Search results for "ELS"

showing 10 items of 12690 documents

Multi-Omics Characterization of the 4T1 Murine Mammary Gland Tumor Model

2020

Background: Tumor models are critical for our understanding of cancer and the development of cancer therapeutics. The 4T1 murine mammary cancer cell line is one of the most widely used breast cancer models. Here, we present an integrated map of the genome, transcriptome, and immunome of 4T1. Results: We found Trp53 (Tp53) and Pik3g to be mutated. Other frequently mutated genes in breast cancer, including Brca1 and Brca2, are not mutated. For cancer related genes, Nav3, Cenpf, Muc5Ac, Mpp7, Gas1, MageD2, Dusp1, Ros, Polr2a, Rragd, Ros1, and Hoxa9 are mutated. Markers for cell proliferation like Top2a, Birc5, and Mki67 are highly expressed, so are markers for metastasis like Msln, Ect2, and P…

0301 basic medicineCancer ResearchBiologylcsh:RC254-282computational immunologyMetastasisTranscriptomeFusion gene03 medical and health sciences0302 clinical medicineBreast cancerMammary tumor virusmedicinecancer modelsTriple-negative breast cancerOriginal Research4T1 murine mammary gland tumor cell lineCancermedicine.diseaselcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogens3. Good health030104 developmental biologyOncology030220 oncology & carcinogenesistriple negative breast cancerCancer researchimmunotherapyCD8Frontiers in Oncology
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Trabectedin triggers direct and NK-mediated cytotoxicity in multiple myeloma

2019

Background Genomic instability is a feature of multiple myeloma (MM), and impairment in DNA damaging response (DDR) has an established role in disease pathobiology. Indeed, a deregulation of DNA repair pathways may contribute to genomic instability, to the establishment of drug resistance to genotoxic agents, and to the escape from immune surveillance. On these bases, we evaluated the role of different DDR pathways in MM and investigated, for the first time, the direct and immune-mediated anti-MM activity of the nucleotide excision repair (NER)-dependent agent trabectedin. Methods Gene-expression profiling (GEP) was carried out with HTA2.0 Affymetrix array. Evaluation of apoptosis, cell cyc…

0301 basic medicineCancer ResearchCell cycle checkpointNatural killerDNA repairmedicine.medical_treatmentMyelomalcsh:RC254-28203 medical and health sciences0302 clinical medicineMicro-RNAmedicineHumansMolecular BiologyAntineoplastic Agents AlkylatingTrabectedin3D-modelChemistrylcsh:RC633-647.5ResearchMicro-RNAsHematologylcsh:Diseases of the blood and blood-forming organsCell cycleNKG2Dlcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensKiller Cells Natural030104 developmental biologyCytokineOncologyApoptosis3D-models030220 oncology & carcinogenesis3D-models; Micro-RNAs; Myeloma; Natural killer; TrabectedinCancer researchDNA fragmentationMultiple Myelomamedicine.drugTrabectedinJournal of Hematology & Oncology
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The phospholipase DDHD1 as a new target in colorectal cancer therapy

2018

Background Our previous study demonstrates that Citrus-limon derived nanovesicles are able to decrease colon cancer cell viability, and that this effect is associated with the downregulation of the intracellular phospholipase DDHD domain-containing protein 1 (DDHD1). While few studies are currently available on the contribution of DDHD1 in neurological disorders, there is no information on its role in cancer. This study investigates the role of DDHD1 in colon cancer. Methods DDHD1 siRNAs and an overexpression vector were transfected into colorectal cancer and normal cells to downregulate or upregulate DDHD1 expression. In vitro and in vivo assays were performed to investigate the functional…

