ReviewHaematologica2023
Leukemic stem cells and therapy resistance in acute myeloid leukemia.
Review in Haematologica, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 161 papers.
What it found
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Who cites it
161 citing papers in PubMed, 176 citations in OpenAlex.
- Integrated computational and experimental identification of a novel ML-IAP-targeting peptide with antiproliferative activity in leukaemia cells.Journal of enzyme inhibition and medicinal chemistry · 2026Article
- Immune Checkpoints in Leukaemia as Gatekeepers of Immuno-Modulation.Immunology · 2026Review
- Targeting ACSF2 overcomes Ara-C resistance in acute myeloid leukemia via the cholesterol metabolism-ERK signaling axis.Leukemia · 2026Article
- Exploiting an epigenetic resistance mechanism to PI3-kinase inhibition in leukemic stem cells.Leukemia · 2026Article
- ANKRD28 interacts with DOCK180 to activate Rac1-STAT3-Myc signaling and sustain stemness of CD34Molecular and cellular biochemistry · 2026Article
- From pumps to networks: ABC transporters in leukemia resistance and microenvironmental adaptation.Medical oncology (Northwood, London, England) · 2026Review
- SIX1 drives acute myeloid leukemia progression by reprogramming glycolytic metabolism and impairing CD8⁺ T-cell effector function.Immunologic research · 2026Article
- Cancer Stem Cell Quiescence: Molecular and Microenvironmental Evidence for an Actively Regulated Adaptive Survival Strategy.Cancer medicine · 2026Review
- Tunable universal OR-gated CAR T cells for AML.iScience · 2026Article
- Oncogenic DHX15 mutation enhances mitochondrial metabolism and sustains leukemia stemness.Leukemia · 2026Article
- PAPOLA-mediated hyperactive polyadenylation promotes leukemogenesis and leukemia stem cell self-renewal through metabolic reprogramming.Nature cancer · 2026Article
- A polyadenylation enzyme rewires metabolism to fuel AML.Nature cancer · 2026Article
- CRISPR integration of an FLT3 CAR into the TRAC locus generates CAR T cells for AML.Genome medicine · 2026Article
- PKM2 modulation regulates leukemia cell survival.Cancer & metabolism · 2026Article
- TRIM24 stabilizes the p110 CUX1 oncoprotein via USP10 to promote chemoresistance in acute myeloid leukemia.Journal of translational medicine · 2026Article
- T-cell miR-155 regulates the response to tumor-specific mRNA vaccines in a murine model of acute myeloid leukemia.Journal of immunology (Baltimore, Md. : 1950) · 2026Article
- Mitochondrial RNA helicase DDX28 promotes cell cycle and DNA repair programs and shapes an immunosuppressive microenvironment in acute myeloid leukemia.Translational oncology · 2026Article
- Resveratrol inhibits aerobic glycolysis and promotes cuproptosis in acute myeloid leukemia via the PI3K/AKT signaling pathway.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Hierarchical lineage tracing reveals diverse pathways of cytarabine resistance.Nature communications · 2026Article
- Diagnosis-Driven Targeted Therapy in Acute Myeloid Leukemia: Clinical Integration of Tyrosine Kinase, BCL-2, and CD33-Directed Strategies with Midostaurin, Venetoclax, and Gemtuzumab Ozogamicin.Journal of clinical medicine · 2026Review
101 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A major obstacle in the treatment of acute myeloid leukemia (AML) is refractory disease or relapse after achieving remission. The latter arises from a few therapy-resistant cells within minimal residual disease (MRD). Resistant cells with long-term self-renewal capacity that drive clonal outgrowth are referred to as leukemic stem cells (LSC). The cancer stem cell concept considers LSC as relapse-initiating cells residing at the top of each genetically defined AML subclone forming epigenetically controlled downstream hierarchies. LSC display significant phenotypic and epigenetic plasticity, particularly in response to therapy stress, which results in various mechanisms mediating treatment resistance. Given the inherent chemotherapy resistance of LSC, targeted strategies must be incorporated into first-line regimens to prevent LSC-mediated AML relapse. The combination of venetoclax and azacitidine is a promising current strategy for the treatment of AML LSC. Nevertheless, the selection of patients who would benefit either from standard chemotherapy or venetoclax + azacitidine treatment in first-line therapy has yet to be established and the mechanisms of resistance still need to be discovered and overcome. Clinical trials are currently underway that investigate LSC susceptibility to first-line therapies. The era of single-cell multi-omics has begun to uncover the complex clonal and cellular architectures and associated biological networks. This should lead to a better understanding of the highly heterogeneous AML at the inter- and intra-patient level and identify resistance mechanisms by longitudinal analysis of patients' samples. This review discusses LSC biology and associated resistance mechanisms, potential therapeutic LSC vulnerabilities and current clinical trial activities.
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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.