ReviewProtein & cell2015
Leukemia stem cells: the root of chronic myeloid leukemia.
Review in Protein & cell, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers, 1 of them a synthesis 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
55 citing papers in PubMed, 1 synthesis or guideline pooled it, 106 citations in OpenAlex.
- The importance of evaluating specific myeloid malignancies in epidemiological studies of environmental carcinogens.BMC cancer · 2021Pooled it
- Trial
- Leveraging Model-Informed Drug Development to Predict Asciminib Efficacy in Second-Line Treatment of Chronic Myeloid Leukemia in Chronic Phase.Clinical pharmacokinetics · 2026Article
- Targeting Musashi-2 to counteract senescence and resistance in chronic myeloid leukemia: enhancing the efficacy of imatinib therapy.BMC cancer · 2025Article
- Lactate-mediated activation of GPR81 regulates BCR/Abl protein expression in chronic myeloid leukemia cells selected under low oxygen tension.The Journal of pathology · 2025Article
- Targeting DDX3X eliminates leukemia stem cells in chronic myeloid leukemia by blocking NT5DC2 mRNA translation.Oncogene · 2025Article
- Chronic myeloid leukemia in a patient treated with palbociclib and exemestane: a case report.AME case reports · 2025Article
- The Anti-Leukemic Potential of Bee Venom.International journal of general medicine · 2025Review
- Potential signaling pathways, biomarkers, natural drugs, and chronic myeloid leukemia therapeutics.Frontiers in pharmacology · 2025Review
- Chiglitazar diminishes the warburg effect through PPARγ/mTOR/PKM2 and increases the sensitivity of imatinib in chronic myeloid leukemia.Experimental hematology & oncology · 2024Article
- Combined targeting of GPX4 and BCR-ABL tyrosine kinase selectively compromises BCR-ABL+ leukemia stem cells.Molecular cancer · 2024Article
- Blockade of PD-1 and TIM-3 Ameliorates CD8Cell biochemistry and biophysics · 2024Article
- The mGenes & diseases · 2024Article
- Long non-coding RNA small nucleolar RNA host gene 29 drives chronic myeloid leukemia progression via microRNA-483-3p/Casitas B-lineage Lymphoma axis-mediated activation of the phosphoinositide 3-kinase/Akt pathway.Medical oncology (Northwood, London, England) · 2024Article
- Article
- Identification of ubiquitination-related hub genes in chronic myeloid leukemia cell by bioinformatics analysis.Journal of Cancer · 2024Article
- The dark side of stemness - the role of hematopoietic stem cells in development of blood malignancies.Frontiers in oncology · 2024Review
- Screening and Activity Evaluation of Novel BCR-ABL/T315I Tyrosine Kinase Inhibitors.Current medicinal chemistry · 2024Article
- Article
- IGFBP-6 Alters Mesenchymal Stromal Cell Phenotype Driving Dasatinib Resistance in Chronic Myeloid Leukemia.Life (Basel, Switzerland) · 2023Article
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 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chronic myeloid leukemia (CML) is a clonal myeloproliferative disorder characterized by a chromosome translocation that generates the Bcr-Abl oncogene encoding a constitutive kinase activity. Despite remarkable success in controlling CML at chronic phase by Bcr-Abl tyrosine kinase inhibitors (TKIs), a significant proportion of CML patients treated with TKIs develop drug resistance due to the inability of TKIs to kill leukemia stem cells (LSCs) that are responsible for initiation, drug resistance, and relapse of CML. Therefore, there is an urgent need for more potent and safer therapies against leukemia stem cells for curing CML. A number of LSC-associated targets and corresponding signaling pathways, including CaMKII-γ, a critical molecular switch for co-activating multiple LSC-associated signaling pathways, have been identified over the past decades and various small inhibitors targeting LSC are also under development. Increasing evidence shows that leukemia stem cells are the root of CML and targeting LSC may offer a curable treatment option for CML patients. This review summarizes the molecular biology of LSC and its-associated targets, and the potential clinical application in chronic myeloid leukemia.
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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.