Evidence map›Paper›PMID 31648336›Full record

ArticleBlood advances2019

Serum Flt3 ligand is a biomarker of progenitor cell mass and prognosis in acute myeloid leukemia.

Paul Milne, Charlotte Wilhelm-Benartzi, Michael R Grunwald, Venetia Bigley, Richard Dillon, Sylvie D Freeman, Kathleen Gallagher, Amy Publicover, Sarah Pagan, Helen Marr and 8 more

Open access · goldAbstract read
In one paragraph

Article in Blood advances, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.5field-weighted citation impact, top 17% 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

17 citing papers in PubMed, 22 citations in OpenAlex.

  1. Review
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  9. Immune therapy: a new therapy for acute myeloid leukemia.Blood science (Baltimore, Md.) · 2023
    Review
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  11. Article
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  16. Review
  17. Driver mutations in acute myeloid leukemia.Current opinion in hematology · 2020
    Review
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

18 authors at 9 institutions in 2 countries.

Paul MilneInstitute of Cellular Medicine, Newcastle University, Newcastle upon Tyne, United Kingdom.
Charlotte Wilhelm-BenartziCentre for Trials Research, College of Biomedical and Life Sciences, Cardiff University, Cardiff, United Kingdom.
Michael R GrunwaldDepartment of Hematologic Oncology and Blood Disorders, Levine Cancer Institute, Atrium Health, Charlotte, NC.
Venetia BigleyInstitute of Cellular Medicine, Newcastle University, Newcastle upon Tyne, United Kingdom.
Richard DillonDepartment of Medical and Molecular Genetics, King's College, Strand, London, United Kingdom.
Sylvie D FreemanClinical Immunology Service, Institute of Immunology and Immunotherapy, College of Medical and Dental Sciences, University of Birmingham Edgbaston, Birmingham, United Kingdom.
Kathleen GallagherImmune Monitoring Laboratory, Massachusetts General Hospital Center for Cancer Research, Boston, MA.
Amy PublicoverNorthern Centre for Cancer Care, Freeman Hospital, Newcastle upon Tyne Hospitals NHS Foundation Trust, Newcastle upon Tyne, United Kingdom.
Sarah PaganInstitute of Cellular Medicine, Newcastle University, Newcastle upon Tyne, United Kingdom.
Helen MarrNorthern Centre for Cancer Care, Freeman Hospital, Newcastle upon Tyne Hospitals NHS Foundation Trust, Newcastle upon Tyne, United Kingdom.
Gail L JonesNorthern Centre for Cancer Care, Freeman Hospital, Newcastle upon Tyne Hospitals NHS Foundation Trust, Newcastle upon Tyne, United Kingdom.
Anne M DickinsonInstitute of Cellular Medicine, Newcastle University, Newcastle upon Tyne, United Kingdom.
Angela GrechDepartment of Haematology, Cardiff University School of Medicine, Cardiff, United Kingdom.
Alan K BurnettDepartment of Haematology, Cardiff University School of Medicine, Cardiff, United Kingdom.
Nigel H RussellDepartment of Haematology, Nottingham University Hospital, Nottingham, United Kingdom; and.
Mark LevisDivision of Hematological Malignancies, Johns Hopkins Sidney Kimmel Cancer Center, Baltimore, MD.
Steven KnapperDepartment of Haematology, Cardiff University School of Medicine, Cardiff, United Kingdom.
Matthew CollinInstitute of Cellular Medicine, Newcastle University, Newcastle upon Tyne, United Kingdom.
Newcastle upon Tyne Hospital · GBCardiff University · GBNewcastle upon Tyne Hospitals NHS Foundation Trust · GBKing's College Hospital · GBLevine Cancer Institute · USMassachusetts General Hospital · USSidney Kimmel Cancer Center · USUniversity of Birmingham · GBUniversity of Nottingham · GB

Funding

Cancer Research UK 15954Cancer Research UK 21025Cancer Research UK 25350Cancer Research UK 25643Cancer Research UK C30484/A21025
6 · The paper itself

Abstract

Fms-like tyrosine kinase 3 (Flt3) is expressed on progenitor cells and acute myeloid leukemia (AML) blasts. Fms-like tyrosine kinase 3 ligand (Flt3L) is detectable during homeostasis and increases in hypoplasia due to genetic defects or treatment with cytoreductive agents. Conversely, Flt3+ AML is associated with depletion of Flt3L to undetectable levels. After induction chemotherapy, Flt3L is restored in patients entering complete remission (CR) but remains depressed in those with refractory disease. Weekly sampling reveals marked differences in the kinetics of Flt3L response during the first 6 weeks of treatment, proportionate to the clearance of blasts and cellularity of the bone marrow. In the UK NCRI AML17 trial, Flt3L was measured at day 26 in a subgroup of 140 patients with Flt3 mutation randomized to the tyrosine kinase inhibitor lestaurtinib or placebo. In these patients, attainment of CR was associated with higher Flt3L at day 26 (Mann-Whitney UP < .0001). Day 26 Flt3L was also associated with survival; Flt3L ≤291 pg/mL was associated with inferior event-free survival (EFS), and Flt3L >1185 pg/mL was associated with higher overall survival (OS; P = .0119). The separation of EFS and OS curves increased when minimal residual disease (MRD) status was combined with Flt3L measurement, and Flt3L retained a near-significant association with survival after adjusting for MRD in a proportional hazards model. Serial measurement of Flt3L in patients who had received a hematopoietic stem cell transplant for AML illustrates the potential value of monitoring Flt3L to identify relapse. Measurement of Flt3L is a noninvasive test with the potential to inform clinical decisions in patients with AML.

Indexed as

BiomarkersGene ExpressionHematopoietic Stem Cell TransplantationHumansImmunophenotypingInduction ChemotherapyLeukemia, Myeloid, AcuteMembrane ProteinsNeoplastic Stem CellsPrognosisProportional Hazards ModelsTreatment OutcomeBiomarkersflt3 ligand proteinMembrane Proteins

Identifiers

PMID31648336
PMCPMC6849950
OpenAlexW2982232092

What OpenQuestion holds

Textmetadata
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Registered trials

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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.