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Daunorubicin inserts itself into the strands of genetic material (DNA) inside the cancerous cells and binds them together.
Relationship of adriamycin concentrations to the DNA lesions induced in hypoxic and euoxic L1210 cells.Qualitative and quantitative aspects of intercalator-induced DNA strand breaks.Cytotoxicity and DNA strand breaks by 5-iminodaunorubicin in mouse leukemia L1210 cells: comparison with adriamycin and 4′-(9-acridinylamino)- methanesulfon-m-aniside.Daunorubicin-induced internucleosomal DNA fragmentation in acute myeloid cell lines.Lack of correlation between expression and function of P-glycoprotein in acute myeloid leukemic cells.Ionizing radiation acts on cellular membranes to generate ceramide and initiate apoptosis.Daunorubicin induced apoptosis: triggering of ceramide generation through sphingomyelin hydrolysis.Lysosomal sphingomyelinase is not solicited for apoptosis signaling.Ceramide synthase mediates daunorubicin-induced apoptosis: an alternative mechanism for generating death signals.Involvement of de novo ceramide biosynthesis in tumor necrosis factor-α/cycloheximide-induced cerebral endothelial cell death.Tumor necrosis factor induces ceramide oscillations and negatively controls sphingolipid synthases by caspases in apoptotic Kym-1 cells.Positive feedback control sphingomyelinase activity by ceramide.Requirement for ceramide-initiated SAPK/JNK signalling in stress-induced apoptosis.Requirement of AP-1 for ceramide-induced apoptosis in human leukemia HL-60 cells.Ras-dependent growth factor regulation of MEK kinase in PC12 cells.Signal transduction pathways regulated by mitogen-activated/extracellular response kinase kinase kinase induce cell death.Induction of apoptosis by ASK1, a mammalian MAPKKK that activates SAPK/JNK and p38 signalling pathways.Role of the stress-activated/c-Jun NH2-terminal protein kinase pathway in the cellular response to adriamycin and other chemotherapeutic drugs.Adriamycin activates c-jun N-terminal kinase in human leukemia cells: a relevance to apoptosis.Implication of radical oxygen species in ceramide generation, c-Jun N-terminal kinase activation and apoptosis induced by daunorubicin.The mammalian ultraviolet response is triggered by activation of Src tyrosine kinases.Activation of the c-Abl tyrosine kinase in the stress response to DNA-damaging agents.Defective induction of stress-activated protein kinase activity in ataxia-telangiectasia cells exposed to ionizing radiation.Persistant activation of c-Jun N-terminal kinase 1 (JNK1) in γ radiation-induced apoptosis.c-Abl activation regulates induction of the SEK1/stress-activated protein kinase pathway in the cellular response to 1-β-D-arabinofuranosylcytosine.Transient stimulation of the c-Jun-NH2-terminal kinase/activator protein 1 pathway and inhibition of extracellular signal-regulated kinase are early effects in paclitaxel-mediated apoptosis in human B lymphoblasts.Paclitaxel (Taxol)-induced gene expression and cell death are both mediated by the activation of c-Jun NH2-terminal kinase (JNK/SAPK).Sounding the alarm: protein kinase cascades activated by stress and inflammation.The protein kinase C activators phorbol esters and phosphatidylserine inhibit neutral sphingomyelinase activation, ceramide generation, and apoptosis triggered by daunorubicin.Protein kinase C inhibition induces apoptosis and ceramide production through activation of a neutral sphingomyelinase.Identification of a distinct pool of sphingomyelin involved in the sphingomyelin cycle.Natural resistance of acute myeloid leukemia cell lines to mitoxantrone is associated with lack of apoptosis.Opposite effects of tumor necrosis factor α on the sphingomyelin-ceramide pathway in two myeloid leukemia cell lines: role of transverse sphingomyelin distribution in the plasma membrane.Restoration of TNF-α-induced ceramide generation in resistant human leukemia KG1a cells by the P-glycoprotein blocker PSC833.Sphingomyelin hydrolysis to ceramide during the execution phase of apoptosis results from phospholipid scrambling and alters cell-surface morphology.Sphingomyelin synthase, a potential regulator of intracellular levels of ceramide and diacylglycerol during SV40 transformation: