Evidence map›Paper›PMID 31336846›Full record

ReviewInternational journal of molecular sciences2019

Targeting Tyrosine Kinases in Acute Myeloid Leukemia: Why, Who and How?

Solène Fernandez, Vanessa Desplat, Arnaud Villacreces, Amélie V Guitart, Noël Milpied, Arnaud Pigneux, Isabelle Vigon, Jean-Max Pasquet, Pierre-Yves Dumas

Registry-linked trialAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT05042531 (Clinical Research for Azacitidine Combined With Low-dose Dasatinib in Maintenance Therapy of Acute Myeloid Leukemia), which is not on this map. Cited by 28 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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.

NCT05042531 naunknown statusnot on this mapstarted 2021, after this paper: background citation

Clinical Research for Azacitidine Combined With Low-dose Dasatinib in Maintenance Therapy of Acute Myeloid Leukemia

TypeinterventionalSponsorLanZhou UniversityRan2021 to 2023Enrolled30ConditionsAcute Myeloid LeukemiaArmsAzacitidine, Dasatinib
3 · Its place in the literature

Who cites it

28 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
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  6. Molecular medicine reports · 2024
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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

9 authors.

Solène FernandezInstitut National de la Santé et de la Recherche Médicale, U1035 Bordeaux, France.
Vanessa DesplatInstitut National de la Santé et de la Recherche Médicale, U1035 Bordeaux, France.
Arnaud VillacrecesInstitut National de la Santé et de la Recherche Médicale, U1035 Bordeaux, France.ORCID 0000-0002-2868-2264
Amélie V GuitartInstitut National de la Santé et de la Recherche Médicale, U1035 Bordeaux, France.ORCID 0000-0002-1451-8789
Noël MilpiedInstitut National de la Santé et de la Recherche Médicale, U1035 Bordeaux, France.
Arnaud PigneuxInstitut National de la Santé et de la Recherche Médicale, U1035 Bordeaux, France.
Isabelle VigonInstitut National de la Santé et de la Recherche Médicale, U1035 Bordeaux, France.
Jean-Max PasquetInstitut National de la Santé et de la Recherche Médicale, U1035 Bordeaux, France.ORCID 0000-0002-1345-3776
Pierre-Yves DumasInstitut National de la Santé et de la Recherche Médicale, U1035 Bordeaux, France. pierre-yves.dumas@u-bordeaux.fr.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Acute myeloid leukemia (AML) is a myeloid malignancy carrying a heterogeneous molecular panel of mutations participating in the blockade of differentiation and the increased proliferation of myeloid hematopoietic stem and progenitor cells. The historical "3 + 7" treatment (cytarabine and daunorubicin) is currently challenged by new therapeutic strategies, including drugs depending on the molecular landscape of AML. This panel of mutations makes it possible to combine some of these new treatments with conventional chemotherapy. For example, the FLT3 receptor is overexpressed or mutated in 80% or 30% of AML, respectively. Such anomalies have led to the development of targeted therapies using tyrosine kinase inhibitors (TKIs). In this review, we document the history of TKI targeting, FLT3 and several other tyrosine kinases involved in dysregulated signaling pathways.

Indexed as

Biomarkers, TumorMolecular Targeted TherapyAnimalsAntineoplastic AgentsClinical Trials as TopicGene Expression Regulation, LeukemicHumansLeukemia, Myeloid, AcuteProtein Kinase InhibitorsProtein-Tyrosine KinasesProteomeSignal TransductionTranscriptomeTreatment OutcomeAntineoplastic AgentsBiomarkers, TumorProtein Kinase InhibitorsProtein-Tyrosine KinasesProteomeacute myeloid leukemiainhibitorstargeted therapytyrosine kinase

Identifiers

PMID31336846
PMCPMC6679203

What OpenQuestion holds

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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.