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showing 10 items of 2193 documents

The new iodoacetamidobenzofuran derivative TR120 decreases STAT5 expression and induces antitumor effects in imatinib-sensitive and imatinib-resistan…

2013

The identification of novel compounds modulating the expression/activity of molecular targets downstream to BCR-ABL could be a new approach in the treatment of chronic myeloid leukemias (CMLs) resistant to imatinib or other BCR-ABL-targeted molecules. Recently, we synthesized a new class of substituted 2-(3,4,5-trimethoxybenzoyl)-2-N,N-dimethylamino-benzo[b]furans, and among these 3-iodoacetylamino-6-methoxybenzofuran-2-yl(3,5-trimethoxyphenyl)methanone (TR120) showed marked cytotoxic activity in BCR-ABL-expressing cells. Interestingly, TR120 was more potent than imatinib in cell growth inhibition and apoptosis induction in both BCR-ABL-expressing K562 and KCL22 cells. Moreover, it showed a…

Cancer ResearchFusion Proteins bcr-ablApoptosisPiperazinesSettore MED/15 - Malattie Del Sanguechemistry.chemical_compoundhemic and lymphatic diseasesSTAT5 Transcription FactorCytotoxic T cellPharmacology (medical)Cyclin D1STAT5biologyDrug SynergismCell cycleNeoplasm ProteinsGene Expression Regulation NeoplasticLeukemiaOncologyProto-Oncogene Proteins c-bcl-2BenzamidesImatinib MesylateGrowth inhibitionmedicine.drugbcl-X ProteinDown-RegulationAntineoplastic AgentsBone Marrow CellsResting Phase Cell CycleColony-Forming Units AssayBenzophenonesNecrosisCell Line TumorLeukemia Myelogenous Chronic BCR-ABL PositivemedicineHumansneoplasmsBenzofuransPharmacologyG1 PhaseImatinibBCR-ABL chronic myeloid leukemia imatinib resistance STAT5 tyrosine kinase inhibitorsmedicine.diseaseSettore CHIM/08 - Chimica FarmaceuticaGenes bcl-1Genes bcl-2PyrimidineschemistryApoptosisDrug Resistance NeoplasmSettore BIO/14 - FarmacologiaCancer researchbiology.proteinK562 CellsK562 cells
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STAT5 is crucial to maintain leukemic stem cells in acute myelogenous leukemias induced by MOZ-TIF2.

2012

Abstract MOZ-TIF2 is a leukemogenic fusion oncoprotein that confers self-renewal capability to hematopoietic progenitor cells and induces acute myelogenous leukemia (AML) with long latency in bone marrow transplantation assays. Here, we report that FLT3-ITD transforms hematopoietic cells in cooperation with MOZ-TIF2 in vitro and in vivo. Coexpression of FLT3-ITD confers growth factor independent survival/proliferation, shortens disease latency, and results in an increase in the number of leukemic stem cells (LSC). We show that STAT5, a major effector of aberrant FLT3-ITD signal transduction, is both necessary and sufficient for this cooperative effect. In addition, STAT5 signaling is essent…

Cancer ResearchMyeloidOncogene Proteins Fusionmedicine.medical_treatmentArticleMyelogenousMicehemic and lymphatic diseasesmedicineSTAT5 Transcription FactorAnimalsSTAT5Mice Inbred BALB CbiologyGrowth factormedicine.diseaseFlow CytometryHaematopoiesisLeukemiaBlotting SouthernLeukemia Myeloid Acutemedicine.anatomical_structureCell Transformation NeoplasticOncologyCancer researchbiology.proteinNeoplastic Stem CellsSignal transductionStem cellSignal TransductionCancer research
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Uncommon Synchronous Association between Ovarian Carcinoma and Gastrointestinal Stromal Tumor: A Case Study and Literature Review

2013

Background The association of gastrointestinal stromal tumors (GIST) and other cancers is well known, but its synchronous occurrence with gynecological malignancies is very uncommon. Usually, the diagnosis is accidentally established. We describe a patient with GIST and concurrent ovarian cancer and discuss the clinical implications of this finding. Case report A 64-year-old woman with a prior diagnosis of ovarian cancer developed a second recurrence after having undergone two operations and adjuvant chemotherapy. While tumor debulking was performed, a small, nonsuspicious lesion was removed from the greater curvature of the stomach. Histology revealed a GIST. Conclusion The association of …

