Evidence map›Paper›PMID 31821677›Full record

ReviewCancer science2020

FLT3 mutations in acute myeloid leukemia: Therapeutic paradigm beyond inhibitor development.

Hitoshi Kiyoi, Naomi Kawashima, Yuichi Ishikawa

Open access · goldAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Cancer science, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 180 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
180citing papers in PubMed, 3 pooled it
13.1field-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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

180 citing papers in PubMed, 3 syntheses or guidelines pooled it, 282 citations in OpenAlex.

  1. Pooled it
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  9. FLT3-Mutated AML: Transplanting with Precision in the Targeted Era.Current hematologic malignancy reports · 2026
    Review
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  15. 6-(2-Aminoethyl)-6Biomolecules · 2026
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  18. Review
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120 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

3 authors at 1 institution in 1 country.

Hitoshi KiyoiDepartment of Hematology and Oncology, Nagoya University Graduate School of Medicine, Nagoya, Japan.ORCID https://orcid.org/0000-0001-6382-9498
Naomi KawashimaDepartment of Hematology and Oncology, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Yuichi IshikawaDepartment of Hematology and Oncology, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Nagoya University · JP

Funding

Japan Agency for Medical Research and DevelopmentJapan Science and Technology AgencyMinistry of Education, Culture, Sports, Science and Technology 17K09921Nagoya University Hospital
6 · The paper itself

Abstract

FMS-like tyrosine kinase 3 (FLT3) is a type III receptor tyrosine kinase that plays an important role in hematopoietic cell survival, proliferation and differentiation. The most clinically important point is that mutation of the FLT3 gene is the most frequent genetic alteration and a poor prognostic factor in acute myeloid leukemia (AML) patients. There are two major types of FLT3 mutations: internal tandem duplication mutations in the juxtamembrane domain (FLT3-ITD) and point mutations or deletion in the tyrosine kinase domain (FLT3-TKD). Both mutant FLT3 molecules are activated through ligand-independent dimerization and trans-phosphorylation. Mutant FLT3 induces the activation of multiple intracellular signaling pathways, mainly STAT5, MAPK and AKT signals, leading to cell proliferation and anti-apoptosis. Because high-dose chemotherapy and allogeneic hematopoietic stem cell transplantation cannot sufficiently improve the prognosis, clinical development of FLT3 kinase inhibitors expected. Although several FLT3 inhibitors have been developed, it takes more than 20 years from the first identification of FLT3 mutations until FLT3 inhibitors become clinically available for AML patients with FLT3 mutations. To date, three FLT3 inhibitors have been clinically approved as monotherapy or combination therapy with conventional chemotherapeutic agents in Japan and/or Europe and United states. However, several mechanisms of resistance to FLT3 inhibitors have already become apparent during their clinical trials. The resistance mechanisms are complex and emerging resistant clones are heterogenous. Further basic and clinical studies are required to establish the best therapeutic strategy for AML patients with FLT3 mutations.

Indexed as

Clinical Trials as TopicDrug Resistance, Neoplasmfms-Like Tyrosine Kinase 3HumansLeukemia, Myeloid, AcutePoint MutationProtein DomainsProtein Kinase InhibitorsSegmental Duplications, GenomicSequence DeletionSignal TransductionFLT3 protein, humanfms-Like Tyrosine Kinase 3Protein Kinase Inhibitorsacute myeloid leukemiaFMS-like tyrosine kinaseinhibitorresistancetyrosine kinase

Identifiers

PMID31821677
PMCPMC7004512
OpenAlexW2995587299

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

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.