Search results for "Neoplasm Protein"

showing 10 items of 247 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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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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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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Mechanisms of tumor invasion: evidence from in vivo observations.

1985

The major mechanisms of tumor invasion in vivo are discussed in the present review. A special emphasis is placed on tumor dedifferentiation which has proved to be of paramount importance for the invasion process. Based on in vivo observations obtained from various human and animal tumors a concept for the mechanism of tumor invasion is proposed which mainly comprises the following basic events: the first and essential step in tumor invasion is the tumor dedifferentiation and dissociation at the invasion front. This apparently temporary and reversible process mobilizes the tumor cells out of the main tumor bulk and enables them to invade the host tissue by active locomotion. This mechanism i…

Cancer ResearchPathologymedicine.medical_specialtyCell divisionColonCellular differentiationBiologyHost tissueBasement MembraneExtracellular matrixIn vivoCell MovementmedicineAnimalsEdemaHumansNeoplasm InvasivenessProcess (anatomy)Cells CulturedDimethylhydrazinesCell DifferentiationMuscle SmoothCell biology12-DimethylhydrazineExtracellular MatrixNeoplasm ProteinsRatsOxygenInterstitial edemaIntercellular JunctionsOncologyColonic NeoplasmsAtrophyIntracellularCell DivisionPeptide HydrolasesCancer metastasis reviews
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Cathepsin D expression levels in nongynecological solid tumors: clinical and therapeutic implications.

2004

Cathepsin D is a lysosomal acid proteinase which is involved in the malignant progression of breast cancer and other gynecological tumors. Clinical investigations have shown that in breast cancer patients cathepsin D overexpression was significantly correlated with a shorter free-time disease and overall survival, whereas in patients with ovarian or endometrial cancer this phenomenon was associated with tumor aggressiveness and a degree of chemoresistance to various antitumor drugs such as anthracyclines, cis-platinum and vinca alkaloids. Therefore, a lot of research has been undertaken to evaluate the role and the prognostic value of cathepsin D also in other solid neoplasms. However, conf…

Cancer ResearchPathologymedicine.medical_specialtyLung NeoplasmsSkin NeoplasmsCathepsin DAntineoplastic AgentsBiologyDigestive System NeoplasmsCathepsin DMetastasisCentral Nervous System NeoplasmsBreast cancerSurgical oncologyNeoplasmsmedicineBiomarkers TumorNeoplasmHumansClinical significanceThyroid NeoplasmsMelanomaEndometrial cancerGeneral Medicinecathepsin D lysosomal proteinases matrix-metalloproteinases metastasis neoplasm plasminogen activator prognosis tumor progressionmedicine.diseaseNeoplasm ProteinsOncologyTumor progressionHead and Neck NeoplasmsDrug DesignCancer researchDisease ProgressionLysosomesUrogenital NeoplasmsClinicalexperimental metastasis
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Cytoskeletal differences between human neuroendocrine tumors: A cytoskeletal protein of molecular weight 46,000 distinguishes cutaneous from pulmonar…

1985

The cytoskeletons of various human neuroendocrine (NE) tumors were analyzed immunohistochemically using antibodies against intermediate-filament (IF) proteins as well as by two-dimensional gel electrophoresis of proteins from microdissected tissue samples. All of the tumors studied were found to contain cytokeratin filaments and are therefore referred to as 'NE tumors of the epithelial type'. In addition, neurofilaments were found in most cutaneous and some pulmonary NE tumors, as well as in medullary carcinomas of the thyroid and in pancreatic islet cell tumors. The neurofilament staining was frequently concentrated in cytoplasmic IF aggregates. Gel-electrophoretic analyses showed that all…

Cancer ResearchPathologymedicine.medical_specialtyLung NeoplasmsSkin NeoplasmsNeurofilamentCarcinoid TumorHistogenesisBiologyNeuroendocrine tumorsDiagnosis DifferentialCytokeratinIntestinal NeoplasmsKeratinmedicineCarcinomaHumansThyroid NeoplasmsCarcinoma Small CellMolecular Biologychemistry.chemical_classificationThyroidCell Biologymedicine.diseaseNeoplasm ProteinsMolecular WeightPancreatic NeoplasmsCytoskeletal Proteinsmedicine.anatomical_structurechemistryImmunologyPancreasDevelopmental BiologyDifferentiation
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Mcl-1 is an anti-apoptotic factor for human hepatocellular carcinoma

2005

Defects in apoptosis signaling in hepatocytes contribute to tumorigenesis in hepatocellular carcinoma (HCC). In addition, treatment with chemotherapeutic drugs is often ineffective in HCC patients due to the apoptosis resistance of cancer cells. Anti-apoptotic members of the Bcl-2 family, including myeloid cell leukemia-1 (Mcl-1), which regulate intrinsic apoptosis induction at the mito-chondrial level, are often overexpressed in human cancer, and are implicated with disease grade and prognosis. Yet, little is known about the role of Mcl-1 in HCC. In this study, we analyzed the relevance of Mcl-1 expression for the apop-tosis resistance of human HCC. Mcl-1 protein expression was considerabl…

