Search results for "Neoplastic"

showing 10 items of 2901 documents

A catch-22: Interleukin-22 and cancer.

2017

Barrier surfaces of multicellular organisms are in constant contact with the environment and infractions to the integrity of epithelial surfaces is likely a frequent event. Interestingly, components of the immune system, that can be activated by environmental compounds such as the microbiota or nutrients, are interspersed among epithelial cells or directly underlie the epithelium. It is now appreciated that immune cells continuously receive and integrate signals from the environment. Curiously, such continuous reception of stimulation does not normally trigger an inflammatory response but mediators produced by immune cells in response to such signals seem to rather promote barrier integrity…

0301 basic medicineOncologymedicine.medical_specialtymedicine.medical_treatmentImmunologyBiologyPolymorphism Single NucleotideEpitheliumMalignant transformationTight JunctionsInterleukin 2203 medical and health sciences0302 clinical medicineImmune systemInternal medicineNeoplasmsmedicineImmunology and AllergyAnimalsHumansLymphocytesIntestinal MucosaReceptorWound HealingInterleukinsMicrobiotaInnate lymphoid cellEpithelial CellsEpitheliumImmunity InnateCell biology030104 developmental biologyCytokinemedicine.anatomical_structureCell Transformation NeoplasticWound healing030215 immunologyEuropean journal of immunology
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A two-gene epigenetic signature for the prediction of response to neoadjuvant chemotherapy in triple-negative breast cancer patients

2019

Background Pathological complete response (pCR) after neoadjuvant chemotherapy (NAC) in triple-negative breast cancer (TNBC) varies between 30 and 40% approximately. To provide further insight into the prediction of pCR, we evaluated the role of an epigenetic methylation-based signature. Methods Epigenetic assessment of DNA extracted from biopsy archived samples previous to NAC from TNBC patients was performed. Patients included were categorized according to previous response to NAC in responder (pCR or residual cancer burden, RCB = 0) or non-responder (non-pCR or RCB > 0) patients. A methyloma study was performed in a discovery cohort by the Infinium HumanMethylation450 BeadChip (450K arra…

0301 basic medicineOncologymedicine.medical_treatmentADNlcsh:MedicineTriple Negative Breast NeoplasmsEpigenesis Genetic0302 clinical medicineGenetics (clinical)Triple-negative breast cancermedicine.diagnostic_testHigh-Throughput Nucleotide SequencingNuclear ProteinsMethylationMiddle AgedNeoadjuvant TherapyGene Expression Regulation NeoplasticTreatment OutcomeMyogenic Regulatory FactorsEfectes secundaris dels medicaments030220 oncology & carcinogenesisCohortFemaleTaxoidsMetilacióMicrotubule-Associated ProteinsAdultmedicine.medical_specialtylcsh:QH426-470MethylationMinor Histocompatibility Antigens03 medical and health sciencesBreast cancerTriple-negative breast cancerInternal medicineCell Line TumorBiopsyGeneticsmedicineHumansEpigeneticsMolecular BiologyEpigenetic signatureAgedChemotherapybusiness.industryGene Expression ProfilingResearchlcsh:RSequence Analysis DNADNADNA Methylationmedicine.diseaseHuman geneticsRepressor Proteinslcsh:Genetics030104 developmental biologyDrug side effectsbusinessPredictionDevelopmental Biology
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5-Fluorouracil and recombinant alpha interferon-2a in the treatment of advanced colorectal carcinoma: a dose optimization study

1990

A dose optimization study was carried out with the aim of identifying the maximally tolerated dose of recombinant alpha interferon-2a (raIFN-2a) in combination with 5-fluorouracil (5FU). 5FU was given at the dose of 750 mg/m2 over a 4-hour infusion on day 1- - greater than 5 followed by 750 mg/m2 weekly i.v. bolus. Recombinant aIFN-2a was started at 3 x 10(6) IU subcutaneously three times/week. 12 patients with advanced colorectal carcinoma were included in the study. 10 patients had previously received chemotherapy for advanced disease. Severe fatigue, most likely attributable to rIFN, was the dose-limiting toxicity. The dosage of raIFN-2a could not be further escalated above 12 x 10(6) IU…

0301 basic medicineOncologymyalgiamedicine.medical_specialtymedicine.medical_treatmentInjections Subcutaneous030106 microbiologyAlpha interferonInterferon alpha-2Gastroenterology03 medical and health sciences0302 clinical medicineBolus (medicine)Internal medicineAntineoplastic Combined Chemotherapy ProtocolsmedicineCarcinomaHumansPharmacology (medical)PharmacologyChemotherapyPerformance statusbusiness.industryCarcinomaInterferon-alphamedicine.diseaseRecombinant ProteinsInfectious DiseasesOncologyFluorouracil030220 oncology & carcinogenesisToxicityFluorouracilmedicine.symptombusinessColorectal Neoplasmsmedicine.drug
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Epigenomic landscape of human colorectal cancer unveils an aberrant core of pan-cancer enhancers orchestrated by YAP/TAZ

