ReviewStem cell research & therapy2021
Chronic myeloid leukemia stem cells: targeting therapeutic implications.
Review in Stem cell research & therapy, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 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
47 citing papers in PubMed, 81 citations in OpenAlex.
- Antileukemic Activity ofMolecules (Basel, Switzerland) · 2026Article
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- Discovery of a Novel 4,5-Dihydro-1Biomedicines · 2026Article
- c-Medical sciences (Basel, Switzerland) · 2026Review
- The disulfonic acid ANDS disrupts ANP32B-p53 interaction to suppress chronic myeloid leukemia.Nature communications · 2026Article
- A Novel CIP2A and BCL-XL Clinical Diagnostic Toolkit to Predict Disease Progression and Treatment-Free Remission in Chronic Myeloid Leukaemia.International journal of molecular sciences · 2026Article
- Potential utility of PPARγ agonists in targeting chronic myeloid leukemia stem cells.Annals of hematology · 2026Article
- Decoding Leukemic Stem Cells in AML: From Identification to Targeted Eradication.Diseases (Basel, Switzerland) · 2026Review
- Advances in Targeting BCR-ABLMolecules (Basel, Switzerland) · 2026Review
- Role of essential and trace elements in chronic myeloid leukemia: associations with serum trace element profiles and hematological parameters.Frontiers in aging · 2026Article
- Under ONIOM Layers: Analysis of BCR-ABL Enzyme Inhibitors Through Bond-Critical Points and Natural Orbitals.Molecules (Basel, Switzerland) · 2025Article
- Article
- Deciphering and targeting oncogenic pathways through integrated approaches and amino acid metabolism in hematologic malignancies.Discover oncology · 2025Review
- Rationally designed BCR-ABL kinase inhibitors for improved leukemia treatment via covalent and pro-/dual-drug targeting strategies.Journal of advanced research · 2025Article
- Article
- PRMT1 Promotes the Self-renewal of Leukemia Stem Cells by Regulating Protein Synthesis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Review
- Article
- Potential signaling pathways, biomarkers, natural drugs, and chronic myeloid leukemia therapeutics.Frontiers in pharmacology · 2025Review
- Mechanisms and signaling pathways of tyrosine kinase inhibitor resistance in chronic myeloid leukemia: A comprehensive review.Leukemia research reports · 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
3 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chronic myeloid leukemia (CML) is a clonal myeloproliferative neoplasm driven by BCR-ABL1 oncoprotein, which plays a pivotal role in CML pathology, diagnosis, and treatment as confirmed by the success of tyrosine kinase inhibitor (TKI) therapy. Despite advances in the development of more potent tyrosine kinase inhibitors, some mechanisms particularly in terms of CML leukemic stem cell (CML LSC) lead to intrinsic or acquired therapy resistance, relapse, and disease progression. In fact, the maintenance CML LSCs in patients who are resistance to TKI therapy indicates the role of CML LSCs in resistance to therapy through survival mechanisms that are not completely dependent on BCR-ABL activity. Targeting therapeutic approaches aim to eradicate CML LSCs through characterization and targeting genetic alteration and molecular pathways involving in CML LSC survival in a favorable leukemic microenvironment and resistance to apoptosis, with the hope of providing a functional cure. In other words, it is possible to develop the combination therapy of TKs with drugs targeting genes or molecules more specifically, which is required for survival mechanisms of CML LSCs, while sparing normal HSCs for clinical benefits along with TKIs.
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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.