Search results for "Neoplastic"

showing 10 items of 2901 documents

SOCS2 controls proliferation and stemness of hematopoietic cells under stress conditions and its deregulation marks unfavorable acute leukemias

2015

Abstract Hematopoietic stem cells (HSC) promptly adapt hematopoiesis to stress conditions, such as infection and cancer, replenishing bone marrow–derived circulating populations, while preserving the stem cell reservoir. SOCS2, a feedback inhibitor of JAK–STAT pathways, is expressed in most primitive HSC and is upregulated in response to STAT5-inducing cytokines. We demonstrate that Socs2 deficiency unleashes HSC proliferation in vitro, sustaining STAT5 phosphorylation in response to IL3, thrombopoietin, and GM-CSF. In vivo, SOCS2 deficiency leads to unrestricted myelopoietic response to 5-fluorouracil (5-FU) and, in turn, induces exhaustion of long-term HSC function along serial bone marro…

Cancer ResearchMyeloidSuppressor of Cytokine Signaling ProteinsMice TransgenicNeoplasm ProteinMiceBone MarrowSuppressor of Cytokine Signaling ProteinmedicineAnimalsHumansMEF2 Transcription FactorThrombopoietinSTAT5Cell ProliferationRegulation of gene expressionABLLeukemiabiologyMEF2 Transcription FactorsAnimalMedicine (all)Animals; Bone Marrow; Cell Differentiation; Cell Proliferation; Fluorouracil; Gene Expression Regulation Neoplastic; Hematopoietic Stem Cells; Humans; Leukemia; MEF2 Transcription Factors; Mice; Mice Transgenic; Neoplasm Proteins; Neoplastic Stem Cells; Suppressor of Cytokine Signaling Proteins; Cancer Research; Oncology; Medicine (all)breakpoint cluster regionCell DifferentiationHematopoietic Stem CellHematopoietic Stem CellsNeoplasm ProteinsGene Expression Regulation NeoplasticHaematopoiesismedicine.anatomical_structureOncologyImmunologybiology.proteinCancer researchNeoplastic Stem CellsFluorouracilNeoplastic Stem CellStem cellHuman
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Hybrid Magnetic Nanostructures For Cancer Diagnosis And Therapy.

2017

Cancer is the second disease in the world from the point of view of mortality. The conventional routes of treatment were found to be not sufficient and thus alternative ways are imposed. The use of hybrid, magnetic nanostructures is a promising way for simultaneous targeted diagnosis and treatment of various types of cancer. For this reason, the development of core@shell structures was found to be an efficient way to develop stable, biocompatible, non-toxic carriers with shell-dependent internalization capacity in cancer cells. So, the multicomponent approach can be the most suitable way to assure the multifunctionality of these nanostructures to achieve the desired/necessary properties. T…

Cancer ResearchNanostructureMaterials sciencePolymersmedia_common.quotation_subjectNanotechnologyAntineoplastic Agents02 engineering and technologyengineering.material010402 general chemistry01 natural sciencesCoatingNeoplasmsmedicineAnimalsHumansInternalizationMagnetite Nanoparticlesmedia_commonPharmacologychemistry.chemical_classificationCancerPolymer021001 nanoscience & nanotechnologyBiocompatible materialmedicine.disease0104 chemical sciencesMagnetic corechemistryFolic acidengineeringMolecular Medicine0210 nano-technologyAnti-cancer agents in medicinal chemistry
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Notch inhibition restores TRAIL-mediated apoptosis via AP1-dependent upregulation of DR4 and DR5 TRAIL receptors in MDA-MB-231 breast cancer cells.

2013

Notch is a family of transmembrane receptors whose activation through proteolytic cleavage by γ-secretase targets genes which participate in cell development, differentiation and tumorigenesis. Notch signaling is constitutively activated in various cancers, including breast cancer and its upregulation is usually related with poor clinical outcomes. Therefore, targeting Notch signaling with γ-secretase inhibitors (GSIs) is considered a promising strategy for cancer treatment. We report that the γ-secretase inhibitor-I (GSI-I) sensitizes human breast cancer cells to apoptosis mediated by tumor necrosis factor-related apoptosis-inducing ligand (TRAIL). The antiproliferative GSI-I/TRAIL synergi…

Cancer ResearchNotch signaling pathwayApoptosisBreast NeoplasmsBiologymedicine.disease_causeTNF-Related Apoptosis-Inducing LigandDownregulation and upregulationGenes junSettore BIO/10 - BiochimicaSurvivinmedicineHumansTranscription factorReceptors NotchCell DifferentiationCell biologyGene Expression Regulation NeoplasticReceptors TNF-Related Apoptosis-Inducing LigandOncologyApoptosisCancer cellMCF-7 CellsFemalenotch signaling γ-secretase inhibitor-I/TRAIL combined treatment apoptosis breast cancer cells AP-1Signal transductionAmyloid Precursor Protein SecretasesCarcinogenesisSignal TransductionInternational journal of oncology
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Redistribution of CD95, DR4 and DR5 in rafts accounts for the synergistic toxicity of resveratrol and death receptor ligands in colon carcinoma cells.