2021

Cancer is characterized by pervasive epigenetic alterations with enhancer dysfunction orchestrating the aberrant cancer transcriptional programs and transcriptional dependencies. Here, we epigenetically characterize human colorectal cancer (CRC) using de novo chromatin state discovery on a library of different patient-derived organoids. By exploring this resource, we unveil a tumor-specific deregulated enhancerome that is cancer cell-intrinsic and independent of interpatient heterogeneity. We show that the transcriptional coactivators YAP/TAZ act as key regulators of the conserved CRC gained enhancers. The same YAP/TAZ-bound enhancers display active chromatin profiles across diverse human t…

0301 basic medicineOrganoidEpigenomicsTranscription FactorGeneral Physics and AstronomyColorectal NeoplasmAdaptor Proteins Signal Transducing; Colorectal Neoplasms; Gene Expression Regulation Neoplastic; Histone Code; Humans; Models Genetic; Organoids; RNA-Seq; Single-Cell Analysis; Trans-Activators; Transcription Factors; Tumor Cells Cultured; Enhancer Elements Genetic; Epigenesis GeneticEpigenesis Genetic0302 clinical medicineModelsAdaptor Proteins Signal Transducing Colorectal Neoplasms Gene Expression Regulation NeoplasticHistone Code Humans Models Genetic Organoids RNA-Seq Single-Cell Analysis Trans-Activators Transcription Factors Tumor Cells Cultured Enhancer Elements Genetic Epigenesis GeneticTumor Cells CulturedCancer genomicsHistone codeRNA-SeqEpigenomicsAdaptor Proteins Signal Transducing; Colorectal Neoplasms; Gene Expression Regulation Neoplastic; Histone Code; Humans; Models Genetic; Organoids; RNA-Seq; Single-Cell Analysis; Trans-Activators; Transcription Factors; Transcriptional Coactivator with PDZ-Binding Motif Proteins; Tumor Cells Cultured; YAP-Signaling Proteins; Enhancer Elements Genetic; Epigenesis GeneticMultidisciplinaryCulturedQAdaptor Proteins3. Good healthChromatinTumor CellsGene Expression Regulation NeoplasticHistone CodeOrganoidsSingle-Cell AnalysiEnhancer Elements GeneticTrans-Activator030220 oncology & carcinogenesisSingle-Cell AnalysisColorectal NeoplasmsHumanEnhancer ElementsScienceTumour heterogeneityBiologyGeneral Biochemistry Genetics and Molecular BiologyArticle03 medical and health sciencesGeneticmedicineHumansEpigeneticsEnhancerTranscription factorAdaptor Proteins Signal TransducingNeoplasticModels GeneticSignal TransducingCancerYAP-Signaling ProteinsGeneral Chemistrymedicine.diseaseColorectal cancerdigestive system diseases030104 developmental biologyGene Expression RegulationTranscriptional Coactivator with PDZ-Binding Motif ProteinsCancer cellCancer researchTrans-ActivatorsEpigenesisTranscription Factors
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Can Immunogenic Chemotherapies Relieve Cancer Cell Resistance to Immune Checkpoint Inhibitors?

2019

The unprecedented clinical activity of checkpoint blockade in several types of cancers has formally demonstrated that anti-tumor immune responses are crucial in cancer therapy. Durable responses seen in patients treated with immune checkpoint inhibitors (ICI) show that they can trigger the establishment of long-lasting immunologic memory. This beneficial outcome is however achieved for a limited number of patients. In addition, late relapses are emerging suggesting the development of acquired resistances that compromise the anticancer efficacy of ICI. How can this be prevented through combination therapies? We here review the functions of immune checkpoints, the successes of ICI in treating…