Cancer ResearchPaclitaxelGastrointestinal Stromal TumorsOvariectomyAntigens CD34Carcinoma Ovarian EpithelialCystectomyHysterectomyCarboplatin030218 nuclear medicine & medical imagingNeoplasms Multiple PrimarySalpingectomy03 medical and health sciencesPancreatectomy0302 clinical medicineOvarian cancerSynchronous occurrenceStomach NeoplasmGastrectomyStomach NeoplasmsAntineoplastic Combined Chemotherapy ProtocolsGastrointestinal Stromal TumorBiomarkers TumorHumansNeoplasms Glandular and EpithelialColectomyOvarian NeoplasmsAntineoplastic Combined Chemotherapy ProtocolOvarian NeoplasmGeneral MedicineMiddle AgedImmunohistochemistryProto-Oncogene Proteins c-kitTreatment OutcomeOncologyChemotherapy AdjuvantCA-125 Antigen030220 oncology & carcinogenesisSplenectomyLymph Node ExcisionFemaleHumanTumori Journal
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Cancer-cell traffic in the liver. I. Growth kinetics of cancer cells after portal-vein delivery

1992

Following the intrasplenic injection of B16F10 melanoma cells into mice, at first single cells, and later multicellular tumor foci were observed at different times in the liver. Cell numbers and tumor volumes were determined over the next 12 days, by confocal microscopy of thick liver sections. Fifteen minutes after injection, approximately 20% of the melanoma cells were identified in the liver microvasculature; after 48 hr, only 0.68% of these retained morphologic integrity; by 5 days only 0.13% of the originally detected cells incorporated BUdR; and, by 12 days, these subsequently grew into tumor nodules. Tumor volume changes with time were not exponential and, following a non-replicative…

Cancer ResearchPathologymedicine.medical_specialtyTime FactorsPopulationMelanoma ExperimentalMetastasisMiceMesenteric VeinsParenchymaAnimalsMedicineeducationeducation.field_of_studyPortal Veinbusiness.industryCell growthMelanomaLiver Neoplasmsmedicine.diseaseExtravasationMice Inbred C57BLTransplantationOncologySplenic VeinInjections IntravenousCancer cellFemalebusinessCell DivisionNeoplasm TransplantationInternational Journal of Cancer
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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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Galangin increases the cytotoxic activity of imatinib mesylate in imatinib-sensitive and imatinib-resistant Bcr-Abl expressing leukemia cells

2008

Resistance to imatinib mesylate is an emergent problem in the treatment of Bcr-Abl expressing myelogenous leukemias and additional therapeutic strategies are required. We observed that galangin, a non-toxic, naturally occurring flavonoid was effective as anti-proliferative, and apoptotic agent in Bcr-Abl expressing K562 and KCL22 cells and in imatinib mesylate resistant K562-R and KCL22-R cells. Galangin induced an arrest of cells in G0–G1phase of cell cycle and a decrease in pRb, cdk4, cdk1, cycline B levels; moreover, it was able to induce a monocytic differentiation of leukemic Bcr-Abl+ cells. Of note, galangin caused a decrease in Bcl-2 levels and markedly increased the apoptotic activi…

Cancer ResearchSettore MED/17 - Malattie InfettiveSettore MED/06 - Oncologia MedicaApoptosisPharmacologyResting Phase Cell CyclePiperazineschemistry.chemical_compoundCell Line TumorLeukemia Myelogenous Chronic BCR-ABL Positivehemic and lymphatic diseasesAntineoplastic Combined Chemotherapy ProtocolsmedicineHumansCytotoxic T cellChrysinneoplasmsFlavonoidsLeukemiaG1 PhaseApoptosiCell DifferentiationImatinibmedicine.diseaseSettore CHIM/08 - Chimica FarmaceuticaGalanginLeukemiaPyrimidinesImatinib mesylateOncologychemistryDrug Resistance NeoplasmImatinibBenzamidesSettore BIO/14 - FarmacologiaImatinib MesylateK562 CellsFisetinBcr-AblK562 cellsmedicine.drugCancer Letters
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Second St. Gallen European Organisation for Research and Treatment of Cancer Gastrointestinal Cancer Conference: consensus recommendations on controv…

2016

Contains fulltext : 171468pub.pdf (Publisher’s version ) (Open Access) Primary treatment of rectal cancer was the focus of the second St. Gallen European Organisation for Research and Treatment of Cancer (EORTC) Gastrointestinal Cancer Conference. In the context of the conference, a multidisciplinary international expert panel discussed and voted on controversial issues which could not be easily answered using published evidence. Main topics included optimal pretherapeutic imaging, indication and type of neoadjuvant treatment, and the treatment strategies in advanced tumours. Here we report the key recommendations and summarise the related evidence. The treatment strategy for localised rect…