0301 basic medicineCancer ResearchColorectal cancerApoptosisMiceSettore BIO/13 - Biologia ApplicataGene Regulatory NetworksMolecular Targeted TherapyCitrus-limon nanovesicleTransfectionlcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogens3. Good healthCitrus-limon nanovesicles; Colorectal cancer; Phospholipase DDHD1; Oncology; Cancer ResearchOncologyPhospholipasesCitrus-limon nanovesicles; Colorectal cancer; Phospholipase DDHD1; Animals; Antineoplastic Agents; Apoptosis; Cell Line Tumor; Cell Proliferation; Colorectal Neoplasms; Computational Biology; Disease Models Animal; Female; Gene Expression Profiling; Gene Ontology; Gene Regulatory Networks; Gene Silencing; Humans; MAP Kinase Signaling System; Mice; Phospholipases; Signal Transduction; Xenograft Model Antitumor Assays; Biomarkers Tumor; Molecular Targeted TherapyFemaleColorectal NeoplasmsSignal TransductionMAP Kinase Signaling SystemAntineoplastic Agentslcsh:RC254-282Citrus-limon nanovesicles03 medical and health sciencesDownregulation and upregulationIn vivoCell Line TumorBiomarkers TumormedicineAnimalsHumansGene silencingGene SilencingPhospholipase DDHD1Cell Proliferationbusiness.industryCell growthGene Expression ProfilingResearchComputational BiologyCancermedicine.diseaseXenograft Model Antitumor AssaysColorectal cancerDisease Models AnimalGene Ontology030104 developmental biologyApoptosisCancer researchbusiness
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In silico RNA-seq and experimental analyses reveal the differential expression and splicing of EPDR1 and ZNF518B genes in relation to KRAS mutations …

2016

Several drugs used for the treatment of colorectal cancer (CRC) are targeted at the epidermal growth factor receptor, but mutations in genes of the RAS family cause resistance to these drugs. Thus, extensive research is being carried out to counterbalance this resistance. The G13D mutation of KRAS is common in humans, and we previously reported that this mutation results in the epigenetic modification of hnRNP proteins, involved in RNA splicing. As aberrant splicing often results in oncogenicity, the present study aimed to identify the genes which show altered splicing patterns in connection with the G13D KRAS mutation. To accomplish this, we first carried out an in silico analysis of RNA-s…

0301 basic medicineCancer ResearchIn silicoMutation MissenseGene ExpressionNerve Tissue ProteinsBiologymedicine.disease_causeProto-Oncogene Proteins p21(ras)03 medical and health sciences0302 clinical medicinemedicineHumansProtein IsoformsComputer SimulationEpigeneticsGeneGeneticsMutationBase SequenceModels GeneticSequence Analysis RNAAlternative splicingGeneral Medicinedigestive system diseasesNeoplasm ProteinsDNA-Binding ProteinsAlternative Splicing030104 developmental biologyOncology030220 oncology & carcinogenesisRNA splicingCancer researchKRASCarcinogenesisColorectal NeoplasmsOncology reports
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Trabectedin Overrides Osteosarcoma Differentiative Block and Reprograms the Tumor Immune Environment Enabling Effective Combination with Immune Check…

2016

Abstract Purpose: Osteosarcoma, the most common primary bone tumor, is characterized by an aggressive behavior with high tendency to develop lung metastases as well as by multiple genetic aberrations that have hindered the development of targeted therapies. New therapeutic approaches are urgently needed; however, novel combinations with immunotherapies and checkpoint inhibitors require suitable preclinical models with intact immune systems to be properly tested. Experimental Design: We have developed immunocompetent osteosarcoma models that grow orthotopically in the bone and spontaneously metastasize to the lungs, mimicking human osteosarcoma. These models have been used to test the effica…

