ReviewCell death discovery2022
The genesis and evolution of acute myeloid leukemia stem cells in the microenvironment: From biology to therapeutic targeting.
Review in Cell death discovery, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 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
37 citing papers in PubMed, 44 citations in OpenAlex.
- Article
- Bispecific Antibodies for Acute Myeloid Leukemia: From Bone Marrow Immune Niche to Clinical Translation.Antibodies (Basel, Switzerland) · 2026Review
- Ferumoxytol enhances NF-κB-responsive GBA-targeted ferroptosis gene therapy in acute myeloid leukemia.Journal of nanobiotechnology · 2026Article
- Prognostic significance of inflammatory cytokine polymorphisms in AML: a study of IFNG, TNFA, and IL1B polymorphisms.BMC immunology · 2026Article
- Overcoming vascular niche-mediated TKI resistance in acute myeloid leukemia through miR-126 inhibition.NPJ systems biology and applications · 2026Article
- Clinical and genetic insights into novel TP53 mutations in De Novo AML patients.Clinical and experimental medicine · 2026Article
- Decoding Leukemic Stem Cells in AML: From Identification to Targeted Eradication.Diseases (Basel, Switzerland) · 2026Review
- Hijacking the helpers: platelet and neutrophil trafficking in AML and therapeutic exploitation.Experimental hematology & oncology · 2026Review
- Leukemia stem cells in acute myeloid leukemia: biology, therapeutic resistance, and barriers to durable remission.Journal of biomed research · 2026Article
- Baseline Extracellular HMGB-1 Levels Associated with Induction Chemotherapy Response in Adult Acute Myeloid Leukemia.F1000Research · 2026Article
- Editorial: Exploiting biomarkers for targeted therapies in acute myeloid leukemia.Frontiers in medicine · 2026Article
- Harnessing the power of exosomes in leukemia: from molecular messengers to clinical applications.Discover oncology · 2025Review
- Ex vivo evaluation of Allium sativum extract on acute myeloid leukemia cells and leukemia stem cell populations.Medical oncology (Northwood, London, England) · 2025Article
- Obesity and Metabolic Syndrome in Childhood Leukemia and in Long-Term Survivors: Causes and Personalized Treatments.Cancers · 2025Review
- Functions, mechanisms, and therapeutic implications of noncoding RNA in acute myeloid leukemia.Fundamental research · 2025Review
- Review
- The Role of the Sirtuin Family Histone Deacetylases in Acute Myeloid Leukemia-A Promising Road Ahead.Cancers · 2025Review
- Crosstalk between genomic variants and DNA methylation in FLT3 mutant acute myeloid leukemia.Briefings in functional genomics · 2025Article
- Multiplex immunophenotyping of human acute myeloid leukemia patients revealed single -cell heterogeneity with special attention on therapy sensitive and therapy resistant subpopulations.Frontiers in immunology · 2025Article
- Lysosome targeted therapies in hematological malignancies.Frontiers in oncology · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Acute myeloid leukemia (AML) is a hematological malignancy characterized by cytogenetic and genomic alterations. Up to now, combination chemotherapy remains the standard treatment for leukemia. However, many individuals diagnosed with AML develop chemotherapeutic resistance and relapse. Recently, it has been pointed out that leukemic stem cells (LSCs) are the fundamental cause of drug resistance and AML relapse. LSCs only account for a small subpopulation of all leukemic cells, but possess stem cell properties, including a self-renewal capacity and a multi-directional differentiation potential. LSCs reside in a mostly quiescent state and are insensitive to chemotherapeutic agents. When LSCs reside in a bone marrow microenvironment (BMM) favorable to their survival, they engage into a steady, continuous clonal evolution to better adapt to the action of chemotherapy. Most chemotherapeutic drugs can only eliminate LSC-derived clones, reducing the number of leukemic cells in the BM to a normal range in order to achieve complete remission (CR). LSCs hidden in the BM niche can hardly be targeted or eradicated, leading to drug resistance and AML relapse. Understanding the relationship between LSCs, the BMM, and the generation and evolution laws of LSCs can facilitate the development of effective therapeutic targets and increase the efficiency of LSCs elimination in AML.
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.