2004

The natural phytoalexin resveratrol (3, 5, 4'-trihydroxystilbene) exhibits both chemopreventive and antitumor activities through a variety of mechanisms. We have shown previously that resveratrol-induced apoptosis of a human colon cancer cell line involved the redistribution of CD95 (Fas/Apo-1) into lipid rafts. Here, we show that, in colon cancer cells that resist to resveratrol-induced apoptosis, the polyphenol also induces a redistribution of death receptors into lipid rafts. This effect sensitizes these tumor cells to death receptor-mediated apoptosis. In resveratrol-treated cells, tumor necrosis factor (TNF), anti-CD95 antibodies and TNF-related apoptosis-inducing ligand (TRAIL) activa…

Cancer ResearchNystatinTime FactorsApoptosisResveratrolmedicine.disease_causeLigandsReceptors Tumor Necrosis FactorTNF-Related Apoptosis-Inducing Ligandchemistry.chemical_compoundStilbenesReceptorLipid raftCaspaseMembrane GlycoproteinsbiologyFas receptorFlow CytometryLipidsMitochondriaProto-Oncogene Proteins c-bcl-2CaspasesColonic Neoplasmslipids (amino acids peptides and proteins)Tumor necrosis factor alphaSignal Transductionmedicine.medical_specialtyBlotting WesternTransfectionMembrane MicrodomainsInternal medicineCell Line TumorGeneticsmedicineHumansfas ReceptorMolecular BiologyTumor Necrosis Factor-alphaCarcinomaLipid MetabolismAntineoplastic Agents PhytogenicReceptors TNF-Related Apoptosis-Inducing LigandEndocrinologychemistryApoptosisResveratrolCancer researchbiology.proteinCarcinogenesisApoptosis Regulatory ProteinsOncogene
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Oligodendroglioma cells synthesize the differentiation-specific linker histone H1˚ and release it into the extracellular environment through shed ves…

2013

Chromatin remodelling can be involved in some of the epigenetic modifications found in tumor cells. One of the mechanisms at the basis of chromatin dynamics is likely to be synthesis and incorporation of replacement histone variants, such as the H1° linker histone. Regulation of the expression of this protein can thus be critical in tumorigenesis. In developing brain, H1° expression is mainly regulated at the post-transcriptional level and RNA-binding proteins (RBPs) are involved. In the past, attention mainly focused on the whole brain or isolated neurons and little information is available on H1° expression in other brain cells. Even less is known relating to tumor glial cells. In this st…

Cancer ResearchOligodendrogliomaGene Expressionmedicine.disease_causeHistonessheddingHistone H1Settore BIO/10 - BiochimicaGene expressionmedicineAnimalsRNA MessengerEpigeneticsRats WistarSettore BIO/06 - Anatomia Comparata E CitologiaTransport Vesicleshistone variantsCells CulturedCell NucleusMessenger RNAbiologyBrain NeoplasmsastrocytesBrainRNA-Binding ProteinsArticlesH1° histoneCell cycleChromatin Assembly and DisassemblyRatsChromatinCell biologyCell Transformation Neoplasticoligodendroglioma cellsHistoneOncologyoligodendroglioma cells astrocytes post-transcriptional regulation histone variants H1˚ histone RNA-binding proteins extracellular vesicles sheddingbiology.proteinextracellular vesiclesCarcinogenesispost-transcriptional regulation
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MLL-Rearranged Leukemia Is Dependent on Aberrant H3K79 Methylation by DOT1L

2011

SummaryThe histone 3 lysine 79 (H3K79) methyltransferase Dot1l has been implicated in the development of leukemias bearing translocations of the Mixed Lineage Leukemia (MLL) gene. We identified the MLL-fusion targets in an MLL-AF9 leukemia model, and conducted epigenetic profiling for H3K79me2, H3K4me3, H3K27me3, and H3K36me3 in hematopoietic progenitor and leukemia stem cells (LSCs). We found abnormal profiles only for H3K79me2 on MLL-AF9 fusion target loci in LSCs. Inactivation of Dot1l led to downregulation of direct MLL-AF9 targets and an MLL translocation-associated gene expression signature, whereas global gene expression remained largely unaffected. Suppression of MLL translocation-a…

Cancer ResearchOncogene Proteins FusionCellular differentiationApoptosisBiologyMethylationArticleHistonesMice03 medical and health sciences0302 clinical medicinehemic and lymphatic diseasesmedicineAnimalsHumansEpigeneticsMyeloid Ecotropic Viral Integration Site 1 ProteinneoplasmsMyeloid Progenitor Cells030304 developmental biologyGene RearrangementHomeodomain Proteins0303 health sciencesLysineMyelodysplastic syndromesCell CycleCell DifferentiationCell BiologyHistone-Lysine N-MethyltransferaseMethyltransferasesMethylationDOT1Lmedicine.diseaseMolecular biologyHematopoiesisNeoplasm Proteins3. Good healthLeukemiaCell Transformation NeoplasticOncologyGenetic Loci030220 oncology & carcinogenesisHistone methyltransferaseCancer researchH3K4me3Protein Processing Post-TranslationalMyeloid-Lymphoid Leukemia ProteinCancer Cell
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Broad-spectrum Cross-resistance to Anticancer Drugs Mediated by Epidermal Growth Factor Receptor

