ArticleBritish journal of pharmacology2009
Metabolic characteristics of imatinib resistance in chronic myeloid leukaemia cells.
Article in British journal of pharmacology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 68 citations in OpenAlex.
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- Nutritional approaches in combating therapeutic resistance and enhancing treatment efficacy in cancer: the impact of ketogenic diets.Nutrition & metabolism · 2025Review
- BCR-ABL triggers a glucose-dependent survival program during leukemogenesis through the suppression of TXNIP.Cell death & disease · 2023Article
- Molecular subtypes predict therapeutic responses and identifying and validating diagnostic signatures based on machine learning in chronic myeloid leukemia.Cancer cell international · 2023Article
- Identification of an endoplasmic reticulum stress-related signature associated with clinical prognosis and immune therapy in glioma.BMC neurology · 2022Article
- The Differential Metabolic Profiles Between Deltamethrin-Resistant and -Susceptible Strains of Aedes albopictus (Diptera: Culicidae) by 1H-NMR.Journal of medical entomology · 2021Article
- Characterization of an endoplasmic reticulum stress-related signature to evaluate immune features and predict prognosis in glioma.Journal of cellular and molecular medicine · 2021Article
- Glycolysis-induced drug resistance in tumors-A response to danger signals?Neoplasia (New York, N.Y.) · 2021Review
- Lyn regulates creatine uptake in an imatinib-resistant CML cell line.Biochimica et biophysica acta. General subjects · 2020Article
- Hexokinase II inhibition by 3-bromopyruvate sensitizes myeloid leukemic cells K-562 to anti-leukemic drug, daunorubicin.Bioscience reports · 2019Article
- SWATH-MS based quantitative proteomics analysis reveals that curcumin alters the metabolic enzyme profile of CML cells by affecting the activity of miR-22/IPO7/HIF-1α axis.Journal of experimental & clinical cancer research : CR · 2018Article
- Structural homologies between phenformin, lipitor and gleevec aim the same metabolic oncotarget in leukemia and melanoma.Oncotarget · 2017Review
- Exploring cancer metabolism using stable isotope-resolved metabolomics (SIRM).The Journal of biological chemistry · 2017Review
- ROS homeostasis and metabolism: a critical liaison for cancer therapy.Experimental & molecular medicine · 2016Review
- ATM/G6PD-driven redox metabolism promotes FLT3 inhibitor resistance in acute myeloid leukemia.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- Resistance to chemotherapy is associated with altered glucose metabolism in acute myeloid leukemia.Oncology letters · 2016Article
- Metabolic Imaging to Assess Treatment Response to Cytotoxic and Cytostatic Agents.Frontiers in oncology · 2016Review
- Triomics Analysis of Imatinib-Treated Myeloma Cells Connects Kinase Inhibition to RNA Processing and Decreased Lipid Biosynthesis.Analytical chemistry · 2015Article
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 3 countries.
Funding
Abstract
background and purposeEarly detection of resistance development is crucial for imatinib-based treatment in chronic myeloid leukaemia (CML) patients. We aimed to distinguish metabolic markers of cell resistance to imatinib. EXPERIMENTAL APPROACH: Two human imatinib-sensitive CML cell lines: LAMA84-s and K562-s, and their resistant counterparts: LAMA84-r and K562-r (both resistant to 1 microM imatinib), and K562-R (5 microM) were analysed by nuclear magnetic resonance spectroscopy to assess global metabolic profiling, including energy state, glucose and phospholipid metabolism. KEY
resultsWe found, by Western blotting and flow cytometry, that the levels of Bcr-Abl tyrosine kinase and multi-drug resistance p-glycoprotein were inconsistent among resistant clones. On the other hand, phospholipid metabolism and lactate production were highly predictive for cell response to imatinib. As previously reported, sensitive cells showed significantly decreased glycolytic activity (lactate) and phospholipid synthesis (phosphocholine) as well as increased phospholipid catabolism (glycerophosphocholine) after 24 h of 1 microM imatinib treatment, which correlated with inhibition of cell proliferation and induction of apoptosis. In contrast to their sensitive counterparts, the K562-r, K562-R and LAMA84-r maintained increased phospholipid synthesis and glycolytic lactate production in the presence of 1 microM (K562-r and LAMA84-r) and 5 microM (K562-R) imatinib. CONCLUSIONS AND IMPLICATIONS: Specific metabolic markers for early detection of imatinib resistance, including increased glycolytic activity and phospholipid turnover, can be identified in resistant clones. Once validated in human isolated leukocytes, they may be used to monitor the responsiveness of CML patients to treatment.
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