Search results for "Western"

showing 10 items of 1138 documents

The expression of HSP60 and HSP10 in large bowel carcinomas with lymph node metastase

2005

Abstract Background The involvement of Heat Shock Proteins (HSP) in cancer development and progression is a widely debated topic. The objective of the present study was to evaluate the presence and expression of HSP60 and HSP10 in a series of large bowel carcinomas and locoregional lymph nodes with and without metastases. Methods 82 Astler and Coller's stage C2 colorectal cancers, of which 48 well-differentiated and 34 poorly-differentiated, were selected along with 661 lymph nodes, including 372 with metastases and 289 with reactive hyperplasia only, from the same tumours. Primitive tumours and both metastatic and reactive lymph nodes were studied; specifically, three different compartment…

Cancer ResearchPathologymedicine.medical_specialtyTime FactorsColonColorectal cancerBlotting Westernlcsh:RC254-282Surgical oncologyIntestinal NeoplasmsBiomarkers TumorChaperonin 10GeneticsmedicineCarcinomaHumansIntestine LargeNeoplasm MetastasisStage (cooking)Lymph nodeInflammationAnalysis of VarianceHyperplasiabusiness.industryCarcinomaCell DifferentiationChaperonin 60Hyperplasialcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensmedicine.diseaseImmunohistochemistryGene Expression Regulation Neoplasticmedicine.anatomical_structureOncologyLymphatic MetastasisDisease ProgressionImmunohistochemistryhspLymph NodesLymphbusinessResearch ArticleBMC Cancer
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Diorganotin(IV) and triorganotin(IV) complexes of meso-tetra(4-sulfonatophenyl) porphine induce apoptosis in A375 human melanoma cells

2006

The cytotoxic effect of several diorganotin(IV) and triorganotin(IV)-meso-tetra(4-sulfonatophenyl)porphine derivatives was tested and only the (Bu(2)Sn)(2)TPPS and the (Bu(3)Sn)(4)TPPS showed cytotoxicity on A375 human melanoma cells. To examine the pathway of (Bu(2)Sn)(2)TPPS or (Bu(3)Sn)(4)TPPS induced A375 cell death, DNA fragmentation analysis, Annexin V binding and PI uptake as well as caspases activation analysis by Western blot were carried out. A375 cells treated exhibited several typical characteristics of apoptosis. Both the (Bu(2)Sn)(2)TPPS and the (Bu(3)Sn)(4)TPPS compounds activate caspase-8 and caspase-9 leading to caspase-3 activation. Thus, we propose that these two porphiri…

Cancer ResearchPorphyrinsCytotoxicityMelamoma cellAntineoplastic AgentsApoptosisDNA FragmentationWestern blotAnnexinCell Line TumorOrganotin CompoundsPimedicineHumansCytotoxic T cellCytotoxicityMelanomaCaspasebiologymedicine.diagnostic_testTriorganotin(IV)ApoptosiFlow CytometryMolecular biologyMicroscopy FluorescenceOncologyApoptosisCaspasesbiology.proteinDNA fragmentationDiorganotin(IV)
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In BCR-ABL-positive cells, STAT-5 tyrosine-phosphorylation integrates signals induced by imatinib mesylate and Ara-C.

2003

In BCR-ABL-positive cells, the transcription factor STAT-5 is constitutively activated by tyrosine phosphorylation. STAT-5 activation results in upregulation of bcl-X(L) and increased resistance to induction of apoptosis. Here, we investigated the effects of imatinib mesylate and cytosine arabinoside (Ara-C) on STAT-5 tyrosine-phosphorylation, cellular proliferation and induction of apoptosis in cell lines and primary hematopoietic cells. Imatinib mesylate treatment strongly suppressed STAT-5 tyrosine-phosphorylation in K562 and primary CML blasts. In contrast to JAK-2 and PI-3-kinase inhibition, exposure of K562 cells to imatinib mesylate resulted in obvious suppression of proliferation. R…

