ArticlePloS one2010
Chronic myeloid leukemia patients sensitive and resistant to imatinib treatment show different metabolic responses.
Article in PloS one, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed.
- Different In Vitro Models of Chronic Myeloid Leukemia Show Different Characteristics: Biological Replicates Are Not Biologically Equivalent.Cell biology international · 2025Article
- Review
- Metabolomic and transcriptomic response to imatinib treatment of gastrointestinal stromal tumour in xenograft-bearing mice.Translational oncology · 2023Article
- To metabolomics and beyond: a technological portfolio to investigate cancer metabolism.Signal transduction and targeted therapy · 2023Review
- Metabonomic analysis of tumor microenvironments: a mini-review.Frontiers in oncology · 2023Review
- In silico identification of potential inhibitor for TP53-induced glycolysis and apoptosis regulator in head and neck squamous cell carcinoma.3 Biotech · 2021Article
- Decitabine Downregulates TIGAR to Induce Apoptosis and Autophagy in Myeloid Leukemia Cells.Oxidative medicine and cellular longevity · 2021Article
- Recent Metabolomics Analysis in Tumor Metabolism Reprogramming.Frontiers in molecular biosciences · 2021Review
- Overexpression of P-glycoprotein and resistance to Imatinib in chronic myeloid leukemia patients.Journal of clinical laboratory analysis · 2020Article
- Druggable Biochemical Pathways and Potential Therapeutic Alternatives to Target Leukemic Stem Cells and Eliminate the Residual Disease in Chronic Myeloid Leukemia.International journal of molecular sciences · 2019Review
- Fumarate hydratase deficiency induces chronic myeloid leukemia progression.Translational cancer research · 2019Article
- Resistance to the Antiproliferative In Vitro Effect of PI3K-Akt-mTOR Inhibition in Primary Human Acute Myeloid Leukemia Cells Is Associated with Altered Cell Metabolism.International journal of molecular sciences · 2018Article
- Regulatory network analysis of microRNAs and genes in imatinib-resistant chronic myeloid leukemia.Functional & integrative genomics · 2017Article
- TIGAR cooperated with glycolysis to inhibit the apoptosis of leukemia cells and associated with poor prognosis in patients with cytogenetically normal acute myeloid leukemia.Journal of hematology & oncology · 2016Article
- Co-expression Pattern Analysis of miR-17-92 Target Genes in Chronic Myelogenous Leukemia.Frontiers in genetics · 2016Article
- Triomics Analysis of Imatinib-Treated Myeloma Cells Connects Kinase Inhibition to RNA Processing and Decreased Lipid Biosynthesis.Analytical chemistry · 2015Article
- [Expression and significance of TIGAR in hematological malignancis].Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi · 2015Article
- Review of mass spectrometry-based metabolomics in cancer research.Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2013Review
- Cross talk between Wnt/β-catenin and Irf8 in leukemia progression and drug resistance.The Journal of experimental medicine · 2013Article
- Metabolomic approach to evaluating adriamycin pharmacodynamics and resistance in breast cancer cells.Metabolomics : Official journal of the Metabolomic Society · 2013Article
Corrections and comments
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Authors and funding
16 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The BCR-ABL tyrosine kinase inhibitor imatinib is highly effective for chronic myeloid leukemia (CML). However, some patients gradually develop resistance to imatinib, resulting in therapeutic failure. Metabonomic and genomic profiling of patients' responses to drug interventions can provide novel information about the in vivo metabolism of low-molecular-weight compounds and extend our insight into the mechanism of drug resistance. Based on a multi-platform of high-throughput metabonomics, SNP array analysis, karyotype and mutation, the metabolic phenotypes and genomic polymorphisms of CML patients and their diverse responses to imatinib were characterized. The untreated CML patients (UCML) showed different metabolic patterns from those of healthy controls, and the discriminatory metabolites suggested the perturbed metabolism of the urea cycle, tricarboxylic acid cycle, lipid metabolism, and amino acid turnover in UCML. After imatinib treatment, patients sensitive to imatinib (SCML) and patients resistant to imatinib (RCML) had similar metabolic phenotypes to those of healthy controls and UCML, respectively. SCML showed a significant metabolic response to imatinib, with marked restoration of the perturbed metabolism. Most of the metabolites characterizing CML were adjusted to normal levels, including the intermediates of the urea cycle and tricarboxylic acid cycle (TCA). In contrast, neither cytogenetic nor metabonomic analysis indicated any positive response to imatinib in RCML. We report for the first time the associated genetic and metabonomic responses of CML patients to imatinib and show that the perturbed in vivo metabolism of UCML is independent of imatinib treatment in resistant patients. Thus, metabonomics can potentially characterize patients' sensitivity or resistance to drug intervention.
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