0301 basic medicineCancer ResearchLung Neoplasmsmedicine.medical_treatmentCellular differentiationT-LymphocytesProgrammed Cell Death 1 ReceptorBone NeoplasmsCore Binding Factor Alpha 1 SubunitDioxolesBiology03 medical and health sciences0302 clinical medicineImmune systemCell Line TumorTetrahydroisoquinolinesmedicineTumor MicroenvironmentHumansTrabectedinTumor microenvironmentOsteosarcomaCancerCell DifferentiationImmunotherapymedicine.diseaseCellular ReprogrammingPrimary tumor030104 developmental biologyOncology030220 oncology & carcinogenesisImmunologyCancer researchOsteosarcomaImmunotherapyOsteosarcoma Trabectedin tumor mouse models immune cells immune checkpoint inhibitors.Tumor Suppressor Protein p53medicine.drugTrabectedinClinical cancer research : an official journal of the American Association for Cancer Research
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Potential of induced metabolic bioluminescence imaging to uncover metabolic effects of antiangiogenic therapy in tumors

2016

Tumor heterogeneity at the genetic level has been illustrated by a multitude of studies on the genomics of cancer, but whether tumors can be heterogeneous at the metabolic level is an issue which has been less systematically investigated so far. A burning related question is whether the metabolic features of tumors can change either following natural tumor progression (i.e. in primary tumors versus metastasis) or therapeutic interventions. In this regard, recent findings by independent teams indicate that anti-angiogenic drugs cause metabolic perturbations in tumors as well as metabolic adaptations associated with increased malignancy. Induced metabolic bioluminescence imaging (imBI) is an …

0301 basic medicineCancer ResearchPathologymedicine.medical_specialtyAngiogenesisMini ReviewBiologyMalignancylcsh:RC254-282MetastasisImaging03 medical and health sciencesAngiogenesis; Cancer mouse models; Glycolysis; Imaging; MetabolismmedicineBioluminescence imagingGlycolysismouse modelsCancerCancerMetabolismlcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensmedicine.disease030104 developmental biologyMetabolismOncologyTumor progressionCancer researchAngiogenesisGlycolysis
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Preclinical models for precision oncology

2018

Precision medicine approaches have revolutionized oncology. Personalized treatments require not only identification of the driving molecular alterations, but also development of targeted therapies and diagnostic tests to identify the appropriate patient populations for clinical trials and subsequent therapeutic implementation. Preclinical in vitro and in vivo models are widely used to predict efficacy of newly developed treatments. Here we discuss whether, and to what extent, preclinical models including cell lines, organoids and tumorgrafts recapitulate key features of human tumors. The potential of preclinical models to anticipate treatment efficacy and clinical benefit is also presented,…

0301 basic medicineCancer ResearchPreclinical modelsMedical OncologyBioinformaticsModels Biological03 medical and health sciences0302 clinical medicineCell Line TumorNeoplasmsGeneticsAnimalsHumansMedicinePrecision Medicinebusiness.industryOrganoids; Patient-derived xenografts (PDX); Preclinical models; Oncology; Genetics; Cancer ResearchDiagnostic testPrecision medicineKey featuresTreatment efficacy3. Good healthClinical trialOrganoids030104 developmental biologyOncologyPrecision oncologyPatient-derived xenografts (PDX)030220 oncology & carcinogenesisHeterograftsbusinessBiochimica et Biophysica Acta (BBA) - Reviews on Cancer
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HDAC1 and HDAC2 integrate the expression of p53 mutants in pancreatic cancer.

2015

Mutation of p53 is a frequent genetic lesion in pancreatic cancer being an unmet clinical challenge. Mutants of p53 have lost the tumour-suppressive functions of wild type p53. In addition, p53 mutants exert tumour-promoting functions, qualifying them as important therapeutic targets. Here, we show that the class I histone deacetylases HDAC1 and HDAC2 contribute to maintain the expression of p53 mutants in human and genetically defined murine pancreatic cancer cells. Our data reveal that the inhibition of these HDACs with small molecule HDAC inhibitors (HDACi), as well as the specific genetic elimination of HDAC1 and HDAC2, reduce the expression of mutant p53 mRNA and protein levels. We fur…