Cancer ResearchProgrammed cell deathBlotting WesternFusion Proteins bcr-ablDown-RegulationAntineoplastic AgentsApoptosisBiologyPiperazineschemistry.chemical_compoundDownregulation and upregulationhemic and lymphatic diseasesLeukemia Myelogenous Chronic BCR-ABL PositivemedicineIn Situ Nick-End LabelingSTAT5 Transcription FactorHumansEnzyme InhibitorsPhosphorylationCell growthCytarabineImatinibTyrosine phosphorylationDrug SynergismHematologyDNAU937 CellsProtein-Tyrosine KinasesMilk ProteinsPrecipitin TestsDNA-Binding ProteinsImatinib mesylatePyrimidinesOncologychemistryApoptosisCaspasesBenzamidesCancer researchImatinib MesylateTrans-ActivatorsTyrosinePoly(ADP-ribose) PolymerasesK562 CellsCell Divisionmedicine.drugK562 cellsSignal TransductionLeukemia
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Hsp72 controls bortezomib-induced HepG2 cell death via interaction with pro-apoptotic factors.

2007

The proteasome inhibitor bortezomib is an efficacious inducer of apoptosis in the hepatoma HepG2 cell line. This study shows that bortezomib increased in these cells the level of the survival factor Hsp72 in a time- and dose-dependent manner. In a first phase of treatment, Hsp72 rapidly increased so that at 24 h of incubation with 50 nM bortezomib its level was approximately five-fold higher than the control. In this phase Hsp72 seemed to play a role in preventing HepG2 cell death, since it interacted with and sequestered the pro-apoptotic factors p53, AIF, Bax and Apaf-1. During a second day of treatment, although the nuclear levels of Hsp72, p53 and AIF increased, the interaction of Hsp72…

Cancer ResearchProgrammed cell deathCarcinoma HepatocellularTime FactorsCellBlotting WesternApoptosisHSP72 Heat-Shock ProteinsAmino Acid Chloromethyl KetonesBortezomibCell Line TumormedicineHumansImmunoprecipitationProtease Inhibitorscardiovascular diseasesCaspasebcl-2-Associated X ProteinOncogenebiologyBortezomibReverse Transcriptase Polymerase Chain ReactionLiver NeoplasmsApoptosis Inducing Factorproteasome inhibitor hepatocarcinoma apoptosisGeneral MedicineCell cycleBoronic Acidsmedicine.anatomical_structureApoptotic Protease-Activating Factor 1OncologyApoptosisPyrazinesProteasome inhibitorCancer researchbiology.proteinTumor Suppressor Protein p53Apoptosis Regulatory Proteinsmedicine.drugProtein Binding
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Sodium phenylbutyrate induces apoptosis in human retinoblastoma Y79 cells: The effect of combined treatment with the topoisomerase I-inhibitor topote…

2001

Our results demonstrate that sodium phenylbutyrate, a compound with a low degree of toxicity, exerted a cytotoxic effect on human retinoblastoma Y79 cells in a time- and dose-dependent manner. Treatment of Y79 cells for 72 h with phenylbutyrate reduced cell viability by 63% at 2 mM and 90% at 4 mM. Cell death caused by phenylbutyrate exhibited the typical features of apoptosis, as shown by light and fluorescent microscopy. Western blot analysis demonstrated that exposure of Y79 cells to phenylbutyrate decreased the level of the antiapoptotic factor Bcl-2 and induced the activation of caspase-3, a key enzyme in the execution phase of apoptosis. Moreover, treatment with phenylbutyrate markedl…

Cancer ResearchProgrammed cell deathCell SurvivalBlotting WesternApoptosisPhenylbutyrateHistonesSettore BIO/10 - BiochimicamedicineTumor Cells CulturedHumansretinoblastoma apoptosis sodium phenylbutirateViability assayEnzyme InhibitorsbiologyCaspase 3TopoisomeraseRetinoblastomaSodium phenylbutyrateAcetylationDrug SynergismCell cyclePhenylbutyrateseye diseasesEnzyme ActivationOncologyProto-Oncogene Proteins c-bcl-2ApoptosisCaspasesbiology.proteinCancer researchTopotecanDrug Therapy CombinationTopoisomerase I InhibitorsTumor Suppressor Protein p53Topotecanmedicine.drug
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The effect of 3-aminobenzamide, inhibitor of poly(ADP-ribose) polymerase, on human osteosarcoma cells

