ArticleLeukemia2009
The hematopoietic stem cell in chronic phase CML is characterized by a transcriptional profile resembling normal myeloid progenitor cells and reflecting loss of quiescence.
Article in Leukemia, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
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Who cites it
45 citing papers in PubMed, 84 citations in OpenAlex.
- Simultaneous capture of single cell RNA-seq, ATAC-seq, and CRISPR perturbation enables multiomic screens to identify gene regulatory relationships.Cell reports methods · 2025Article
- Developing therapeutic approaches for chronic myeloid leukemia: a review.Molecular and cellular biochemistry · 2023Review
- TSPAN32 suppresses chronic myeloid leukemia pathogenesis and progression by stabilizing PTEN.Signal transduction and targeted therapy · 2023Article
- Molecular regulation of hematopoietic stem cell quiescence.Cellular and molecular life sciences : CMLS · 2022Review
- Article
- miRNome profiling of LSC-enriched CD34Frontiers in pharmacology · 2020Article
- Mechanisms of Disease Progression and Resistance to Tyrosine Kinase Inhibitor Therapy in Chronic Myeloid Leukemia: An Update.International journal of molecular sciences · 2019Review
- Identification of key candidate targets and pathways for the targeted treatment of leukemia stem cells of chronic myelogenous leukemia using bioinformatics analysis.Molecular genetics & genomic medicine · 2019Article
- Chronic myelogenous leukemia, a still unsolved problem: pitfalls and new therapeutic possibilities.Drug design, development and therapy · 2019Review
- Bone mesenchymal stromal cells exhibit functional inhibition but no chromosomal aberrations in chronic myelogenous leukemia.Oncology letters · 2019Article
- ICAM-1 Deficiency in the Bone Marrow Niche Impairs Quiescence and Repopulation of Hematopoietic Stem Cells.Stem cell reports · 2018Article
- Differential proteomic profile of leukemic CD34+ progenitor cells from chronic myeloid leukemia patients.Oncotarget · 2018Article
- Article
- Wide-transcriptome analysis and cellularity of bone marrow CD34+/lin- cells of patients with chronic-phase chronic myeloid leukemia at diagnosis vs. 12 months of first-line nilotinib treatment.Cancer biomarkers : section A of Disease markers · 2017Article
- Time-series analysis in imatinib-resistant chronic myeloid leukemia K562-cells under different drug treatments.Journal of Huazhong University of Science and Technology. Medical sciences = Hua zhong ke ji da xue xue bao. Yi xue Ying De wen ban = Huazhong keji daxue xuebao. Yixue Yingdewen ban · 2017Article
- Expression of CD25 on leukemic stem cells in BCR-ABL1Experimental hematology · 2017Review
- Single-cell transcriptomics uncovers distinct molecular signatures of stem cells in chronic myeloid leukemia.Nature medicine · 2017Article
- Article
- Cellular and Molecular Networks in Chronic Myeloid Leukemia: The Leukemic Stem, Progenitor and Stromal Cell Interplay.Current drug targets · 2017Review
- Identification of CD25 as STAT5-Dependent Growth Regulator of Leukemic Stem Cells in Ph+ CML.Clinical cancer research : an official journal of the American Association for Cancer Research · 2016Article
Corrections and comments
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Authors and funding
17 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We found that composition of cell subsets within the CD34+ cell population is markedly altered in chronic phase (CP) chronic myeloid leukemia (CML). Specifically, proportions and absolute cell counts of common myeloid progenitors (CMP) and megakaryocyte-erythrocyte progenitors (MEP) are significantly greater in comparison to normal bone marrow whereas absolute numbers of hematopoietic stem cells (HSC) are equal. To understand the basis for this, we performed gene expression profiling (Affymetrix HU-133A 2.0) of the distinct CD34+ cell subsets from six patients with CP CML and five healthy donors. Euclidean distance analysis revealed a remarkable transcriptional similarity between the CML patients' HSC and normal progenitors, especially CMP. CP CML HSC were transcriptionally more similar to their progeny than normal HSC to theirs, suggesting a more mature phenotype. Hence, the greatest differences between CP CML patients and normal donors were apparent in HSC including downregulation of genes encoding adhesion molecules, transcription factors, regulators of stem-cell fate and inhibitors of cell proliferation in CP CML. Impaired adhesive and migratory capacities were functionally corroborated by fibronectin detachment analysis and transwell assays, respectively. Based on our findings we propose a loss of quiescence of the CML HSC on detachment from the niche leading to expansion of myeloid progenitors.
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