0301 basic medicineOrganoplatinum CompoundsImmune checkpoint inhibitorsmedicine.medical_treatmentProgrammed Cell Death 1 ReceptorLeucovorinReviewLymphocyte ActivationchemotherapyimmunomodulationB7-H1 AntigenMice0302 clinical medicineAntineoplastic Agents ImmunologicalcheckpointT-Lymphocyte SubsetsNeoplasmsAntineoplastic Combined Chemotherapy ProtocolsTumor MicroenvironmentImmunology and AllergyCTLA-4 AntigenMolecular Targeted TherapyClinical Trials as TopicLymphokinesDrug Synergism3. Good healthNeoplasm ProteinsFluorouracillcsh:Immunologic diseases. AllergyImmunologyCancer therapyT cells03 medical and health sciencesImmune systemmedicineAnimalsHumanscancerIn patientChemotherapybusiness.industryCancermedicine.diseaseIpilimumabBlockade030104 developmental biologyDrug Resistance NeoplasmCancer cellCancer researchlcsh:RC581-607business030215 immunologyFrontiers in immunology
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Anticancer properties of 4-thiazolidinone derivatives depend on peroxisome proliferator-activated receptor gamma (PPARγ)

2017

Peroxisome proliferator-activated receptors (PPARs) play an important role in numerous chronic diseases such as diabetes, obesity, atherosclerosis and cancer, and PPAR modulators are among the approved drugs and drug-candidates for their treatment. The aim of this study was to elucidate the involvement of PPARs in the mechanism of cytotoxic and pro-apoptotic action of novel anticancer 4-thiazolidinone derivatives (Les-2194, Les-3377, Les-3640) and approved 4-thiazolidinones (Rosiglitazone, Pioglitazone) towards the human squamous carcinoma (SCC-15) cell line. Experiments with 4-thiazaolidinone derivatives and PPAR-specific siRNA were conducted and PPARα, PPARβ and PPARγ mRNA expression was …

0301 basic medicinePPARsCytotoxicityPeroxisome proliferator-activated receptorAntineoplastic AgentsApoptosisPharmacologySCC-1503 medical and health sciencesStructure-Activity Relationship0302 clinical medicineCell Line TumorDrug DiscoverymedicineGene silencingHumansViability assayRNA MessengerReceptorCell ProliferationPharmacologychemistry.chemical_classificationGene knockdownDose-Response Relationship DrugMolecular StructureThiazolothiopyranesOrganic ChemistryGeneral MedicineSquamous carcinomaPPAR gamma030104 developmental biologychemistryCell cultureThiazolidinone030220 oncology & carcinogenesisThiazolidinesDrug Screening Assays AntitumorRosiglitazonemedicine.drugEuropean Journal of Medicinal Chemistry
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Gene Expression (mRNA) Markers for Differentiating between Malignant and Benign Follicular Thyroid Tumours

2017

Distinguishing between follicular thyroid cancer (FTC) and follicular thyroid adenoma (FTA) constitutes a long-standing diagnostic problem resulting in equivocal histopathological diagnoses. There is therefore a need for additional molecular markers. To identify molecular differences between FTC and FTA, we analyzed the gene expression microarray data of 52 follicular neoplasms. We also performed a meta-analysis involving 14 studies employing high throughput methods (365 follicular neoplasms analyzed). Based on these two analyses, we selected 18 genes differentially expressed between FTA and FTC. We validated them by quantitative real-time polymerase chain reaction (qRT-PCR) in an independe…

0301 basic medicinePathologyMicroarrayThyroid Glandlaw.inventionlawFollicular phaseGene expressionAdenocarcinoma Follicularfollicular thyroid adenoma; follicular thyroid cancer; gene expression; microarray; meta-analysisSpectroscopyPolymerase chain reactionOligonucleotide Array Sequence Analysisfollicular thyroid cancerGeneral MedicineCANCERComputer Science ApplicationsGene Expression Regulation NeoplasticCARCINOMASFUSION ONCOGENEmicroarrayNEOPLASMSmedicine.medical_specialtyMOLECULAR MARKERSASPIRATIONBiologyCatalysisCLASSIFICATIONArticleInorganic Chemistry03 medical and health sciencesNODULESADENOMASmedicineBiomarkers TumorHumansRNA MessengerThyroid NeoplasmsPhysical and Theoretical ChemistryFollicular thyroid cancerMolecular BiologyGeneGene Expression ProfilingOrganic ChemistryThyroid adenomaACVRL1medicine.diseaseMODELmeta-analysis030104 developmental biologyfollicular thyroid adenomaMutationgene expressionInternational Journal of Molecular Sciences
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Pivotal roles of glycogen synthase-3 in hepatocellular carcinoma

2017

Hepatocellular carcinoma (HCC) is one of the most common cancers in the world, and represents the second most frequently cancer and third most common cause of death from cancer worldwide. At advanced stage, HCC is a highly aggressive tumor with a poor prognosis and with very limited response to common therapies. Therefore, there is still the need for new effective and well-tolerated therapeutic strategies. Molecular-targeted therapies hold promise for HCC treatment. One promising molecular target is the multifunctional serine/threonine kinase glycogen synthase kinase 3 (GSK-3). The roles of GSK-3β in HCC remain controversial, several studies suggested a possible role of GSK-3β as a tumor …