2003

This study demonstrates that in human osteosarcoma cells treatment with 3-aminobenzamide (3-AB), a potent inhibitor of poly(ADP-ribose) polymerase (PARP), induces morphological and biochemical features of differentiation, the duration of which depends on whether or not the normal RB gene is expressed. In Saos-2 cells expressing a non-functional Rb protein, 3-AB treatment induced the formation of transient, short dendritic-like protrusions. In RB-transfected-Saos-2 cells (a clone previously generated in our laboratory that shows stable expression of wild-type Rb protein), 3-AB induced marked and prolonged changes with the formation of long dendritic-like protrusions and the appearance of ste…

Cancer ResearchProgrammed cell deathCell typeTime FactorsTranscription GeneticCell SurvivalPoly ADP ribose polymeraseCellular differentiationBlotting WesternApoptosisDNA FragmentationPoly(ADP-ribose) Polymerase InhibitorsBiologyTransfectionPolymerase Chain ReactionRetinoblastoma Proteinchemistry.chemical_compoundCell Line TumorProto-Oncogene ProteinsHumansMicroscopy Phase-ContrastRNA MessengerEnzyme Inhibitorsbcl-2-Associated X ProteinOsteosarcomaLamin Type BCaspase 3Reverse Transcriptase Polymerase Chain ReactionCell DifferentiationDendritesCell cycleAlkaline PhosphataseFlow CytometryMolecular biologyChromatinHyaluronan ReceptorsProto-Oncogene Proteins c-bcl-2OncologychemistryApoptosis3-AminobenzamideCaspasesBenzamides3-aminobenzamide osteosarcoma cells PARP activityAlkaline phosphataseInternational Journal of Oncology
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Temozolomide- and fotemustine-induced apoptosis in human malignant melanoma cells: response related to MGMT, MMR, DSBs, and p53

2009

Malignant melanomas are highly resistant to chemotherapy. First-line chemotherapeutics used in melanoma therapy are the methylating agents dacarbazine (DTIC) and temozolomide (TMZ) and the chloroethylating agents BCNU and fotemustine. Here, we determined the mode of cell death in 11 melanoma cell lines upon exposure to TMZ and fotemustine. We show for the first time that TMZ induces apoptosis in melanoma cells, using therapeutic doses. For both TMZ and fotemustine apoptosis is the dominant mode of cell death. The contribution of necrosis to total cell death varied between 10 and 40%. The O(6)-methylguanine-DNA methyltransferase (MGMT) activity in the cell lines was between 0 and 1100 fmol m…

Cancer ResearchProgrammed cell deathDNA repairDacarbazineBlotting WesternApoptosistemozolomideBiologyCollagen Type XIDNA Mismatch RepairNecrosisGliomaAntineoplastic Combined Chemotherapy ProtocolsTumor Cells CulturedmedicineHumansDNA Breaks Double-StrandedEverolimusPhosphorylationDNA Modification MethylasesMelanomaneoplasmsSirolimusTemozolomideTumor Suppressor ProteinsMelanomafotemustinemelanoma therapymedicine.diseaseDacarbazineEnzyme Activationmismatch repairDNA Repair EnzymesOncologyApoptosisCaspasesCancer researchFotemustineTumor Suppressor Protein p53Translational TherapeuticsMGMTmedicine.drugBritish Journal of Cancer
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Sodium butyrate induces apoptosis in human hepatoma cells by a mitochondria/caspase pathway, associated with degradation of beta-catenin, pRb and Bcl…

2004

Butyrate can promote programmed cell death in a number of tumour cells in vitro. This paper provides evidence that butyrate induces apoptosis in human hepatoma HuH-6 and HepG2 cells but is ineffective in Chang liver cells, an immortalised non-tumour cell line. In both HuH-6 and HepG2 cells, apoptosis appeared after a lag period of approximately 16 h and increased rapidly during the second day of treatment. In particular, the effect was stronger in HuH-6 cells, which were, therefore, chosen for ascertaining the mechanism of butyrate action. In HuH-6 cells, beta-catenin seemed to exert an important protective role against apoptosis, since pretreatment with beta-catenin antisense ODN reduced t…