Cancer ResearchProgrammed cell deathCarcinoma HepatocellularApoptosisBiologyPhosphatidylinositol 3-KinasesEpidermal growth factorhemic and lymphatic diseasesTumor Cells CulturedmedicineHumansneoplasmsProtein kinase BPI3K/AKT/mTOR pathwayAkt/PKB signaling pathwayGene Expression ProfilingLiver NeoplasmsIntrinsic apoptosisPrognosisdigestive system diseasesNeoplasm ProteinsProto-Oncogene Proteins c-bcl-2OncologyImmunologyCancer cellCancer researchMyeloid Cell Leukemia Sequence 1 ProteinHepatocyte growth factorProto-Oncogene Proteins c-aktmedicine.drugInternational Journal of Oncology
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Nupr1-Aurora Kinase A Pathway Provides Protection against Metabolic Stress-Mediated Autophagic-Associated Cell Death

2012

Abstract Purpose: The limited supply of oxygen and nutrients is thought to result in rigorous selection of cells that will eventually form the tumor. Experimental Design: Nupr1 expression pattern was analyzed in human tissue microarray (TMA) and correlated with survival time of the patient. Microarray analysis was conducted on MiaPaCa2 cells subjected to metabolic stress in Nupr1-silenced conditions. DNA repair and cell cycle–associated gene expression was confirmed by real-time quantitative PCR (qRT-PCR). Nupr1 and AURKA protective role were analyzed using RNA interference (RNAi) silencing or overexpression. DNA damage and autophagy were analyzed by Western blot analysis and immunofluoresc…

Cancer ResearchProgrammed cell deathCell SurvivalDNA damageDNA repairAdenocarcinomaProtein Serine-Threonine KinasesBiologyAurora KinasesStress PhysiologicalCell Line TumorAutophagyBasic Helix-Loop-Helix Transcription FactorsHumansGene silencingAurora Kinase ARegulation of gene expressionGene knockdownMicroarray analysis techniquesAURKA GeneMolecular biologyCell HypoxiaNeoplasm ProteinsCell biologyGene Expression Regulation NeoplasticGlucoseOncologyRNA InterferenceCarcinoma Pancreatic DuctalClinical Cancer Research
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Dynamic survivin in head and neck cancer: Molecular mechanism and therapeutic potential

2007

Although disease management of head and neck squamous cell carcinomas (HNSCC) has improved significantly, therapy resistance leading to tumor recurrence still counteracts improvement of long-term survival. Consequently, identification of molecular markers that signal increased risk of treatment failure or, which can be exploited by targeted therapy, is urgently needed. Survivin is strongly expressed in HNSCC, and its proposed dual role as an apoptosis inhibitor and a mitotic effector positioned survivin in the front line of cancer research. Notably, survivin is detected as a cytoplasmic and as a nuclear protein in HNSCC patients, which stimulated numerous studies to investigate and to specu…

Cancer ResearchProgrammed cell deathPathologymedicine.medical_specialtyApoptosis InhibitorSurvivinmedicine.medical_treatmentCellBiologyInhibitor of Apoptosis ProteinsTargeted therapySurvivinBiomarkers TumormedicineAnimalsHumansNuclear proteinneoplasmsHead and neck cancerCell cyclePrognosismedicine.diseaseNeoplasm Proteinsmedicine.anatomical_structureOncologyHead and Neck NeoplasmsCancer researchMicrotubule-Associated ProteinsBiologie
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Resistance to diverse apoptotic triggers in multidrug resistant HL60 cells and its possible relationship to the expression of P-glycoprotein, Fas and…

2002

We studied the human HL60 leukemia cell line and its multidrug resistant (MDR) variant HL60R. In contrast to the HL60, HL60R showed an inability to undergo apoptosis from doxorubicin (Dox) or other different stimuli, including cisplatin, Fas ligation and serum withdrawal. HL60R cells lost surface Fas expression, but we found no evidence that Fas/FasL mediates the apoptotic effects of Dox in HL60. P-glycoprotein (P-gp) did not seem to play a major role as a specific inhibitor of apoptosis. In fact, the P-gp inhibitor verapamil reversed only partially the resistance to Dox-induced apoptosis of the MDR cells. In addition, it did not modify the rate of apoptosis induced from the other stimuli i…

Cancer ResearchProgrammed cell deathTime FactorsChromosomal Proteins Non-HistoneSurvivinDown-RegulationAntineoplastic AgentsApoptosisHL-60 CellsNerve Tissue ProteinsBiologyInhibitor of apoptosisFas ligandInhibitor of Apoptosis ProteinsInhibitory Concentration 50SurvivinTumor Cells CulturedHumansATP Binding Cassette Transporter Subfamily B Member 1RNA Messengerfas ReceptorP-glycoproteinInhibitor of apoptosis domainCaspase 3Reverse Transcriptase Polymerase Chain ReactionProteinsFlow CytometryNeuronal Apoptosis-Inhibitory ProteinNeoplasm ProteinsCell biologyProto-Oncogene Proteins c-bcl-2OncologyDoxorubicinDrug Resistance NeoplasmApoptosisCaspasesbiology.proteinInsect ProteinsNAIPCisplatinMicrotubule-Associated ProteinsCancer Letters
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