Cancer ResearchStagingColorectal cancermedicine.medical_treatmentNeoplasias Gastrointestinais030230 surgerySYNCHRONOUS LIVER METASTASESImagingCOLORECTAL-CANCER0302 clinical medicineADJUVANT CHEMOTHERAPYTumours of the digestive tract Radboud Institute for Molecular Life Sciences [Radboudumc 14]SHORT-COURSE RADIOTHERAPYRectal cancerNeoadjuvant therapyGastrointestinal NeoplasmsRectal Neoplasms/drug therapyCombination chemotherapyChemoradiotherapyCombined Modality TherapyTotal mesorectal excisionNeoadjuvant TherapyEuropeNeoplasias do Recto/quimioterapiaOncology030220 oncology & carcinogenesisMEDIAN FOLLOW-UPLife Sciences & BiomedicineDiagnostic Imagingmedicine.medical_specialtyAntineoplastic AgentsLOCAL RECURRENCERisk AssessmentCOURSE PREOPERATIVE RADIOTHERAPY03 medical and health sciencesmedicineHumansGastrointestinal cancerOncology & CarcinogenesisRadiochemotherapyNeoplasm StagingScience & TechnologyRadiotherapyRectal Neoplasmsbusiness.industryGeneral surgeryTOTAL MESORECTAL EXCISIONCancerRANDOMIZED PHASE-IIImedicine.diseaseSurgeryRadiation therapySurgerybusiness1112 Oncology And CarcinogenesisChemoradiotherapyPOSTOPERATIVE CHEMORADIOTHERAPY
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Influence of interferon-alpha on cytokine expression by the bone marrow microenvironment--impact on treatment of myeloproliferative disorders.

1996

Myeloproliferative disorders (MPD) are characterized by several common clinical and biological features, although at the molecular level, each disease entity exhibits distinct abnormalities. IFN-alpha exerts beneficial therapeutic effects in chronic myelogenous leukemia, polycythemia vera and essential thrombocythemia, resulting in control of hematopoietic hyperplasia and, in a minority of patients, in induction of cytogenetic remission. The mechanism of action of IFN-alpha in MPD is poorly defined. Recently published in vitro findings suggest that IFN-alpha interacts with the regulation of hematopoiesis by multiple ways. Its antiproliferative activity is well known for more than a decade, …

Cancer ResearchStromal cellAlpha interferonBiologyPolycythemia veraMyeloproliferative DisordersBone Marrowhemic and lymphatic diseasesmedicineCell AdhesionHumansImmunologic FactorsProgenitor cellMyeloproliferative DisordersEssential thrombocythemiaInterferon-alphaHematologymedicine.diseaseHematopoietic Stem Cellsmedicine.anatomical_structureOncologyAdipose TissueGene Expression RegulationConnective TissueImmunologyCytokinesBone marrowCell DivisionChronic myelogenous leukemiaLeukemialymphoma
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Carboxyamidotriazole inhibits cell growth of imatinib-resistant chronic myeloid leukaemia cells including T315I Bcr-Abl mutant by a redox-mediated me…

2010

Mutation of the Bcr–Abl oncoprotein is one of most frequent mechanisms by which chronic myelogenous leukemia (CML) cells become resistant to imatinib. Here, we show that treat- ment of cell lines harbouring wild type or mutant BCR–ABL with carboxyamidotriazole (CAI), a calcium influx and signal transduction inhibitor, inhibits cell growth, the expres- sion of Bcr–Abl and its downstream signalling, and induces apoptosis. Moreover, we show that CAI acts by increasing intracellular ROS. Clinically significant, CAI has also inhibitory effects on T315I Bcr–Abl mutant, a mutation that causes CML cells to become insensitive to imatinib and second generation abl kinase inhibitors.

Cancer Researchbcr-abl Carboxyamidotriazole chronic myeloid leukemia cells imatinibBlotting WesternFusion Proteins bcr-ablAntineoplastic AgentsApoptosisSignal transduction inhibitorBiologyPiperazineschemistry.chemical_compoundMicehemic and lymphatic diseasesCell Line TumorLeukemia Myelogenous Chronic BCR-ABL PositivemedicineAnimalsHumansneoplasmsCell ProliferationSettore MED/04 - Patologia GeneraleABLCarboxyamidotriazoleCell growthWild typeImatinibTriazolesmedicine.diseaseImatinib mesylatePyrimidinesOncologychemistryDrug Resistance NeoplasmBenzamidesMutationCancer researchImatinib MesylateReactive Oxygen SpeciesOxidation-ReductionChronic myelogenous leukemiamedicine.drug
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Can curcumin induces selective packaging of miRNAs in exosomes? A pilot study in chronic myelogenous leukemia cells.

2015

e13563 Background: Chronic myeloid leukemia is a myeloproliferative disorder that comes from a hematopoietic stem cell or a multipotent progenitor. Exosomes are biological nanovescicles (40-100 nm)...

Cancer Researchbusiness.industryHematopoietic stem cellMyeloid leukemiamedicine.diseaseMicrovesicleschemistry.chemical_compoundmedicine.anatomical_structureOncologychemistryhemic and lymphatic diseasesmicroRNAmedicineCurcuminCancer researchbusinessChronic myelogenous leukemiaProgenitorJournal of Clinical Oncology
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