Cancer ResearchProgrammed cell deathbeta-CateninCarcinoma HepatocellularBlotting Westernbcl-X ProteinCaspase 3Bcl-xLApoptosisButyrateCell LineMembrane Potentialschemistry.chemical_compoundSettore BIO/10 - BiochimicaCyclin DCyclinsCyclin EHumansCaspasebeta CateninbiologyReverse Transcriptase Polymerase Chain ReactionCytochrome cLiver NeoplasmsSodium butyrateMolecular biologyButyratesCytoskeletal ProteinspRbOncologychemistryProto-Oncogene Proteins c-bcl-2ApoptosisCaspasesbiology.proteinTrans-ActivatorsPoly(ADP-ribose) PolymerasesEuropean journal of cancer (Oxford, England : 1990)
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The role of oxidative stress in apoptosis induced by the histone deacetylase inhibitor suberoylanilide hydroxamic acid in human colon adenocarcinoma …

2008

Histone deacetylase inhibitors (HDACIs) activate genes that promote cell cycle arrest and apoptosis in a number of tumor cells. This study showed that suberoylanilide hydroxamic acid (SAHA), a potent and commonly used HDACI, induced apoptosis in human colon adenocarcinoma HT-29 cells in a time- and dose-dependent manner. This effect was accompanied by the induction of oxidative stress, dissipation of mitochondrial transmembrane potential and activation of executioner caspases. Moreover, SAHA increased the levels of phosphorylated active forms of p38 and JNK. The addition of either the antioxidant N-acetylcysteine or the specific inhibitor of NADPH oxidase diphenylene iodonium chloride reduc…

Cancer ResearchProgrammed cell deathmedicine.drug_classCell Survivalp38 mitogen-activated protein kinasesBlotting WesternApoptosisAdenocarcinomamedicine.disease_causeHydroxamic AcidsAntioxidantsSettore BIO/10 - BiochimicamedicineHumansEnzyme InhibitorsProtein kinase BCaspaseMembrane Potential MitochondrialVorinostatbiologyHistone deacetylase inhibitorEnzyme ActivationHistone Deacetylase InhibitorsOxidative StressOncologyBiochemistryApoptosisCaspasesColonic NeoplasmsCancer researchbiology.proteinHistone deacetylaseReactive Oxygen Speciescolon adenomacarcinoma cells histone deacetylase inhibitors apoptosisHT29 CellsOxidative stressSignal TransductionInternational journal of oncology
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Large-scale proteomic identification of S100 proteins in breast cancer tissues

2010

Abstract Background Attempts to reduce morbidity and mortality in breast cancer is based on efforts to identify novel biomarkers to support prognosis and therapeutic choices. The present study has focussed on S100 proteins as a potentially promising group of markers in cancer development and progression. One reason of interest in this family of proteins is because the majority of the S100 genes are clustered on a region of human chromosome 1q21 that is prone to genomic rearrangements. Moreover, there is increasing evidence that S100 proteins are often up-regulated in many cancers, including breast, and this is frequently associated with tumour progression. Methods Samples of breast cancer t…

Cancer ResearchProteomeBlotting WesternBreast NeoplasmsBioinformaticsS100 proteinlcsh:RC254-282Cohort StudiesBreast cancerSurgical oncologyBiomarkers TumorGeneticsmedicineHumansElectrophoresis Gel Two-DimensionalBreastNeoplasm MetastasisSettore BIO/06 - Anatomia Comparata E CitologiaGeneproteomicbusiness.industryS100 ProteinsChromosomePrognosismedicine.diseaselcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensPrimary tumorS100 proteinOncologybreast cancer tissuesSpectrometry Mass Matrix-Assisted Laser Desorption-IonizationProteomeFemaleStem cellbusinessResearch ArticleBMC Cancer
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