does sphingomyelin synthase account for the putative phosphatidylcholine-specific phospholipase C?Stress-induced apoptosis is not mediated by endolysosomal ceramide.Differential regulation of sphingomyelinase and ceramidase activities by growth factors and cytokines: implications for cellular proliferation and differentiation.Suppression of ceramide-mediated programmed cell death by sphingosine-1-phosphate.Sphingosine 1-phosphate inhibits activation of caspases that cleave poly(ADP-ribose) polymerase and lamins during Fas- and ceramide-mediated apoptosis in Jurkat T lymphocytes.1α,25-dihydroxyvitamin D3 inhibits programmed cell death in HL-60 cells by activation of sphingosine kinase.Apoptosis-associated signaling pathways are required for chemotherapy-mediated female germ cell destruction.Modulation of renal epithelial cell growth by glucosylceramide: association with protein kinase C, sphingosine, and diacylglycerol.Structural and stereochemical studies of potent inhibitors of glucosylceramide synthase and tumor cell growth.Cell cycle arrest induced by an inhibitor of glucosylceramide synthase: correlation with cyclin-dependent kinases.Expression of glucosylceramide synthase, converting ceramide to glucosylceramide, confers adriamycin resistance in human breast cancer cells.Agents that reverse multidrug resistance, tamoxifen, verapamil, and cyclosporin A, block glycosphingolipid metabolism by inhibiting ceramide glycosylation in human cancer cells.Uncoupling ceramide glycosylation by transfection of glucosylceramide synthase antisense reverses adriamycin resistance.Alteration of the daunorubicin-triggered sphingomyelin-ceramide pathway and apoptosis in MDR cells: influence of drug transport abnormalities.Accumulation of glucosylceramide in multidrug-resistant cancer cells.Glucosylceramide: a marker for multiple-drug resistant cancers.Modification of ceramide metabolism increases cancer cell sensitivity to cytotoxics.Multidrug resistance modulators and doxorubicin synergize to elevate ceramide levels and elicit apoptosis in drug-resistant cancer cells.SDZ PSC 833, the cyclosporin A analogue and multidrug resistance modulator, activates ceramide synthesis and increases vinblastine sensitivity in drug-sensitive and drug-resistant cancer cells.Inhibition of P-glycoprotein activity and chemosensitization of multidrug-resistant ovarian carcinoma 2780 AD cells by dexanoyl glucosylceramide.Influence of Bcl-2 overexpression on the ceramide pathway in daunorubicin-induced apoptosis of leukemic cells.Attenuation of ceramide-induced apoptosis by diglyceride in human myeloid leukemia cells.Induction of apoptosis and potentiation of ceramide-mediated cytotoxicity by sphingoid bases in human myeloid leukemia cells.Receptors for granulo-macrophage colony-stimulating factor, interleukin-3, and interleukin-5.Hematopoietic cytokines inhibit apoptosis induced by transforming growth factor β1 and cancer chemotherapy compounds in myeloid leukemic cells.Protection of human myeloid leukemic cells against doxorubicin-induced apoptosis by granulocyte-macrophage colony-stimulating factor and interleukin 3.Effect of the protein kinase C inhibitor staurosporine on chemosensitivity to daunorubicin of normal and leukemic fresh myeloid cells.Kit activation inhibits daunorubicin-induced sphingomyelin cycle and apoptosis through a phospholipase Cγ and protein kinase C-dependent mechanism.Free radicals and anticancer drug resistance: oxygen free radicals in the mechanisms of drug cytotoxicity and resistance by certain tumors.Generation of daunomycin radicals on the outer side of the erythrocyte membrane.Lipid peroxidation and possible hydroxyl radical formation stimulated by the self-reduction of a doxorubicin-iron (III) complex.Glutathione regulation of neutral sphingomyelinase in tumor necrosis factor-α-induced cell death.Cytokine-mediated induction of ceramide production is redox-sensitive.Direct effect of ceramide on the mitochondrial electron transport chain leads to generation of reactive species.Implication of mitochondrial hydrogen peroxide generation in ceramide-induced apoptosis.Inhibition of apoptosis by antioxidants in the human HL-60 leukaemia cell line.Hydrogen peroxide- and fetal bovine serum-induced DNA synthesis