0301 basic medicineCancer ResearchProteasome Endopeptidase ComplexMutantHistone Deacetylase 2Histone Deacetylase 1Biologymedicine.disease_causeMolecular oncologyProto-Oncogene Proteins c-myc03 medical and health sciencesMicePancreatic cancerGeneticsmedicineAnimalsHumansRNA MessengerPromoter Regions GeneticMolecular BiologyRegulation of gene expressionMice KnockoutMutationWild typeCancerProto-Oncogene Proteins c-mdm2medicine.diseaseGenes p53HDAC13. Good healthGene Expression Regulation NeoplasticHistone Deacetylase InhibitorsPancreatic NeoplasmsDisease Models Animal030104 developmental biologyMutationCancer researchOncogene
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Lack of a peroxiredoxin suppresses the lethality of cells devoid of electron donors by channelling electrons to oxidized ribonucleotide reductase

2017

The thioredoxin and glutaredoxin pathways are responsible of recycling several enzymes which undergo intramolecular disulfide bond formation as part of their catalytic cycles such as the peroxide scavengers peroxiredoxins or the enzyme ribonucleotide reductase (RNR). RNR, the rate-limiting enzyme of deoxyribonucleotide synthesis, is an essential enzyme relying on these electron flow cascades for recycling. RNR is tightly regulated in a cell cycle-dependent manner at different levels, but little is known about the participation of electron donors in such regulation. Here, we show that cytosolic thioredoxins Trx1 and Trx3 are the primary electron donors for RNR in fission yeast. Unexpectedly,…

0301 basic medicineCancer ResearchThioredoxin reductaseSynthesis PhaseYeast and Fungal ModelsBiochemistryElectron DonorsSchizosaccharomyces PombeThioredoxinsGlutaredoxinCell Cycle and Cell DivisionGenetics (clinical)Chemical ReactionsOxidesPeroxidesNucleic acidsChemistryRibonucleotide reductaseBiochemistryExperimental Organism SystemsCell ProcessesSchizosaccharomyces pombePhysical SciencesSynthesis phaseThioredoxinOxidation-ReductionResearch ArticleDNA Replicationlcsh:QH426-470DNA transcriptionElectron donorsBiologyDNA replicationResearch and Analysis MethodsCatalysisElectron Transport03 medical and health sciencesModel OrganismsSchizosaccharomycesRibonucleotide ReductasesOxidationGeneticsMolecular BiologyEcology Evolution Behavior and SystematicsGlutaredoxinsCell growthDNA replicationChemical CompoundsOrganismsFungiBiology and Life SciencesCell BiologyDNAPeroxiredoxinsbiology.organism_classificationYeastCell cycle and cell divisionCheckpoint Kinase 2lcsh:Genetics030104 developmental biologySchizosaccharomyces pombeGene expressionSchizosaccharomyces pombe ProteinsPeroxiredoxin
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The organoid era permits the development of new applications to study glioblastoma

2020

Simple Summary Glioblastoma is the most lethal primary adult brain tumor. The great number of mutations involved and the aggressiveness of glioblastoma render this type of cancer especially difficult to investigate. To address this problem, cerebral organoids have emerged as promising tools to investigate brain biology and to recapitulates the major steps involved in glioblastoma tumorigenesis. This review focuses on methods of cerebral organoid development, describes the protocols used for inducing glioblastoma, the approach used to derive glioblastoma organoids directly from patients’ biopsies and discusses their limitations and potential future direction. Abstract Glioblastoma (GB) is th…

0301 basic medicineCancer ResearchTranslational researchContext (language use)ReviewStem cellsBiologylcsh:RC254-28203 medical and health sciences0302 clinical medicineGenome editingGliomaOrganoidmedicinePreclinical cancer modelsPrecision medicineCancerTranslational researchlcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensmedicine.diseasePrecision medicineBiobankOrganoids030104 developmental biologyTumoroidsOncologyGlioblastomaNeuroscience030217 neurology & neurosurgeryCancers
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