Evidence map›Paper›PMID 31919472›Full record

ReviewLeukemia2020

FLT3 inhibitors in acute myeloid leukemia: ten frequently asked questions.

Ahmad I Antar, Zaher K Otrock, Elias Jabbour, Mohamad Mohty, Ali Bazarbachi

Registry-linked trialAbstract readReview
PubMed Publisher
In one paragraph

Review in Leukemia, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT07320235 (IMetelstat and Azacitidine With or Without Venetoclax GIveN in rElapsed Acute Myeloid Leukemia), which is not on this map. Cited by 126 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
126citing papers in PubMed, 4 pooled it
20.0field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

NCT07320235 phase1recruitingnot on this mapstarted 2026, after this paper: background citation

IMetelstat and Azacitidine With or Without Venetoclax GIveN in rElapsed Acute Myeloid Leukemia (IMAGINE Trial)

TypeinterventionalSponsorDouglas TremblayRan2026 to 2035Enrolled36ConditionsRelapsed Acute Myeloid LeukemiaArmsImetelstat, Azacitidine, Venetoclax
3 · Its place in the literature

Who cites it

126 citing papers in PubMed, 4 syntheses or guidelines pooled it, 233 citations in OpenAlex.

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  8. The Mutational Landscape of Acute Myeloid Leukemia and Its Impact.International journal of molecular sciences · 2026
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66 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 5 institutions in 3 countries.

Ahmad I AntarDepartment of Hematology and Oncology, Hammoud Hospital University Medical Center, Saida, Lebanon.
Zaher K OtrockDepartment of Pathology and Laboratory Medicine, Henry Ford Hospital, Wayne State University, Detroit, MI, USA.
Elias JabbourDepartment of Leukemia, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Mohamad MohtyService d'hématologie clinique et thérapie cellulaire, Hôpital Saint-Antoine, INSERM UMRs 938 and université Sorbonne, Paris, France.
Ali BazarbachiBone Marrow Transplantation Program, Department of Internal Medicine, American University of Beirut Medical Center, Beirut, Lebanon. bazarbac@aub.edu.lb.
American University of Beirut Medical Center · LBHammoud Hospital University Medical Center · LBInserm · FRThe University of Texas MD Anderson Cancer Center · USWayne State University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The FMS-like tyrosine kinase 3 (FLT3) gene is mutated in approximately one third of patients with acute myeloid leukemia (AML), either by internal tandem duplications (FLT3-ITD), or by a point mutation mainly involving the tyrosine kinase domain (FLT3-TKD). Patients with FLT3-ITD have a high risk of relapse and low cure rates. Several FLT3 tyrosine kinase inhibitors have been developed in the last few years with variable kinase inhibitory properties, pharmacokinetics, and toxicity profiles. FLT3 inhibitors are divided into first generation multi-kinase inhibitors (such as sorafenib, lestaurtinib, midostaurin) and next generation inhibitors (such as quizartinib, crenolanib, gilteritinib) based on their potency and specificity of FLT3 inhibition. These diverse FLT3 inhibitors have been evaluated in myriad clinical trials as monotherapy or in combination with conventional chemotherapy or hypomethylating agents and in various settings, including front-line, relapsed or refractory disease, and maintenance therapy after consolidation chemotherapy or allogeneic stem cell transplantation. In this practical question-and-answer-based review, the main issues faced by the leukemia specialists on the use of FLT3 inhibitors in AML are addressed.

Indexed as

Aniline CompoundsAntineoplastic AgentsBenzimidazolesBenzothiazolesCarbazolesDNA MethylationEnzyme Inhibitorsfms-Like Tyrosine Kinase 3FuransHumansLeukemia, Myeloid, AcuteMutationNeoplasm Recurrence, LocalPhenylurea CompoundsPiperidinesPrognosisAniline CompoundsAntineoplastic AgentsBenzimidazolesBenzothiazolesCarbazolescrenolanibEnzyme InhibitorsFLT3 protein, humanfms-Like Tyrosine Kinase 3FuransgilteritiniblestaurtinibmidostaurinPhenylurea CompoundsPiperidinesPyrazinesquizartinibSorafenibStaurosporine

Identifiers

PMID31919472
OpenAlexW3000653492

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.