ArticleNature2016
A 17-gene stemness score for rapid determination of risk in acute leukaemia.
Article in Nature, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 584 papers, 2 of them syntheses that pooled 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.
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
584 citing papers in PubMed, 2 syntheses or guidelines pooled it, 896 citations in OpenAlex.
- Prognostic value of measuring LSC frequency in AML: a systematic review and meta-analysis.Blood advances · 2026Pooled it
- Epithelial membrane protein 1 in human cancer: a potential diagnostic biomarker and therapeutic target.Biomarkers in medicine · 2024Pooled it
- Azacitidine, Venetoclax, and Magrolimab in Newly Diagnosed and Relapsed Refractory Acute Myeloid Leukemia: Phase Ib/II Study and Correlative Analysis.Clinical cancer research : an official journal of the American Association for Cancer Research · 2025Trial
- Genetic deletion of JAM-C in preleukemic cells rewires leukemic stem cell gene expression program in AML.Blood advances · 2024Trial
- Imetelstat-mediated alterations in fatty acid metabolism to induce ferroptosis as a therapeutic strategy for acute myeloid leukemia.Nature cancer · 2024Trial
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- Unifying multimodal single-cell data with a mixture-of-experts β-variational autoencoder framework.Genome research · 2026Article
- Inflammatory Network Remodeling in AML Is Driven by Neutrophil-Centric Self-Amplifying Circuits.International journal of molecular sciences · 2026Article
- Non-genetic remodeling drives leukemia propagation and reveals actionable vulnerabilities in acute myeloid leukemia.Cell reports. Medicine · 2026Article
- Messenger RNA From Canine Cytology Lymph Node Specimens Can Be Utilised for Gene Expression Profiling Using Digital RNA Counting.Veterinary and comparative oncology · 2026Article
- A parallel-risk framework accurately predicts hematopoietic stem cell transplantation outcomes and identifies benefiting patients in pediatric AML.Genes & diseases · 2026Article
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- Putting the I in AML: Artificial Intelligence and Machine Learning in Acute Myeloid Leukemia.Cells · 2026Review
- Multilayer modeling reveals an endogenous retrovirus signature predictive of induction chemotherapy failure in AML.Blood neoplasia · 2026Article
- Article
- Co-option of lineage plasticity as a hallmark of multipotent acute leukemias.Blood neoplasia · 2026Review
- DNA Methylation of Pharmacologic and Leukemia-Related Genes Predicts Clinical Outcomes in Pediatric Acute Myeloid Leukemia.Cancers · 2026Article
- Single-cell long-read genotyping of transcripts reveals discrete mechanisms of clonal evolution in post-MPN AML.Blood advances · 2026Article
524 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
30 authors at 12 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Refractoriness to induction chemotherapy and relapse after achievement of remission are the main obstacles to cure in acute myeloid leukaemia (AML). After standard induction chemotherapy, patients are assigned to different post-remission strategies on the basis of cytogenetic and molecular abnormalities that broadly define adverse, intermediate and favourable risk categories. However, some patients do not respond to induction therapy and another subset will eventually relapse despite the lack of adverse risk factors. There is an urgent need for better biomarkers to identify these high-risk patients before starting induction chemotherapy, to enable testing of alternative induction strategies in clinical trials. The high rate of relapse in AML has been attributed to the persistence of leukaemia stem cells (LSCs), which possess a number of stem cell properties, including quiescence, that are linked to therapy resistance. Here, to develop predictive and/or prognostic biomarkers related to stemness, we generated a list of genes that are differentially expressed between 138 LSC
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Identifiers
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.