Abnormalities in glucose uptake and metabolism in imatinib-resistant human BCR-ABL-positive cells.
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Metabolic Imaging to Assess Treatment Response to Cytotoxic and Cytostatic AgentsIntegration of Mitochondrial Targeting for Molecular Cancer TherapeuticsTargeting glycogen metabolism in bladder cancerYeast toxicogenomics: genome-wide responses to chemical stresses with impact in environmental health, pharmacology, and biotechnologyChronic myeloid leukemia patients sensitive and resistant to imatinib treatment show different metabolic responsesDynamics of resistance development to imatinib under increasing selection pressure: a combination of mathematical models and in vitro dataSubmolecular regulation of cell transformation by deuterium depleting water exchange reactions in the tricarboxylic acid substrate cycle.Immunosuppressant neurotoxicity in rat brain models: oxidative stress and cellular metabolismImatinib resistance associated with BCR-ABL upregulation is dependent on HIF-1alpha-induced metabolic reprogramingEffects of lovastatin on breast cancer cells: a proteo-metabonomic study.Exploiting mitochondrial dysfunction for effective elimination of imatinib-resistant leukemic cells.Increased anaerobic metabolism is a distinctive signature in a colorectal cancer cellular model of resistance to antiepidermal growth factor receptor antibody.17-allyamino-17-demethoxygeldanamycin treatment results in a magnetic resonance spectroscopy-detectable elevation in choline-containing metabolites associated with increased expression of choline transporter SLC44A1 and phospholipase A2Tyrosine kinase inhibition in leukemia induces an altered metabolic state sensitive to mitochondrial perturbations.Reactive Oxygen Species and Mitochondrial DNA Damage and Repair in BCR-ABL1 Cells Resistant to Imatinib.Doxorubicin Differentially Induces Apoptosis, Expression of Mitochondrial Apoptosis-Related Genes, and Mitochondrial Potential in BCR-ABL1-Expressing Cells Sensitive and Resistant to Imatinib.Activating oxidative phosphorylation by a pyruvate dehydrogenase kinase inhibitor overcomes sorafenib resistance of hepatocellular carcinoma.(13)C MRS and LC-MS Flux Analysis of Tumor Intermediary Metabolism.The role of mitochondrial DNA damage and repair in the resistance of BCR/ABL-expressing cells to tyrosine kinase inhibitorsSynergistic activity of histone deacetylase and proteasome inhibition against pancreatic and hepatocellular cancer cell lines.Preclinical activity of the rational combination of selumetinib (AZD6244) in combination with vorinostat in KRAS-mutant colorectal cancer models.Systems biology analysis of drivers underlying hallmarks of cancer cell metabolism.Metabolic assessment of the action of targeted cancer therapeutics using magnetic resonance spectroscopyHER Family Receptors are Important Theranostic Biomarkers for Cervical Cancer: Blocking Glucose Metabolism Enhances the Therapeutic Effect of HER InhibitorsUnveiling the Metabolic Changes on Muscle Cell Metabolism Underlying p-Phenylenediamine Toxicity.NMR metabonomics for mammalian cell metabolism studies.MR evaluation of response to targeted treatment in cancer cells.Regulation of mammalian nucleotide metabolism and biosynthesisTargeting of cell metabolism in human acute myeloid leukemia--more than targeting of isocitrate dehydrogenase mutations and PI3K/AKT/mTOR signaling?Metabolomics applications in precision medicine: An oncological perspective.Structural homologies between phenformin, lipitor and gleevec aim the same metabolic oncotarget in leukemia and melanoma.Cell intrinsic and extrinsic regulation of leukemia cell metabolism.Proteomic analysis of imatinib-resistant CML-T1 cells reveals calcium homeostasis as a potential therapeutic target.Resistance to chemotherapy is associated with altered glucose metabolism in acute myeloid leukemia.Triomics Analysis of Imatinib-Treated Myeloma Cells Connects Kinase Inhibition to RNA Processing and Decreased Lipid Biosynthesis.Inhibition of Lipid Oxidation Increases Glucose Metabolism and Enhances 2-Deoxy-2-[(18)F]Fluoro-D-Glucose Uptake in Prostate Cancer Mouse Xenografts.Decreased lactate concentration and glycolytic enzyme expression reflect inhibition of mTOR signal transduction pathway in B-cell lymphoma.S6K1 determines the metabolic requirements for BCR-ABL survival.Bezielle (BZL101)-induced oxidative stress damage followed by redistribution of metabolic fluxes in breast cancer cells: a combined proteomic and metabolomic study.Metabolic assessment of a novel chronic myelogenous leukemic cell line and an imatinib resistant subline by H NMR spectroscopy.
P2860
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P2860
Abnormalities in glucose uptake and metabolism in imatinib-resistant human BCR-ABL-positive cells.
description
2009 nî lūn-bûn
@nan
2009年の論文
@ja
2009年学术文章
@wuu
2009年学术文章
@zh
2009年学术文章
@zh-cn
2009年学术文章
@zh-hans
2009年学术文章
@zh-my
2009年学术文章
@zh-sg
2009年學術文章
@yue
2009年學術文章
@zh-hant
name
Abnormalities in glucose uptak ...... human BCR-ABL-positive cells.
@en
Abnormalities in glucose uptak ...... human BCR-ABL-positive cells.
@nl
type
label
Abnormalities in glucose uptak ...... human BCR-ABL-positive cells.
@en
Abnormalities in glucose uptak ...... human BCR-ABL-positive cells.
@nl
prefLabel
Abnormalities in glucose uptak ...... human BCR-ABL-positive cells.
@en
Abnormalities in glucose uptak ...... human BCR-ABL-positive cells.
@nl
P2093
P1476
Abnormalities in glucose uptak ...... human BCR-ABL-positive cells.
@en
P2093
Douglas J Kominsky
Jaimi L Brown
Jelena Klawitter
Junia V Melo
Laszlo G Boros
Natalie J Serkova
S Gail Eckhardt
P304
P356
10.1158/1078-0432.CCR-08-3291
P407
P577
2009-04-28T00:00:00Z