in vascular smooth muscle cells: positive and negative regulation by protein kinase C isoforms.Three distinct mechanisms for translocation and activation of the delta subspecies of protein kinase C.Tumor necrosis factor-alpha, platelet-activating factor, and hydrogen peroxide activate protein kinase C subtypes alpha and epsilon in human saphenous vein endothelial cells.NF-κB activation by ultraviolet light not dependent on a nuclear signal.Association of Grb2 with Sos and Ras with Raf-1 upon gamma irradiation of breast cancer cells.Activation of protein kinase C by tyrosine phosphorylation in response to H2O2.Oxidative stress activates extracellular signal-regulated kinases through Src and Ras in cultured cardiac myocytes of neonatal rats.Involvement of tyrosine phosphorylation and protein kinase C in the activation of phospholipase D by H2O2 in swiss 3T3 fibroblasts.A p53-independent pathway for activation of WAF1/CIP1 expression following oxidative stress.Activation of mitogen-activated protein kinase by H2O2: role in cell survival following oxidant injury.Function and activation of NF-κB in the immune system.TNF-α and cancer therapy-induced apoptosis: potentiation by inhibition of NF-κB.Protein kinase C in adriamycin action and resistance in mouse sarcoma 180 cells.Daunorubicin- and mitoxantrone-triggered phosphatidylcholine hydrolysis: implication in drug-induced ceramide generation.Evidence for a bifurcation of the mitogenic signaling pathway activated by Ras and phosphatidylcholine-hydrolyzing phospholipase C.Platelet-derived growth factor activation of mitogen-activated protein kinase depends on the sequential activation of phosphatidylcholine-specific phospholipase C, protein kinase C-δ and Raf-1.Opposing effects of ERK and JNK-p38 MAP kinases on apoptosis.Antisense raf oligodeoxyribonucleotide is protected by liposomal encapsulation and inhibits Raf-1 protein expression in vitro and in vivo: implication for gene therapy of radioresistant cancer.Evidence supporting a signal transduction pathway leading to the radiation-resistant phenotype in human tumor cells.Protein kinase C δ isoform is critical for mitogenic signal transduction.Positioning atypical PKC isoforms in the UV-induced apoptotic signaling cascade.Atypical protein kinase C ι protects human leukemia cells against drug-induced apoptosis.Evidence for a role of phosphatidylcholine-hydrolysing phospholipase C in the regulation of protein kinase C by ras and src oncogenes.Human IL-3 receptor signaling: rapid induction of phosphatidylcholine hydrolysis is independent of protein kinase C but dependent on tyrosine phosphorylation in transfected NIH 3T3 cells.Human interleukin-3 stimulates a phosphatidylcholine specific phospholipase C and protein kinase C translocation.Function of the p55 tumor necrosis factor receptor “death domain” mediated by phosphatidylcholine-specific phospholipase C.Direct regulation of the Akt proto-oncogene product by phosphatidylinositol-3,4-biphophate.Activation of protein kinase C family members by the novel polyphosphoinositides PtdIns-3,4-P2 and PtdIns-3,4,5-P3.Activation of the ζ isozyme of protein kinase C by phosphatidylinositol 3,4,5-triphosphate.Activation of phospholipase C-γ by phosphatidylinositol 3,4,5-triphosphate.The phosphatidylinositol 3-kinase inhibitor wortmannin sensitizes murine fibroblasts and human tumor cells to radiation and blocks induction of p53 following DNA damage.Antiapoptotic signalling by the insulin-like growth factor I receptor, phosphatidylinositol 3-kinase, and Akt.Phosphoinositide 3-kinase/Akt-mediated survival pathway is activated by daunorubicin in human acute myeloid leukemia cell lines.Sensitization of HL60 human apoptosis by inhibition of PI3-kinase survival signals.Role of phosphoinositide 3-OH kinase in cell transformation and control of the actin cytoskeleton by Ras.Activation of phosphatidylinositol 3-kinase in cells expressing abl oncogene variants.Transformation of hematopoietic cells by BCR/ABL requires activation of a PI-3k/Akt-dependent pathway.Phosphatidylinositol-3 kinase activity is regulated by BCR/ABL and is required for the growth of Philadelphia chromosome-positive cells.Analysis of the mitogenic pathway of the FLT3 receptor and characterization in