Search results for " Neoplastic"

showing 10 items of 662 documents

An immune escape screen reveals Cdc42 as regulator of cancer susceptibility to lymphocyte-mediated tumor suppression.

2007

Abstract Adoptive cellular immunotherapy inducing a graft-versus-tumor (GVT) effect is the therapeutic mainstay of allogeneic hematopoietic stem cell transplantation (ASCT) for high-risk leukemias. Autologous immunotherapies using vaccines or adoptive transfer of ex vivo–manipulated lymphocytes are clinically explored in patients with various cancer entities. Main reason for failure of ASCT and cancer immunotherapy is progression of the underlying malignancy, which is more prevalent in patients with advanced disease. Elucidating the molecular mechanisms contributing to immune escape will help to develop strategies for the improvement of immunologic cancer treatment. To this end, we have und…

MAPK/ERK pathwayCytotoxicity ImmunologicAdoptive cell transferTranscription GeneticMAP Kinase Signaling Systemmedicine.medical_treatmentImmunologyMolecular Sequence DataApoptosisBiologyBiochemistryMiceImmune systemCancer immunotherapyNeoplasmsmedicineCytotoxic T cellAnimalsHumansLymphocytescdc42 GTP-Binding ProteinCells CulturedBase SequenceCancerCell BiologyHematologymedicine.diseaseGene Expression Regulation NeoplasticMice Inbred C57BLCdc42 GTP-Binding ProteinProto-Oncogene Proteins c-bcl-2ImmunologyCancer cellCancer researchDisease SusceptibilityNeoplasm TransplantationBlood
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Erythropoietin activates cell survival pathways in breast cancer stem-like cells to protect them from chemotherapy

2013

Abstract Recombinant erythropoietin (EPO) analogs [erythropoiesis-stimulating agents (ESA)] are clinically used to treat anemia in patients with cancer receiving chemotherapy. After clinical trials reporting increased adverse events and/or reduced survival in ESA-treated patients, concerns have been raised about the potential role of ESAs in promoting tumor progression, possibly through tumor cell stimulation. However, evidence is lacking on the ability of EPO to directly affect cancer stem–like cells, which are thought to be responsible for tumor progression and relapse. We found that breast cancer stem–like cells (BCSC) isolated from patient tumors express the EPO receptor and respond to …

MAPK/ERK pathwayOncologyCancer Researchmedicine.medical_treatmentFluorescent Antibody TechniqueApoptosisMice SCIDImmunoenzyme TechniquesMiceCell MovementMice Inbred NODhemic and lymphatic diseasesTumor Cells CulturedCulturedBlottingAnemiaFlow CytometryTumor CellsTRIALSOncologyDisease ProgressionNeoplastic Stem CellsFemaleWesternSignal Transductionmedicine.drugSTIMULATING AGENTSEXPRESSIONmedicine.medical_specialtyBlotting WesternAntineoplastic AgentsBreast NeoplasmsSCIDRECOMBINANT-HUMAN-ERYTHROPOIETIN STIMULATING AGENTS EXPRESSION MORTALITY TRIALS ANEMIA ALPHA ALDH1Breast cancerIn vivoInternal medicinemedicineAnimalsHumansBreast cancer Cancer stem cellsALDH1ErythropoietinProtein kinase BCell ProliferationSettore MED/04 - Patologia GeneraleChemotherapybusiness.industryMORTALITYCancerRECOMBINANT-HUMAN-ERYTHROPOIETINmedicine.diseaseALPHAErythropoietinTumor progressionInbred NODAnemia; Animals; Antineoplastic Agents; Apoptosis; Blotting Western; Breast Neoplasms; Cell Movement; Cell Proliferation; Disease Progression; Erythropoietin; Female; Flow Cytometry; Fluorescent Antibody Technique; Humans; Immunoenzyme Techniques; Mice; Mice Inbred NOD; Mice SCID; Neoplastic Stem Cells; Signal Transduction; Tumor Cells Cultured; Cancer Research; Oncologybusiness
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Emerging Raf inhibitors

