Evidence map›Paper›PMID 38112995›Full record

ReviewInternational journal of hematology2024

FLT3 targeting in the modern era: from clonal selection to combination therapies.

Vanessa E Kennedy, Catherine C Smith

Open access · hybridAbstract readReview
In one paragraph

Review in International journal of hematology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
4.4field-weighted citation impact, top 5% 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

12 citing papers in PubMed, 15 citations in OpenAlex.

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  9. Metabolic Signature ofJournal of personalized medicine · 2025
    Review
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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

2 authors at 1 institution in 1 country.

Vanessa E KennedyDivision of Hematology/Oncology, Department of Medicine, University of California San Francisco, 505 Parnassus Ave, Box 1270, San Francisco, CA, 94143, USA.
Catherine C SmithDivision of Hematology/Oncology, Department of Medicine, University of California San Francisco, 505 Parnassus Ave, Box 1270, San Francisco, CA, 94143, USA. catherine.smith@ucsf.edu.ORCID http://orcid.org/0000-0003-0160-7026
University of California, San Francisco · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Fms-like tyrosine kinase 3 (FLT3) is the most frequently mutated gene in acute myeloid leukemia (AML). Modern targeting of FLT3 with inhibitors has improved clinical outcomes and FLT3 inhibitors have been incorporated into the treatment of AML in all phases of the disease, including the upfront, relapsed/refractory and maintenance settings. This review will discuss the current understanding of FLT3 biology, the clinical use of FLT3 inhibitors, resistance mechanisms and emerging combination treatment strategies.

Indexed as

Drug Resistance, Neoplasmfms-Like Tyrosine Kinase 3Leukemia, Myeloid, AcuteMolecular Targeted TherapyProtein Kinase InhibitorsAntineoplastic Combined Chemotherapy ProtocolsHumansMutationFLT3 protein, humanfms-Like Tyrosine Kinase 3Protein Kinase InhibitorsAcute Myeloid LeukemiaAMLClonal EvolutionFLT3FLT3 inhibitor

Identifiers

PMID38112995
PMCPMC11513752
OpenAlexW4389940248

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.