its C terminal region of a specific binding site for the PI3-kinase.Interleukin-3-induced phosphorylation of BAD through the protein kinase Akt.The PI 3-kinase/Akt signaling pathway delivers an apoptotic signal.Regulation of cell death protease caspase-9 by phosphorylation.Inhibition of Akt kinase by cell-permeable ceramide and its implication for ceramide-induced apoptosis.Topoisimerase poisons activate the transcription factor NF-kappaB in ACH-2 and CEM cells.Daunorubicin activates NFκB and induces κB-dependent gene expression in HL-60 promyelocytic and Jurkat T lymphoma cells.Activation of NF-κB by antineoplastic agents: role of protein kinase C.Nuclear factor-κB-dependent regulation of p53 gene expression induced by daunomycin genotoxic drug.Stable inhibition of nuclear factor kB in cancer cells does not increase sensitivity to cytotoxic drugs.Activation of the transcription factor kB in human KG-1 myeloid leukemia cells treated with 1-β-D-Arabinofuranosylcytosine.Constitutive nuclear NF kappa B/rel DNA-binding activity of rat thymocytes is increased by stimuli that promote apoptosis, but not inhibited by pyrrolidine dithiocarbamate.TNF activates NF-κB by phosphatidylcholine-specific phospholipase C-induced “acidic” sphingomyelin breakdown.Serine-protease inhibitors block neutral sphingomyelinase activation, ceramide generation and apoptosis triggered by daunorubicin.Inhibition of ceramide pathway does not affect ability of TNF-α to activate nuclear factor-κB.Dissociation of endogenous cellular ceramide from NF-κB activation.Activation of IkappaB kinase beta by protein kinase C isoforms.NF-κB activation by tumour necrosis factor requires the Akt serine-threonine kinase.NF-κB is a target of AKT in anti-apoptotic PDGF signalling.Inhibition of NF-κB/Rel induces apoptosis of murine B cells.Constitutive nuclear factor-κB-RelA activation is required for proliferation and survival of Hodgkin's disease tumor cells.An essential role for NF-κB in human CD34+ bone marrow cell survival.An essential role for NF-κB in preventing TNF-α-induced cell death.Coupling of a signal response domain in I kappa B alpha to multiple pathways for NF-kappa B activation.The ubiquitin-proteasome pathway is required for processing the NF-kappa B1 precursor protein and the activation of NF-kappa B.Immunosuppression by glucocorticoids: inhibition of NF-κB activity through induction of IκB synthesis.Role of transcriptional activation of IkBa in mediation of immunosuppression by glucocorticoids.Control of inducible chemoresistance: enhanced anti-tumor therapy through increased apoptosis by inhibition of NF-kappaB.Inactivation of the inhibitory κB protein kinase/nuclear factor κB pathway by Par-4 expression potentiates tumor necrosis factor α-induced apoptosis.Involvement of the CD95 (APO-1/FAS) receptor/ligand system in drug-induced apoptosis in leukemia cells.Drug-induced apoptosis in hepatoma cells is mediated by the CD95 (APO-1/Fas) receptor/ligand system and involves activation of wild-type p53.The CD95 (APO-1/Fas) system mediates drug-induced apoptosis in neuroblastoma cells.Activation of CD95 (APO-1/Fas) signaling by ceramide mediates cancer therapy-induced apoptosis.Comparison of apoptosis in wild-type and Fas-resistant cells: chemotherapy-induced apoptosis is not dependent on Fas/Fas ligand interactions.Drug-induced apoptosis is associated with enhanced Fas (APO-1/CD95) ligand expression but occurs independently of Fas (APO-1/CD95) signaling in human T-acute lymphatic leukemia cells.Anticancer drugs induce caspase-8/FLICE activation and apoptosis in the absence of CD95 receptor/ligand interaction.Fas ligand-independent, FADD-mediated activation of the Fas death pathway by anticancer drugs.Ultraviolet radiation-induced apoptosis is mediated by activation of CD-95 (Fas/APO-1).Ultraviolet light induces apoptosis via direct activation of CD95 (Fas/APO-1) independently of its ligand CD95L.The tyrosine kinase Lck is required for CD95-independent caspase-8 activation and apoptosis in response to ionizing radiation.FLICE, a novel FADD-homologous ICE/CED-3-like protease, is recruited to the CD95(Fas/Apo-1) death-inducing signaling complex.FLIP prevents apoptosis induced by death receptors but not by perforin/granzyme B, chemotherapeutic