ReviewFrontiers in oncology2014
Molecular therapeutic approaches for pediatric acute myeloid leukemia.
Review in Frontiers in oncology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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.
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.
Who cites it
23 citing papers in PubMed, 38 citations in OpenAlex.
- A parsimonious 3-gene signature predicts clinical outcomes in an acute myeloid leukemia multicohort study.Blood advances · 2019Trial
- Gemtuzumab ozogamicin in children with relapsed or refractory acute myeloid leukemia: a report by Berlin-Frankfurt-Münster study group.Haematologica · 2019Trial
- MiR-15a-5p, c-MYB, and circHIPK3 Axis as a Potential Diagnostic and Clinicopathological-Related Network in Acute Myeloid Leukemia.Advanced biomedical research · 2025Article
- Diagnostic value of circular RNAs as promising hematological biomarkers in acute myeloid leukemia: A systematic review and meta-analysis.Journal of research in medical sciences : the official journal of Isfahan University of Medical Sciences · 2025Review
- IGF2BP2 promotes lncRNA DANCR stability mediated glycolysis and affects the progression of FLT3-ITD + acute myeloid leukemia.Apoptosis : an international journal on programmed cell death · 2023Article
- METTL3 affects FLT3-ITD+ acute myeloid leukemia by mediating autophagy by regulating PSMA3-AS1 stability.Cell cycle (Georgetown, Tex.) · 2023Article
- Proteomic Profiling Identifies Specific Leukemic Stem Cell-Associated Protein Expression Patterns in Pediatric AML Patients.Cancers · 2022Article
- High-Risk Acute Myeloid Leukemia: A Pediatric Prospective.Biomedicines · 2022Review
- Article
- Paediatric Strategy Forum for medicinal product development of chimeric antigen receptor T-cells in children and adolescents with cancer: ACCELERATE in collaboration with the European Medicines Agency with participation of the Food and Drug Administration.European journal of cancer (Oxford, England : 1990) · 2022Review
- Discovery of LDD-1075 as a potent FLT3 inhibitor.Oncology letters · 2019Article
- Advances in hematopoietic cell transplant for the treatment of hematologic malignancies.Current opinion in pediatrics · 2019Review
- Article
- Discovery of a FLT3 inhibitor LDD1937 as an anti-leukemic agent for acute myeloid leukemia.Oncotarget · 2018Article
- Article
- Epigenetic drug combination induces remission in mouse xenograft models of pediatric acute myeloid leukemia.Leukemia research · 2017Article
- Current Management of Childhood Acute Myeloid Leukemia.Paediatric drugs · 2017Review
- Gene Mutations as Emerging Biomarkers and Therapeutic Targets for Relapsed Acute Myeloid Leukemia.Frontiers in pharmacology · 2017Review
- Collaborative Efforts Driving Progress in Pediatric Acute Myeloid Leukemia.Journal of clinical oncology : official journal of the American Society of Clinical Oncology · 2015Review
- Targeting protein-protein interactions in hematologic malignancies: still a challenge or a great opportunity for future therapies?Immunological reviews · 2015Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 3 institutions in 1 country.
Funding
Abstract
Approximately two-thirds of children with acute myeloid leukemia (AML) are cured with intensive multi-agent chemotherapy. However, refractory and relapsed AML remains a significant source of childhood cancer mortality, highlighting the need for new therapies. Further therapy intensification with traditional cytotoxic chemotherapy in pediatric AML is not feasible given the risks of both short-term and long-term organ dysfunction. Substantial emphasis has been placed upon the development of molecularly targeted therapeutic approaches for adults and children with high-risk subtypes of AML with the goal of improving remission induction and minimizing relapse. Several promising agents are currently in clinical testing or late preclinical development for AML, including monoclonal antibodies against leukemia cell surface proteins, kinase inhibitors, proteasome inhibitors, epigenetic agents, and chimeric antigen receptor engineered T cell immunotherapies. Many of these therapies have been specifically tested in children with relapsed/refractory AML in Phase 1 and 2 trials with a smaller number of new agents under Phase 3 evaluation for children with de novo AML. Although successful identification and implementation of new drugs for children with AML remain a formidable challenge, enthusiasm for novel molecular therapeutic approaches is great given the potential for significant clinical benefit for children who do not have other curative options.
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What OpenQuestion holds
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.