2009

The Raf/MAPK kinase/extracellular-signal-regulated kinase pathway is often activated by genetic alterations in upstream signaling molecules. An integral component of this pathway, BRAF, is also activated by mutation, especially in melanoma and thyroid cancers. The Raf/MAPK kinase/extracellular-signal-regulated kinase pathway has profound effects on proliferative, apoptotic and differentiation pathways as well as the sensitivity and resistance to chemotherapeutic drugs.This review discusses targeting of Raf which could control abnormal proliferation in cancer and other proliferative diseases. The important roles that genetics plays in the response of patients to Raf inhibitors is also evalua…

MAPK/ERK pathwayProto-Oncogene Proteins B-rafCell signalingMAP Kinase Signaling SystemSignal transductionrafmedicine.disease_causemekerkmedicineHumanscancerPharmacology (medical)raf inhibitorsExtracellular Signal-Regulated MAP KinasesMelanomaProtein Kinase InhibitorsPharmacologyapoptosis cancer ERK proliferative disorderssignal transductionMitogen-Activated Protein Kinase KinasesApoptosis; Cancer; ERK; Kinases; MEK; Proliferative disorders; Protein phosphorylation; Raf; Raf inhibitors; Signal transductionMutationproliferative disordersapoptosis; cancer; erk; kinases; mek; proliferative disorders; protein phosphorylation; raf; raf inhibitors; signal transduction read more: http://informahealthcare.com/doi/abs/10.1517/14728210903232633business.industryKinaseMelanomaapoptosisCancermedicine.diseaseXenograft Model Antitumor Assaysprotein phosphorylationCell Transformation Neoplastickinasessignal transduction read more: http://informahealthcare.com/doi/abs/10.1517/14728210903232633ApoptosisDrug Resistance NeoplasmCancer researchSignal transductionMitogen-Activated Protein Kinasesbusiness
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Expression of spindle assembly checkpoint proteins BubR1 and Mad2 expression as potential biomarkers of malignant transformation of oral leukoplakia:…

2021

Background The Spindle Assembly Checkpoint (SAC) is a surveillance mechanism essential to ensure the accuracy of chromosome segregation during mitosis. Our aim was to evaluate the expression of SAC proteins in oral carcinogenesis, and to assess their potential in predicting malignant transformation of oral leukoplakia. Material and Methods We analysed the immunoexpression of BubR1, Mad2, Bub3, and Spindly proteins in 64 oral biopsies from 52 oral leukoplakias and 12 normal tissues. Univariate and multivariate analysis were performed to evaluate predictive factors for malignant transformation (MT). Results We observed that BubR1 and Mad2 were more highly expressed in high dysplasia grade les…

Mad2BUB3medicine.disease_causeMalignant transformationOral Cancer and Potentially malignant disordersmedicineoral dysplasiawnt ligandsHumansGeneral DentistryMitosisUNESCO:CIENCIAS MÉDICASLeukoplakiadestruction complexbusiness.industryResearchoral cancermedicine.disease?-cateninSpindle checkpointstomatognathic diseasesCell Transformation NeoplasticOtorhinolaryngologyDysplasiaMad2 ProteinsCancer researchM Phase Cell Cycle CheckpointsSurgeryLeukoplakia OralbusinessCarcinogenesisBiomarkersMedicina Oral, Patología Oral y Cirugía Bucal
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Vitronectin as a molecular player of the tumor microenvironment in neuroblastoma

2019

Background Vitronectin is a multifunctional glycoprotein known in several human tumors for its adhesive role in processes such as cell growth, angiogenesis and metastasis. In this study, we examined vitronectin expression in neuroblastoma to investigate whether this molecule takes part in cell-cell or cell-extracellular matrix interactions that may confer mechanical properties to promote tumor aggressiveness. Methods We used immunohistochemistry and image analysis tools to characterize vitronectin expression and to test its prognostic value in 91 neuroblastoma patients. To better understand the effect of vitronectin, we studied its in vitro expression using commercial neuroblastoma cell lin…

Male0301 basic medicineCancer ResearchAngiogenesislcsh:RC254-282MetastasisExtracellular matrixMice03 medical and health sciencesNeuroblastoma0302 clinical medicineCell Line TumorNeuroblastomaImage Interpretation Computer-AssistedTumor MicroenvironmentGeneticsmedicineAnimalsHumansDigital pathologyVitronectinMigrationTumor microenvironmentbiologyCell growthChemistryExtracellular matrixlcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensPrognosismedicine.diseaseSurvival AnalysisUp-RegulationGene Expression Regulation Neoplastic030104 developmental biologyOncology030220 oncology & carcinogenesisCancer researchbiology.proteinImmunohistochemistryFemaleVitronectinNeoplasm TransplantationResearch Article
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Metabolic Inflammation-Associated IL-17A Causes Non-alcoholic Steatohepatitis and Hepatocellular Carcinoma