drugs, and gamma irradiation.Cross-resistance of CD95- and drug-induced apoptosis as a consequence of deficient activation of caspases (ICE/Ced-3 proteases).Cytokine response modifier A (CrmA) inhibits ceramide formation in response to tumor necrosis factor (TNF)-α: CrmA and Bcl-2 target distinct components in the apoptotic pathway.Ordering of ceramide formation, caspase activation, and mitochondrial changes during CD95- and DNA damage-induced apoptosis.Fas-Fas ligand-based interactions between tumor cells and tumor-specific cytotoxic T lymphocytes: a lethal two-way street.Lymphocyte apoptosis induced by CD95 (APO-1/Fas) ligand-expressing tumor cells—a mechanism of immune evasion?Sensitivity of multidrug-resistant tumor cell lines to immunologic effector cells.Immunosensitisation of prostate carcinoma cell lines for lymphocytes (CTL, TIL, LAK)-mediated apoptosis via the Fas-Fas-ligand pathway of cytotoxicity.Sensitization of cancer cells treated with cytotoxic drugs to Fas-mediated cytotoxicity.Decreased sensitivity of drug-resistant cells towards T cell cytotoxicity.Impairment of Fas-antigen expression in adriamycin-resistant but not TNF-resistant MCF-7 tumor cells.Selection for drug resistance results in resistance to Fas-mediated apoptosis.Expression of Fas/CD95 and Bcl-2 by primitive hematopoietic progenitors freshly isolated from human fetal liver.Expression and function of CD95 (FAS/apo-1) in leukemia-lymphoma tumour lines.Functional expression of Fas (CD95) in acute myeloid leukemia cells in the context of CD34 and CD38 expression: possible correlation with sensitivity to chemotherapy.Antileukemic drugs increase death receptor 5 levels and enhance Apo-2L-induced apoptosis of human acute leukemia cells.p53-dependent and -independent regulation of the death receptor killer/DR5 gene expression in response to genotoxic stress and tumor necrosis factor alpha.Increase in sequence specific DNA binding by p53 following treatment with chemotherapeutic and DNA damaging agents.p53 status and the efficacy of cancer therapy in vivo.p53-dependent apoptosis modulates the cytotoxicity of anticancer agents.Apoptosis, p53, and tumor cell sensitivity to anticancer agents.p53 mutations are associated with resistance to chemotherapy and short survival in hematologic malignancies.Expression of p53 predicts treatment failure in aggressive non-Hodgkin's lymphomas.p53 status affects the rate of the onset but not the overall extent of doxorubicin-induced cell death in Rat-1 fibroblasts constitutively expressing c-Myc.WAF1, a potential mediator of p53 tumor suppression.Decreased cytotoxic effects of doxorubicin in a human ovarian cancer-cell line expressing wild-type p53 and WAF1/CIP1 genes.Induction of the WAF1/CIP1 protein and apoptosis in human T-cell leukemia virus type I-transformed lymphocytes after treatment with adriamycin by using a p53-independent pathway.High levels of constitutive WAF1/Cip1 protein are associated with chemoresistance in acute myelogenous leukemia.Cell cycle-dependent cytotoxicity, G2/M phase arrest, and disruption of p34cdc2/cyclin B1 activity induced by doxorubicin in synchronized P388 cells.Activation of Src-like p56/p53lyn tyrosine kinase by ionizing radiation.p56/p53lyn tyrosine kinase activation in mammalian cells treated with mitomycin C.Extracellular matrix proteins protect small cell lung cancer cells against apoptosis: a mechanism for small cell lung cancer growth and drug resistance in vivo.Cell adhesion mediated drug resistance (CAM-DR): role of integrins and resistance to apoptosis in human myeloma cell lines.Adhesion receptors as regulators of the hematopoietic process.Profiling expression patterns and isolating differentially expressed genes by cDNA microarray system with colorimetry detection.Monitoring the expression profiles of doxorubicin-induced and doxorubicin-resistant cancer cells by cDNA microarray.Copyright © 2001 The American Society of Hematology
these metabolic events play a role in DNR resistance of myeloid leukemic cells.Remarkably, in drug-sensitive cells, DNR also triggers pathways that should negatively regulate apoptosis. ), in part by l'Association pour la Recherche sur le Cancer grant 5526 (G.L.
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