2019

BACKGROUND The oncogenic role of epidermal growth factor receptor (EGFR) has been intensively studied. However, its emerging role in drug resistance has not been fully addressed. MATERIALS AND METHODS This study systematically investigated the correlation of mRNA and protein expression of EGFR, as well as gene amplification and mutations with the log-transformed half-maximal inhibitory concentration (log10IC50) values obtained from the NCI panel of 60 human tumor cell lines against 83 standard anticancer agents and the top 10 natural cytotoxic products previously screened by us. RESULTS EGFR protein expression, rather than other measurements, was most frequently associated with drug respons…

Cancer ResearchOncogenebiologyChemistryTopoisomeraseAntineoplastic AgentsGeneral MedicineDrug resistanceErbB Receptors03 medical and health sciences0302 clinical medicineOncologyDrug Resistance NeoplasmCell cultureCell Line TumorNeoplasms030220 oncology & carcinogenesisPharmacogenomicsbiology.proteinCancer researchHumansCytotoxic T cellRNA MessengerEpidermal growth factor receptorCross-resistanceAnticancer 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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Altered Expression of c-IAP1, Survivin, and Smac Contributes to Chemotherapy Resistance in Thyroid Cancer Cells

2006

Abstract Resistance to chemotherapy predicts an unfavorable outcome for patients with radioiodine-insensitive thyroid cancer. To investigate the mechanisms underlying this resistance, we evaluated the expression of four different inhibitor of apoptosis proteins, and their antagonist, Smac, in thyroid cancer cells that survived 48 hours of exposure to cisplatin, doxorubicin, or taxol. We found high levels of c-IAP1 after cisplatin treatment and increased expression of survivin following exposure to doxorubicin. Cells that endured treatment with taxol showed reduced expression of Smac and released minimal amounts of this protein from the mitochondria. Down-regulation of c-IAP1 and survivin in…

Cancer ResearchPaclitaxelSurvivinmedicine.medical_treatmentAntineoplastic AgentsX-Linked Inhibitor of Apoptosis ProteinBiologyInhibitor of apoptosisInhibitor of Apoptosis ProteinsMitochondrial ProteinsCell Line TumorSurvivinmedicineHumansGene silencingCytotoxic T cellDoxorubicinThyroid NeoplasmsThyroid cancerCisplatinChemotherapyIntracellular Signaling Peptides and Proteinsmedicine.diseaseDrug Resistance MultipleNeoplasm ProteinsOncologyDoxorubicinDrug Resistance NeoplasmCancer researchCisplatinApoptosis Regulatory ProteinsMicrotubule-Associated Proteinsmedicine.drugCancer Research
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The dual PI3K/mTOR inhibitor PKI-587 enhances sensitivity to cetuximab in EGFR-resistant human head and neck cancer models

2014

Background:Cetuximab is the only targeted agent approved for the treatment of head and neck squamous cell carcinomas (HNSCC), but low response rates and disease progression are frequently reported. As the phosphoinositide 3-kinase (PI3K) and the mammalian target of rapamycin (mTOR) pathways have an important role in the pathogenesis of HNSCC, we investigated their involvement in cetuximab resistance.Methods:Different human squamous cancer cell lines sensitive or resistant to cetuximab were tested for the dual PI3K/mTOR inhibitor PF-05212384 (PKI-587), alone and in combination, both in vitro and in vivo.Results:Treatment with PKI-587 enhances sensitivity to cetuximab in vitro, even in the co…

Cancer ResearchPathologyCetuximabApoptosisHNSCCHNSCCMiceAntineoplastic Combined Chemotherapy ProtocolsNeoplasmPhosphoinositide-3 Kinase InhibitorsMice Inbred BALB CCetuximabCaspase 3TriazinesTOR Serine-Threonine KinasesCetuximab resistanceErbB ReceptorsOncologyHead and Neck NeoplasmsMonoclonalCarcinoma Squamous Cellmedicine.drugmedicine.medical_specialtyMorpholinesPI3K-mTOR inhibitorsMice NudeAntineoplastic AgentsBiologyAntibodies Monoclonal HumanizedCell Line TumorAutophagymedicineCarcinomaAnimalsHumansneoplasmsPI3K/AKT/mTOR pathwayCell Proliferationcetuximab resistanceSquamous Cell Carcinoma of Head and Necktarget therapyCell growthAutophagyCancermedicine.diseaseXenograft Model Antitumor Assaysdigestive system diseasesDrug Resistance NeoplasmPI3K7mTOR inhibitorsCancer researchTranslational TherapeuticsBritish Journal of Cancer
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