ArticleHaematologica2011
Glucose availability in hypoxia regulates the selection of chronic myeloid leukemia progenitor subsets with different resistance to imatinib-mesylate.
Article in Haematologica, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 45 citations in OpenAlex.
- 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
- Determination of the Minimum Cell-to-Cell Adhesion Time Using Optical Tweezers in Leukemia and Lymphoma Research.Methods and protocols · 2025Article
- Therapy Resistance and Disease Progression in CML: Mechanistic Links and Therapeutic Strategies.Current hematologic malignancy reports · 2022Review
- Novel GermlineMedicina (Kaunas, Lithuania) · 2022Article
- Metabolic plasticity in blast crisis-chronic myeloid leukaemia cells under hypoxia reduces the cytotoxic potency of drugs targeting mitochondria.Discover oncology · 2022Article
- Lactate Maintains BCR/Abl Expression and Signaling in Chronic Myeloid Leukemia Cells Under Nutrient Restriction.Oncology research · 2022Article
- Article
- In Vitro Comparison of the Effects of Imatinib and Ponatinib on Chronic Myeloid Leukemia Progenitor/Stem Cell Features.Targeted oncology · 2020Article
- Targeting the Extracellular Signal-Regulated Kinase 5 Pathway to Suppress Human Chronic Myeloid Leukemia Stem Cells.Stem cell reports · 2018Article
- Sensitivity to imatinib of KCL22 chronic myeloid leukemia cell survival/growth and stem cell potential under glucose shortage.Data in brief · 2018Article
- Severe hypoxia selects hematopoietic progenitors with stem cell potential from primary Myelodysplastic syndrome bone marrow cell cultures.Oncotarget · 2018Article
- Chronic myeloid leukemia progenitor cells require autophagy when leaving hypoxia-induced quiescence.Oncotarget · 2017Article
- Recent Advances in Comprehending the Signaling Pathways Involved in the Progression of Breast Cancer.International journal of molecular sciences · 2017Review
- Targeting chronic myeloid leukemia stem cells with the hypoxia-inducible factor inhibitor acriflavine.Blood · 2017Article
- The hypoxia signalling pathway in haematological malignancies.Oncotarget · 2017Review
- Tyrosine kinase inhibitors and mesenchymal stromal cells: effects on self-renewal, commitment and functions.Oncotarget · 2017Review
- The Leukemic Stem Cell Niche: Adaptation to "Hypoxia" versus Oncogene Addiction.Stem cells international · 2017Article
- Different BCR/Abl protein suppression patterns as a converging trait of chronic myeloid leukemia cell adaptation to energy restriction.Oncotarget · 2016Article
- Chronic Myeloid Leukemia and Hepatoblastoma: Two Cancer Models to Link Metabolism to Stem Cells.Frontiers in oncology · 2016Review
- Hypoxia and Hypoxia-Inducible Factors in Leukemias.Frontiers in oncology · 2016Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundIncubation of chronic myeloid leukemia cells in hypoxia inhibits growth and selects BCR/Abl-independent cells with stem cell properties which are refractory to imatinib-mesylate. This study aimed to characterize the relationship of this refractoriness with glucose availability in the environment. DESIGN AND
methodsK562 or primary chronic myeloid leukemia cells were cultured at 0.1% O(2), different cell densities and glucose concentrations. The stem and progenitor cell potential of these cultures at different times of incubation in relation to BCR/Abl(protein) expression and sensitivity to imatinib-mesylate was explored by transferring cells to growth-permissive secondary cultures in normoxia, according to the Culture-Repopulating Ability assay methodology.
resultsHypoxia-resistant cells maintained BCR/Abl(protein) expression until glucose was no longer available in primary hypoxic cultures, where glucose availability appeared to regulate cell number and the balance between the enrichment of cells with kinetic properties typical of stem or progenitor cells. Cells surviving merely hypoxic conditions were, upon transfer to secondary cultures, immediately available for numerical expansion due to the maintained BCR/Abl(protein) expression, and were consequently sensitive to imatinib-mesylate. Instead, BCR/Abl(protein)-negative cells selected in primary cultures under oxygen/glucose shortage underwent a delayed numerical expansion in secondary cultures, which was completely refractory to imatinib-mesylate. Cells with the latter properties were also found in primary chronic myeloid leukemia explants.
conclusionsGlucose shortage in hypoxia was shown to represent the condition selecting BCR/Abl(protein)-negative cells refractory to imatinib-mesylate from either chronic myeloid leukemia lines or patients. These cells, exhibiting stem cell properties in vitro, are metabolically suited to home to stem cell niches in vivo and so may represent the chronic myeloid leukemia cell subset responsible for minimal residual disease.
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