Literature DB >> 35258791

Which FLT3 Inhibitor for Treatment of AML?

Jayastu Senapati1, Tapan Mahendra Kadia2.   

Abstract

OPINION STATEMENT: Treatment options in acute myeloid leukemia (AML) have improved significantly over the last decade with better understanding of disease biology and availability of a multitude of targeted therapies. The use of FLT3 inhibitors (FLT3i) in FLT3-mutated (FLT3mut) AML is one such development; however, the clinical decisions that govern their use and dictate the choice of the FLT3i are evolving. Midostaurin and gilteritinib are FDA-approved in specific situations; however, available data from clinical trials also shed light on the utility of sorafenib maintenance post-allogeneic stem cell transplantation (allo-SCT) and quizartinib as part of combination therapy in FLT3mut AML. The knowledge of the patient's concurrent myeloid mutations, type of FLT3 mutation, prior FLT3i use, and eligibility for allo-SCT helps to refine the choice of FLT3i. Data from ongoing studies will further precisely define their use and help in making more informed choices. Despite improvements in FLT3i therapy, the definitive aim is to enable the eligible patient with FLT3mut AML (esp. ITD) to proceed to allo-SCT with regimens containing FLT3i incorporated prior to SCT and as maintenance after SCT.
© 2022. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.

Entities:  

Keywords:  AML; FLT3 inhibitor; Gilteritinib; Midostaurin; Quizartinib; Sorafenib

Mesh:

Substances:

Year:  2022        PMID: 35258791     DOI: 10.1007/s11864-022-00952-6

Source DB:  PubMed          Journal:  Curr Treat Options Oncol        ISSN: 1534-6277


  108 in total

1.  Genomic Classification and Prognosis in Acute Myeloid Leukemia.

Authors:  Elli Papaemmanuil; Moritz Gerstung; Hartmut Döhner; Peter J Campbell; Lars Bullinger; Verena I Gaidzik; Peter Paschka; Nicola D Roberts; Nicola E Potter; Michael Heuser; Felicitas Thol; Niccolo Bolli; Gunes Gundem; Peter Van Loo; Inigo Martincorena; Peter Ganly; Laura Mudie; Stuart McLaren; Sarah O'Meara; Keiran Raine; David R Jones; Jon W Teague; Adam P Butler; Mel F Greaves; Arnold Ganser; Konstanze Döhner; Richard F Schlenk
Journal:  N Engl J Med       Date:  2016-06-09       Impact factor: 91.245

2.  Analysis of FLT3-activating mutations in 979 patients with acute myelogenous leukemia: association with FAB subtypes and identification of subgroups with poor prognosis.

Authors:  Christian Thiede; Christine Steudel; Brigitte Mohr; Markus Schaich; Ulrike Schäkel; Uwe Platzbecker; Martin Wermke; Martin Bornhäuser; Markus Ritter; Andreas Neubauer; Gerhard Ehninger; Thomas Illmer
Journal:  Blood       Date:  2002-06-15       Impact factor: 22.113

3.  Co-occurrence of FLT3-TKD and NPM1 mutations defines a highly favorable prognostic AML group.

Authors:  Prajwal Boddu; Hagop Kantarjian; Gautam Borthakur; Tapan Kadia; Naval Daver; Sherry Pierce; Michael Andreeff; Farhad Ravandi; Jorge Cortes; Steven M Kornblau
Journal:  Blood Adv       Date:  2017-08-17

Review 4.  Differential signaling of Flt3 activating mutations in acute myeloid leukemia: a working model.

Authors:  Perry M Chan
Journal:  Protein Cell       Date:  2011-02-25       Impact factor: 14.870

Review 5.  Acute myeloid leukemia: Treatment and research outlook for 2021 and the MD Anderson approach.

Authors:  Hagop M Kantarjian; Tapan M Kadia; Courtney D DiNardo; Mary Alma Welch; Farhad Ravandi
Journal:  Cancer       Date:  2021-03-18       Impact factor: 6.860

6.  Meta-analysis for the potential application of FLT3-TKD mutations as prognostic indicator in non-promyelocytic AML.

Authors:  Wei Li; Li Zhang; Liang Huang; Yingchang Mi; Jianxiang Wang
Journal:  Leuk Res       Date:  2011-09-09       Impact factor: 3.156

7.  Internal tandem duplication of the flt3 gene found in acute myeloid leukemia.

Authors:  M Nakao; S Yokota; T Iwai; H Kaneko; S Horiike; K Kashima; Y Sonoda; T Fujimoto; S Misawa
Journal:  Leukemia       Date:  1996-12       Impact factor: 11.528

8.  Insertion of FLT3 internal tandem duplication in the tyrosine kinase domain-1 is associated with resistance to chemotherapy and inferior outcome.

Authors:  Sabine Kayser; Richard F Schlenk; Martina Correa Londono; Frank Breitenbuecher; Kerstin Wittke; Juan Du; Silja Groner; Daniela Späth; Jürgen Krauter; Arnold Ganser; Hartmut Döhner; Thomas Fischer; Konstanze Döhner
Journal:  Blood       Date:  2009-07-14       Impact factor: 22.113

Review 9.  Downstream molecular pathways of FLT3 in the pathogenesis of acute myeloid leukemia: biology and therapeutic implications.

Authors:  Shinichiro Takahashi
Journal:  J Hematol Oncol       Date:  2011-04-01       Impact factor: 17.388

10.  FLT3 tyrosine kinase domain mutations are biologically distinct from and have a significantly more favorable prognosis than FLT3 internal tandem duplications in patients with acute myeloid leukemia.

Authors:  Adam J Mead; David C Linch; Robert K Hills; Keith Wheatley; Alan K Burnett; Rosemary E Gale
Journal:  Blood       Date:  2007-04-24       Impact factor: 22.113

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