Effective killing of Gleevec-resistant CML cells with T315I mutation by a natural compound PEITC through redox-mediated mechanism - Wikidata - wikimedia - TriplyDB

Effective killing of Gleevec-resistant CML cells with T315I mutation by a natural compound PEITC through redox-mediated mechanism

Effective killing of Gleevec-resistant CML cells with T315I mutation by a natural compound PEITC through redox-mediated mechanism

http://www.wikidata.org/entity/Q28275023

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Pro-apoptotic activity of α-bisabolol in preclinical models of primary human acute leukemia cells MUC1-C Oncoprotein Blocks Terminal Differentiation of Chronic Myelogenous Leukemia Cells by a ROS-Mediated Mechanism Redox-directed cancer therapeutics: molecular mechanisms and opportunities Dual effect of oxidative stress on leukemia cancer induction and treatment Naturally Occurring Isothiocyanates Exert Anticancer Effects by Inhibiting Deubiquitinating Enzymes DCPIP (2,6-dichlorophenolindophenol) as a genotype-directed redox chemotherapeutic targeting NQO1*2 breast carcinoma Carboxyamidotriazole-orotate inhibits the growth of imatinib-resistant chronic myeloid leukaemia cells and modulates exosomes-stimulated angiogenesis No evident dose-response relationship between cellular ROS level and its cytotoxicity--a paradoxical issue in ROS-based cancer therapy.SAHA and S116836, a novel tyrosine kinase inhibitor, synergistically induce apoptosis in imatinib-resistant chronic myelogenous leukemia cells.Exploiting mitochondrial dysfunction for effective elimination of imatinib-resistant leukemic cells.Systems biology modeling reveals a possible mechanism of the tumor cell death upon oncogene inactivation in EGFR addicted cancers.Terminal differentiation of chronic myelogenous leukemia cells is induced by targeting of the MUC1-C oncoprotein.Preferential killing of cancer cells with mitochondrial dysfunction by natural compounds.Metabolic reprogramming orchestrates cancer stem cell properties in nasopharyngeal carcinoma.Proteins as binding targets of isothiocyanates in cancer prevention.Inhibition of mitochondrial respiration and rapid depletion of mitochondrial glutathione by β-phenethyl isothiocyanate: mechanisms for anti-leukemia activity.Novel use of old drug: Anti-rheumatic agent auranofin overcomes imatinib-resistance of chronic myeloid leukemia cells Effective killing of leukemia cells by the natural product OSW-1 through disruption of cellular calcium homeostasis Redox control of leukemia: from molecular mechanisms to therapeutic opportunities.Hirsutanol A, a novel sesquiterpene compound from fungus Chondrostereum sp., induces apoptosis and inhibits tumor growth through mitochondrial-independent ROS production: hirsutanol A inhibits tumor growth through ROS production Redox Regulation of Stem-like Cells Though the CD44v-xCT Axis in Colorectal Cancer: Mechanisms and Therapeutic Implications The role of mitochondrial DNA damage and repair in the resistance of BCR/ABL-expressing cells to tyrosine kinase inhibitors Abl tyrosine kinase inhibitors for overriding Bcr-Abl/T315I: from the second to third generation.Role of oxidative stress in stem, cancer, and cancer stem cells.Inhibition of cancer antioxidant defense by natural compounds.Development of an effective therapy for chronic myelogenous leukemia NF-κB suppresses ROS levels in BCR-ABL(+) cells to prevent activation of JNK and cell death.Phenethyl isothiocyanate inhibits STAT3 activation in prostate cancer cells.Chaetocin antileukemia activity against chronic myelogenous leukemia cells is potentiated by bone marrow stromal factors and overcomes innate imatinib resistance.Exposure of chronic myelogenous leukemia cells to imatinib results in the post-transcriptional induction of manganese superoxide dismutase.Mitochondrial dysfunction in cancer chemoprevention by phytochemicals from dietary and medicinal plants.Phenethyl isothiocyanate triggers apoptosis in human malignant melanoma A375.S2 cells through reactive oxygen species and the mitochondria-dependent pathways.Apoptosis induced by benzyl isothiocyanate in gefitinib-resistant lung cancer cells is associated with Akt/MAPK pathways and generation of reactive oxygen species.Optimal ROS Signaling Is Critical for Nuclear Reprogramming.Identification of deubiquitinase targets of isothiocyanates using SILAC-assisted quantitative mass spectrometry.Interfering with ROS Metabolism in Cancer Cells: The Potential Role of Quercetin.Mitochondrial respiratory chain involvement in peroxiredoxin 3 oxidation by phenethyl isothiocyanate and auranofin.A pharmacodynamic model of Bcr-Abl signalling in chronic myeloid leukaemia.Reactive oxygen species in haematopoiesis: leukaemic cells take a walk on the wild side.Discovering proteasomal deubiquitinating enzyme inhibitors for cancer therapy: lessons from rational design, nature and old drug reposition

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Effective killing of Gleevec-resistant CML cells with T315I mutation by a natural compound PEITC through redox-mediated mechanism

http://www.wikidata.org/entity/Q28275023

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2008 nî lūn-bûn

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2008 թուականի Յունիսին հրատարակուած գիտական յօդուած

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Effective killing of Gleevec-r ...... rough redox-mediated mechanism

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D Trachootham

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F J Giles

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H Zhang

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P2860

The two major imatinib resistance mutations E255K and T315I enhance the activity of BCR/ABL fusion kinase.

Dasatinib in imatinib-resistant Philadelphia chromosome-positive leukemias

Efficacy and safety of a specific inhibitor of the BCR-ABL tyrosine kinase in chronic myeloid leukemia

Multiple BCR-ABL kinase domain mutations confer polyclonal resistance to the tyrosine kinase inhibitor imatinib (STI571) in chronic phase and blast crisis chronic myeloid leukemia

Clinical resistance to STI-571 cancer therapy caused by BCR-ABL gene mutation or amplification

Overriding imatinib resistance with a novel ABL kinase inhibitor

Caspase-dependent cleavage of c-Abl contributes to apoptosis.

The biology of chronic myeloid leukemia.

Chronic myeloid leukaemia as a model of disease evolution in human cancer.

Mechanisms of BCR-ABL in the pathogenesis of chronic myelogenous leukaemia.

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10.1038/LEU.2008.74

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