2016

Obesity increases hepatocellular carcinoma (HCC) risks via unknown mediators. We report that hepatic unconventional prefoldin RPB5 interactor (URI) couples nutrient surpluses to inflammation and non-alcoholic steatohepatitis (NASH), a common cause of HCC. URI-induced DNA damage in hepatocytes triggers inflammation via T helper 17 (Th17) lymphocytes and interleukin 17A (IL-17A). This induces white adipose tissue neutrophil infiltration mediating insulin resistance (IR) and fatty acid release, stored in liver as triglycerides, causing NASH. NASH and subsequently HCC are prevented by pharmacological suppression of Th17 cell differentiation, IL-17A blocking antibodies, and genetic ablation of t…

Male0301 basic medicineCancer ResearchCarcinoma HepatocellularInflammationWhite adipose tissueDiet High-FatMice03 medical and health sciencesNon-alcoholic Fatty Liver DiseasemedicineAnimalsHumansUnconventional prefoldin RPB5 interactorbiologyInterleukin-17Liver NeoplasmsFatty liverIntracellular Signaling Peptides and ProteinsCell Biologymedicine.diseasedigestive system diseasesGene Expression Regulation NeoplasticRepressor Proteins030104 developmental biologyNeutrophil InfiltrationOncologyHepatocellular carcinomaImmunologybiology.proteinTh17 CellsInterleukin 17SteatosisSteatohepatitismedicine.symptomDNA DamageCancer Cell
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Evidence for PTGER4 ,PSCA, and MBOAT7 as risk genes for gastric cancer on the genome and transcriptome level

2018

Genetic associations between variants on chromosome 5p13 and 8q24 and gastric cancer (GC) have been previously reported in the Asian population. We aimed to replicate these findings and to characterize the associations at the genome and transcriptome level. We performed a fine-mapping association study in 1926 GC patients and 2012 controls of European descent using high dense SNP marker sets on both chromosomal regions. Next, we performed expression quantitative trait locus (eQTL) analyses using gastric transcriptome data from 143 individuals focusing on the GC associated variants. On chromosome 5p13 the strongest association was observed at rs6872282 (P = 2.53 x 10(-04)) and on chromosome …

Male0301 basic medicineCancer ResearchGenotypeQuantitative Trait LocieQTL studyBiologyGPI-Linked ProteinsPolymorphism Single NucleotideGenomeTranscriptome03 medical and health sciencesAntigens NeoplasmStomach NeoplasmsGene expressionmedicineHumansSNPGenetic Predisposition to DiseaseRadiology Nuclear Medicine and imagingGeneGenetic Association StudiesOriginal ResearchCancer BiologyGeneticsGene Expression ProfilingChromosome MappingMembrane ProteinsChromosomeCancermedicine.diseaseNeoplasm ProteinsGene Expression Regulation Neoplastic030104 developmental biologyOncologygenetic association studyCase-Control StudiesExpression quantitative trait locigene expressionChromosomes Human Pair 5FemaleReceptors Prostaglandin E EP4 SubtypeAcyltransferasesChromosomes Human Pair 8Cancer Medicine
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Absence of germline CDKN2A mutation in Sicilian Patients with Familial Malignant Melanoma: could it be a population-specific genetic signature?

2015

Germline CDKN2A mutations have been described in 25% to 40% of melanoma families from several countries. Sicilian population is genetically different from the people of Europe and Northern Italy because of its historical background, therefore familial melanoma could be due to genes different from high-penetrance CDKN2A gene. Four hundred patients with cutaneous melanoma were observed in a 6-years period at the Plastic Surgery Unit of the University of Palermo. Forty-eight patients have met the criteria of the Italian Society of Human Genetics (SIGU) for the diagnosis of familial melanoma and were screened for CDKN2A and CDK4 mutations. Mutation testing revealed that none of the families car…

