» Articles » PMID: 30112274

The Role of FLT3 Inhibitors As Maintenance Therapy Following Hematopoietic Stem Cell Transplant

Overview
Journal Leuk Res Rep
Date 2018 Aug 17
PMID 30112274
Citations 5
Authors
Affiliations
Soon will be listed here.
Abstract

Activating mutations in FLT3 in acute myeloid leukemia (AML) portend a poor prognosis, and targeting FLT3 with a tyrosine kinase inhibitor has been an area of intense research recently. Most FLT3 mutated AML patients undergo hematopoietic stem cell transplantation (HSCT) as standard of care but a significant proportion of patients relapse. Although the use of FLT3 inhibitors in the pre-HSCT perspective is more clearly defined, its use in the post-HSCT scenario, when most relapses occur, remains unclear. In this review, we comprehensively present the data on the recent and ongoing studies evaluating the role of various FLT3 inhibitors in AML with a particular focus in the post-HSCT setting.

Citing Articles

Post-transplant maintenance therapy in patients with FLT3-mutated acute myeloid leukemia: Real-world treatment patterns and outcomes.

Griffin J, Song Y, Yang H, Freimark J, Shah M Eur J Haematol. 2021; 107(5):553-565.

PMID: 34289175 PMC: 9292256. DOI: 10.1111/ejh.13692.


Two Novel Mutations in a Turkish Patient with Acute Myeloid Leukemia.

Tokgun P, Alay M, Atli Tekin S, Guler N, Tokgun O, Demiray A Balkan J Med Genet. 2021; 23(2):99-102.

PMID: 33816079 PMC: 8009566. DOI: 10.2478/bjmg-2020-0024.


Gilteritinib induces PUMA-dependent apoptotic cell death via AKT/GSK-3β/NF-κB pathway in colorectal cancer cells.

Li L, Lin L, Li M, Li W J Cell Mol Med. 2019; 24(3):2308-2318.

PMID: 31881122 PMC: 7011145. DOI: 10.1111/jcmm.14913.


The Interplay Between the Genetic and Immune Landscapes of AML: Mechanisms and Implications for Risk Stratification and Therapy.

Mendez L, Posey R, Pandolfi P Front Oncol. 2019; 9:1162.

PMID: 31781488 PMC: 6856667. DOI: 10.3389/fonc.2019.01162.


Quizartinib (AC220): a promising option for acute myeloid leukemia.

Zhou F, Ge Z, Chen B Drug Des Devel Ther. 2019; 13:1117-1125.

PMID: 31114157 PMC: 6497874. DOI: 10.2147/DDDT.S198950.

References
1.
Wander S, Levis M, Fathi A . The evolving role of FLT3 inhibitors in acute myeloid leukemia: quizartinib and beyond. Ther Adv Hematol. 2014; 5(3):65-77. PMC: 4031904. DOI: 10.1177/2040620714532123. View

2.
Antar A, Otrock Z, El-Cheikh J, Kharfan-Dabaja M, Battipaglia G, Mahfouz R . Inhibition of FLT3 in AML: a focus on sorafenib. Bone Marrow Transplant. 2016; 52(3):344-351. DOI: 10.1038/bmt.2016.251. View

3.
Schiller G, Tuttle P, Desai P . Allogeneic Hematopoietic Stem Cell Transplantation in FLT3-ITD-Positive Acute Myelogenous Leukemia: The Role for FLT3 Tyrosine Kinase Inhibitors Post-Transplantation. Biol Blood Marrow Transplant. 2016; 22(6):982-990. DOI: 10.1016/j.bbmt.2016.01.013. View

4.
Nagel G, Weber D, Fromm E, Erhardt S, Lubbert M, Fiedler W . Epidemiological, genetic, and clinical characterization by age of newly diagnosed acute myeloid leukemia based on an academic population-based registry study (AMLSG BiO). Ann Hematol. 2017; 96(12):1993-2003. PMC: 5691091. DOI: 10.1007/s00277-017-3150-3. View

5.
Chen Y, Huang Y, Reiberger T, Duyverman A, Huang P, Samuel R . Differential effects of sorafenib on liver versus tumor fibrosis mediated by stromal-derived factor 1 alpha/C-X-C receptor type 4 axis and myeloid differentiation antigen-positive myeloid cell infiltration in mice. Hepatology. 2013; 59(4):1435-47. PMC: 3966948. DOI: 10.1002/hep.26790. View