Evidence map›Paper›PMID 30332834›Full record

ReviewInternational journal of molecular sciences2018

Targeting Oncogenic Signaling in Mutant FLT3 Acute Myeloid Leukemia: The Path to Least Resistance.

Dilana Staudt, Heather C Murray, Tabitha McLachlan, Frank Alvaro, Anoop K Enjeti, Nicole M Verrills, Matthew D Dun

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
5.1field-weighted citation impact, top 4% 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

41 citing papers in PubMed, 74 citations in OpenAlex.

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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

7 authors at 2 institutions in 1 country.

Dilana StaudtSchool of Biomedical Sciences and Pharmacy, Faculty of Health and Medicine, University of Newcastle, Callaghan, NSW 2308, Australia. Dilana.StaudtBarreto@uon.edu.au.ORCID 0000-0001-5049-2208
Heather C MurraySchool of Biomedical Sciences and Pharmacy, Faculty of Health and Medicine, University of Newcastle, Callaghan, NSW 2308, Australia. Heather.C.Murray@uon.edu.au.
Tabitha McLachlanSchool of Biomedical Sciences and Pharmacy, Faculty of Health and Medicine, University of Newcastle, Callaghan, NSW 2308, Australia. Tabitha.McLachlan@uon.edu.au.ORCID 0000-0002-6633-974X
Frank AlvaroPriority Research Centre for Cancer Research, Innovation & Translation, Faculty of Health & Medicine, Hunter Medical Research Institute, New Lambton Heights, NSW 2305, Australia. Frank.Alvaro@hnehealth.nsw.gov.au.
Anoop K EnjetiPriority Research Centre for Cancer Research, Innovation & Translation, Faculty of Health & Medicine, Hunter Medical Research Institute, New Lambton Heights, NSW 2305, Australia. Anoop.Enjeti@calvarymater.org.au.
Nicole M VerrillsSchool of Biomedical Sciences and Pharmacy, Faculty of Health and Medicine, University of Newcastle, Callaghan, NSW 2308, Australia. nikki.verrills@newcastle.edu.au.
Matthew D DunSchool of Biomedical Sciences and Pharmacy, Faculty of Health and Medicine, University of Newcastle, Callaghan, NSW 2308, Australia. matt.dun@newcastle.edu.au.ORCID 0000-0002-9063-5370
Hunter Medical Research Institute · AUJohn Hunter Hospital · AU

Funding

Cancer Institute NSW MD00487Hunter Medical Research Institute G1701507 Zebra Equities
6 · The paper itself

Abstract

The identification of recurrent driver mutations in genes encoding tyrosine kinases has resulted in the development of molecularly-targeted treatment strategies designed to improve outcomes for patients diagnosed with acute myeloid leukemia (AML). The receptor tyrosine kinase FLT3 is the most commonly mutated gene in AML, with internal tandem duplications within the juxtamembrane domain (FLT3-ITD) or missense mutations in the tyrosine kinase domain (FLT3-TKD) present in 30⁻35% of AML patients at diagnosis. An established driver mutation and marker of poor prognosis, the FLT3 tyrosine kinase has emerged as an attractive therapeutic target, and thus, encouraged the development of FLT3 tyrosine kinase inhibitors (TKIs). However, the therapeutic benefit of FLT3 inhibition, particularly as a monotherapy, frequently results in the development of treatment resistance and disease relapse. Commonly, FLT3 inhibitor resistance occurs by the emergence of secondary lesions in the

Indexed as

OncogenesSignal TransductionAnimalsDrug Resistance, Neoplasmfms-Like Tyrosine Kinase 3HumansLeukemia, Myeloid, AcuteMutationfms-Like Tyrosine Kinase 3acute myeloid leukemiaFLT3resistancetyrosine kinase inhibitors

Identifiers

PMID30332834
PMCPMC6214138
OpenAlexW2891169131

What Socratic 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 Socratic graph.