0301 basic medicinePathologymedicine.medical_specialtyCancer ResearchCarcinoma HepatocellularEpithelial-Mesenchymal TransitionTumor suppressor geneAntineoplastic Agentsmacromolecular substancesBiologyMetastasisGlycogen Synthase Kinase 303 medical and health sciencesWnt0302 clinical medicineGeneticTransforming Growth Factor betaGSK-3GeneticsmedicineHumansHedgehog ProteinsMolecular Targeted TherapyInsulin-Like Growth Factor IHCCIGFβ-cateninGlycogen synthaseHedgehogMolecular Biologybeta CateninGSK-3Glycogen Synthase Kinase 3 betaReceptors NotchLiver NeoplasmsWnt signaling pathwayCancermedicine.diseaseSurvival Analysisdigestive system diseasesGene Expression Regulation Neoplastic030104 developmental biology030220 oncology & carcinogenesisHepatocellular carcinomabiology.proteinCancer researchMolecular MedicineHedgehogSignal Transduction
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miR-9 and miR-200 regulate PDGFRβ-mediated endothelial differentiation of tumor cells in triple-negative breast cancer

2016

Abstract Organization of cancer cells into endothelial-like cell-lined structures to support neovascularization and to fuel solid tumors is a hallmark of progression and poor outcome. In triple-negative breast cancer (TNBC), PDGFRβ has been identified as a key player of this process and is considered a promising target for breast cancer therapy. Thus, we aimed at investigating the role of miRNAs as a therapeutic approach to inhibit PDGFRβ-mediated vasculogenic properties of TNBC, focusing on miR-9 and miR-200. In MDA-MB-231 and MDA-MB-157 TNBC cell lines, miR-9 and miR-200 promoted and inhibited, respectively, the formation of vascular-like structures in vitro. Induction of endogenous miR-9…

0301 basic medicinePathologymedicine.medical_specialtyCancer ResearchCellular differentiationBlotting WesternFluorescent Antibody TechniqueTriple Negative Breast NeoplasmsMice SCIDBiologySettore MED/08 - Anatomia PatologicaPolymerase Chain ReactionNeovascularizationReceptor Platelet-Derived Growth Factor beta03 medical and health sciencesMice0302 clinical medicinemicroRNAmedicineAnimalsHumansTriple-negative breast cancerIn Situ HybridizationRegulation of gene expressionNeovascularization PathologicCancerEndothelial CellsCell Differentiationmedicine.diseaseImmunohistochemistryGene Expression Regulation NeoplasticMicroRNAs030104 developmental biologyOncologyOncology; Cancer Research030220 oncology & carcinogenesisGene Knockdown TechniquesCancer cellCancer researchHeterograftsEctopic expressionFemalemedicine.symptom
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Increased liver carcinogenesis and enrichment of stem cell properties in livers of Dickkopf 2 (Dkk2) deleted mice.

2013

// Thorsten Maass 1 , Jens Marquardt 2 , Ju-Seog Lee 3 , Markus Krupp 4 , Peter Scholz-Kreisel 2 , Carolin Mogler 5 , Peter Schirmacher 5 , Martina Muller 1 , Heiner Westphal 6 , Peter R. Galle 2 , Andreas Teufel 1 1 Department of Internal Medicine I, University of Regensburg, Regensburg, Germany 2 I. Department of Medicine, University Medical Center Mainz, Mainz, Germany 3 Cancer Biology Program, MD Anderson Cancer Center, Houston, TX, USA 4 Department of Informatics, Johannes Gutenberg University Mainz, Mainz, Germany 5 Institute of Pathology, University of Heidelberg, Heidelberg, Germany 6 Laboratory of Mammalian Genes and Development, National Institute of Child Health and Human Develop…

0301 basic medicinePathologymedicine.medical_specialtyCarcinogenesisBiologymedicine.disease_causeTranscriptome03 medical and health sciencesMicestem cellsmedicineAtypiaAnimalsHumansGene Regulatory Networksprognostic signatureGeneWnt Signaling PathwayMice Knockouttranscriptomics profilingLiver CarcinogenesisDkk2Liver NeoplasmsGastroenterologyWnt signaling pathwaymedicine.diseaseMolecular biologyMice Inbred C57BL030104 developmental biologymedicine.anatomical_structureOncologyHepatocyteCancer researchNeoplastic Stem CellsIntercellular Signaling Peptides and ProteinsStem cellLiver cancerCarcinogenesisgenetic signatureResearch PaperOncotarget
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