Long-term in vitro treatment of human glioblastoma cells with temozolomide increases resistance in vivo through up-regulation of GLUT transporter and aldo-keto reductase enzyme AKR1C expression.
about
Targeting cellular metabolism to improve cancer therapeuticsDinosaurs and ancient civilizations: reflections on the treatment of cancerThe Warburg effect and drug resistanceInhibition of prolyl 4-hydroxylase, beta polypeptide (P4HB) attenuates temozolomide resistance in malignant glioma via the endoplasmic reticulum stress response (ERSR) pathwaysJLK1486, a Bis 8-Hydroxyquinoline-Substituted Benzylamine, Displays Cytostatic Effects in Experimental Gliomas through MyT1 and STAT1 Activation and, to a Lesser Extent, PPARγ ActivationA chalcone-related small molecule that induces methuosis, a novel form of non-apoptotic cell death, in glioblastoma cells.Differential expression of miR200a-3p and miR21 in grade II-III and grade IV gliomas: evidence that miR200a-3p is regulated by O⁶-methylguanine methyltransferase and promotes temozolomide responsiveness.Protein alterations associated with temozolomide resistance in subclones of human glioblastoma cell lines.Temozolomide modifies caveolin-1 expression in experimental malignant gliomas in vitro and in vivo.The interconnectedness of cancer cell signaling.Local delivery of cancer-cell glycolytic inhibitors in high-grade glioma.Enzymes of the AKR1B and AKR1C Subfamilies and Uterine Diseases.In search of a cytostatic agent derived from the alkaloid lycorine: synthesis and growth inhibitory properties of lycorine derivativesBulbispermine: a crinine-type Amaryllidaceae alkaloid exhibiting cytostatic activity toward apoptosis-resistant glioma cells.High levels of cellular proliferation predict pseudoprogression in glioblastoma patientsOphiobolin A induces paraptosis-like cell death in human glioblastoma cells by decreasing BKCa channel activity.Stalling the engine of resistance: targeting cancer metabolism to overcome therapeutic resistance.Temozolomide promotes genomic and phenotypic changes in glioblastoma cells.Expression of dynein, cytoplasmic 2, heavy chain 1 (DHC2) associated with glioblastoma cell resistance to temozolomide.Mitochondrial protein ATPase family, AAA domain containing 3A correlates with radioresistance in glioblastoma.Aldo-keto reductase 1C1 induced by interleukin-1β mediates the invasive potential and drug resistance of metastatic bladder cancer cells.GLUT3 upregulation promotes metabolic reprogramming associated with antiangiogenic therapy resistance.Inhibitors of GLUT/SLC2A Enhance the Action of BCNU and Temozolomide against High-Grade Gliomas.Hepatic expression and cellular distribution of the glucose transporter family.Metabolic implication of tumor:stroma crosstalk in breast cancer.Molecular imaging coupled to pattern recognition distinguishes response to temozolomide in preclinical glioblastoma.Combination of unsaturated fatty acids and ionizing radiation on human glioma cells: cellular, biochemical and gene expression analysis.LRIG1 enhances chemosensitivity by modulating BCL-2 expression and receptor tyrosine kinase signaling in glioma cells.Strategies to Target Glucose Metabolism in Tumor Microenvironment on Cancer by Flavonoids.Hyperoxia resensitizes chemoresistant human glioblastoma cells to temozolomide.Considering temozolomide as a novel potential treatment for esophageal cancer.Hormetic potential of methylglyoxal, a side-product of glycolysis, in switching tumours from growth to death.Overcoming intratumor heterogeneity of polygenic cancer drug resistance with improved biomarker integrationAKR1C1 as a Biomarker for Differentiating the Biological Effects of Combustible from Non-Combustible Tobacco Products.Combined Inhibitions of Glycolysis and AKT/autophagy Can Overcome Resistance to EGFR-targeted Therapy of Lung Cancer.Aldo-Keto Reductase Regulation by the Nrf2 System: Implications for Stress Response, Chemotherapy Drug Resistance, and Carcinogenesis.Molecular characterization of central neurocytomas: potential markers for tumor typing and progression.AKR1C enzymes sustain therapy resistance in paediatric T-ALL.Inhibition of Glycolysis and Glutaminolysis: Emerging Drug Discovery Approach to Combat Cancer.
P2860
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P2860
Long-term in vitro treatment of human glioblastoma cells with temozolomide increases resistance in vivo through up-regulation of GLUT transporter and aldo-keto reductase enzyme AKR1C expression.
description
2010 nî lūn-bûn
@nan
2010 թուականի Սեպտեմբերին հրատարակուած գիտական յօդուած
@hyw
2010 թվականի սեպտեմբերին հրատարակված գիտական հոդված
@hy
2010年の論文
@ja
2010年論文
@yue
2010年論文
@zh-hant
2010年論文
@zh-hk
2010年論文
@zh-mo
2010年論文
@zh-tw
2010年论文
@wuu
name
Long-term in vitro treatment o ...... ctase enzyme AKR1C expression.
@ast
Long-term in vitro treatment o ...... ctase enzyme AKR1C expression.
@en
Long-term in vitro treatment o ...... ctase enzyme AKR1C expression.
@nl
type
label
Long-term in vitro treatment o ...... ctase enzyme AKR1C expression.
@ast
Long-term in vitro treatment o ...... ctase enzyme AKR1C expression.
@en
Long-term in vitro treatment o ...... ctase enzyme AKR1C expression.
@nl
prefLabel
Long-term in vitro treatment o ...... ctase enzyme AKR1C expression.
@ast
Long-term in vitro treatment o ...... ctase enzyme AKR1C expression.
@en
Long-term in vitro treatment o ...... ctase enzyme AKR1C expression.
@nl
P2093
P2860
P50
P356
P1433
P1476
Long-term in vitro treatment o ...... ctase enzyme AKR1C expression.
@en
P2093
Benjamin Le Calvé
Christine Decaestecker
Céline Bruyère
Florence Lefranc
Jean-Marie Ruysschaert
Marie Le Mercier
Michal Rynkowski
Robert Kiss
Thierry Gras
P2860
P304
P356
10.1593/NEO.10526
P407
P577
2010-09-01T00:00:00Z