patients achieving a bone marrow response (17%), while there was no response to second-line treatment with ponatinib.
conclusionThis "real-life" data reflect the continuing challenge of FLT3-ITD-positive AML and confirm the poor outcome even after allogeneic SCT. Furthermore, efficacy of TKI treatment of relapsed or refractory FLT3-ITD AML is still limited and requires substantial improvement, e.g., by the introduction of second-generation inhibitors targeting constitutively active FLT3.
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