Male0301 basic medicineCancer ResearchMutation rateSettore MED/06 - Oncologia MedicaSettore MED/19 - Chirurgia Plasticap14ARFGermline0302 clinical medicineCDKN2ATumor Suppressor Protein p14ARFMedicineMelanomaSicilyfamilial melanomaGeneticseducation.field_of_studyMelanomaMiddle AgedGene Expression Regulation NeoplasticItalyOncologygermline mutation030220 oncology & carcinogenesisMolecular MedicineFemaleResearch PaperSignal TransductionAdultPopulation03 medical and health sciencesCDKN2Acutaneous melanomaGermline mutationp16INK4aHumansGenetic Predisposition to DiseaseeducationneoplasmsCyclin-Dependent Kinase Inhibitor p16Germ-Line MutationAgedPharmacologybusiness.industryGenetic heterogeneityp.R87W mutationmedicine.disease030104 developmental biologyMutationCutaneous melanomaCDKN2A; cutaneous melanoma; familial melanoma; germline mutation; p.R87W mutation; p14ARF; p16INK4a; Cancer Research; Oncology; Molecular Medicine; Pharmacologybusiness
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Abilities of berberine and chemically modified berberines to inhibit proliferation of pancreatic cancer cells.

2018

Berberine (BBR) is a common nutraceutical consumed by millions worldwide. BBR has many different effects on human health, e.g., diabetes, diarrhea, inflammation and now more recently it has been proposed to have potent anti-cancer effects. BBR has been shown to suppress the growth of cancer cells more than normal cells. BBR has been proposed to exert its growth-inhibitory effects by many different biochemical mechanisms including: suppression of cell cycle progression, induction of reactive oxygen species, induction of apoptosis and autophagy and interactions with DNA potentially leading to DNA damage, and altered gene expression. Pancreatic cancer is a leading cancer worldwide associated w…

Male0301 basic medicineCancer ResearchSettore MED/09 - Medicina InternaBerberineDNA damagePopulationSignal transduction inhibitorsApoptosisInflammation03 medical and health sciences0302 clinical medicineCell Line TumorPancreatic cancerGeneticsmedicineHumanseducationChemotherapeutic drugMolecular BiologySignal transduction inhibitorAgededucation.field_of_studybusiness.industryCell CycleAutophagyCancerPDACDNA Neoplasmmedicine.diseaseGene Expression Regulation NeoplasticPancreatic Neoplasms030104 developmental biologyApoptosis030220 oncology & carcinogenesisCancer cellCancer researchMolecular MedicineChemotherapeutic drugsmedicine.symptombusinessDNA DamageSignal Transduction
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CpG islands in MyD88 and ASC/PYCARD/TMS1 promoter regions are differentially methylated in head and neck squamous cell carcinoma and primary lung squ…

2021

Abstract Background Patients with head and neck squamous cell carcinoma (HNSCC) can develop lung squamous cell carcinoma (LuSCC), which could be the second primary tumor or HNSCC metastasis. Morphologically it is difficult to distinguish metastatic HNSCC from a second primary tumor which presents a significant diagnostic challenge. Differentiation of those two malignancies is important because the recommended treatments for metastatic HNSCC and primary LuSCC differ significantly. We investigated if the quantification of the promotor methylation status in HNSCC and LuSCC differs. Methods Primary HNSCC (N = 36) and LuSCC (N = 17) were included in this study. Methylation status in the ASC/TMS1…

Male0301 basic medicinePathologyLung NeoplasmsHNSCCEpigenesis GeneticMetastasis0302 clinical medicinePromoter Regions GeneticLungDiagnostic biomarkerPYCARDGeneral MedicineMethylationMiddle AgedGene Expression Regulation NeoplasticBisulfiteCpG siteHead and Neck Neoplasms030220 oncology & carcinogenesisCarcinoma Squamous CellSecond primary tumorFemalelcsh:RB1-214Adultmedicine.medical_specialtyHistologyShort ReportBiologyMethylationPathology and Forensic Medicine03 medical and health sciencesCpG ; diagnostic biomarker ; HNSCC ; lung ; methylation ; second primary tumorCpGClinical Medical Scienceslcsh:PathologymedicineHumansGeneAdaptor Proteins Signal TransducingAgedSquamous Cell Carcinoma of Head and NeckPromotermedicine.diseaseHead and neck squamous-cell carcinomastomatognathic diseases030104 developmental biologyMyeloid Differentiation Factor 88Cancer researchCpG IslandsDiagnostic Pathology
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