Search results for "HCCS"

showing 10 items of 20 documents

MR-imaging features of hepatocellular carcinoma capsule appearance in cirrhotic liver: comparison of gadoxetic acid and gadobenate dimeglumine.

2016

Purpose: The purpose of the study is to compare the MR-imaging features of hepatocellular carcinoma (HCC) capsule appearance on gadoxetic acid and gadobenate dimeglumine-enhanced MR imaging, using imaging-based presumptive diagnosis of HCC as the reference standard. Methods: Gadoxetic acid and gadobenate dimeglumine-enhanced MR imaging of 51 patients with 71 HCCs were retrospectively reviewed. Three readers graded in consensus, using a five-point scale, the presence (score 4–5) of capsule appearance on images obtained during T1-weighted GRE portal venous phase (PVP), 3-min phase, and hepatobiliary phase (HBP). The Fisher's exact test and the t student unpaired test were performed. Results: …

Gadolinium DTPALiver CirrhosisMaleCirrhotic livermedicine.medical_specialtyGadoxetic acidCarcinoma HepatocellularHepatocellular carcinomaUrologyGadoxetic acidContrast MediaSensitivity and Specificity030218 nuclear medicine & medical imaging03 medical and health sciences0302 clinical medicineMeglumineInternal medicineGadobenate dimegluminemedicineOrganometallic CompoundsHumansRadiology Nuclear Medicine and imagingGADOBENATE DIMEGLUMINECapsuleAgedRetrospective StudiesAged 80 and overRadiological and Ultrasound Technologybusiness.industryLiver NeoplasmsGastroenterologyCapsuleReproducibility of ResultsHepatologyHCCSMiddle Agedmedicine.diseaseImage EnhancementMr imagingMagnetic Resonance Imagingdigestive system diseasesLiver030220 oncology & carcinogenesisHepatocellular carcinomaFemaleRadiologybusinessMR imagingmedicine.drugAbdominal radiology (New York)
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RSPO2 gene rearrangement: a powerful driver of β-catenin activation in liver tumours

2019

ObjectiveWe aimed at the identification of genetic alterations that may functionally substitute for CTNNB1 mutation in ß-catenin-activated hepatocellular adenomas (HCAs) and hepatocellular carcinoma (HCC).DesignLarge cohorts of HCA (n=185) and HCC (n=468) were classified using immunohistochemistry. The mutational status of the CTNNB1 gene was determined in ß-catenin-activated HCA (b-HCA) and HCC with at least moderate nuclear CTNNB1 accumulation. Ultra-deep sequencing was used to characterise CTNNB1wild-type and ß-catenin-activated HCA and HCC. Expression profiling of HCA subtypes was performed.ResultsA roof plate-specific spondin 2 (RSPO2) gene rearrangement resulting from a 46.4 kb microd…

Gene expression profilingGastroenterologyCancer researchWnt signaling pathwayTelomerase reverse transcriptaseGene rearrangementHCCSBiologyRSPO2Malignant transformationRSPO2 GeneGut
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Liver-specific overexpression of matrix metalloproteinase 9 (MMP-9) in transgenic mice accelerates development of hepatocellular carcinoma.

2010

Matrix metalloproteinase-9 (MMP-9) plays a central role in tumor invasion and development of metastases. Expression of MMP-9 had been shown in human hepatocellular carcinomas (HCCs). However, it remained unclear whether MMP-9 could influence development of HCC. In order to address this issue, we generated transgenic mice overexpressing MMP-9 in the liver. In order to avoid embryonic lethality a Cre-lox system was utilized for conditional overexpression of MMP-9 under control of an albumin enhancer and promoter. Induction of MMP-9 overexpression in transgenic mice was achieved by i.v. injection of an adenovirus coding for the Cre recombinase. Initiation of liver carcinogenesis was achieved b…

Genetically modified mouseCancer ResearchLiver tumorTransgeneGenetic VectorsCre recombinaseGene ExpressionMice TransgenicBiologymedicine.disease_causeMiceLiver Neoplasms ExperimentalIn vivoGene OrdermedicineAnimalsHomeostasisHumansHomologous RecombinationMolecular BiologyIntegrasesHCCSmedicine.diseaseMolecular biologyCell Transformation NeoplasticPhenotypeLiverMatrix Metalloproteinase 9Organ SpecificityHepatocellular carcinomaCarcinogenesisMolecular carcinogenesis
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Next generation sequencing of HCC from European and Asian HCC cohorts. Back to p53 and Wnt/β-catenin

2013

Hepatocellular carcinoma (HCC) is the most common pri- mary liver malignancy. Here, we performed high-resolution copy- number analysis on 125 HCC tumors and whole-exome sequencing on 24 of these tumors. We identified 135 homozygous deletions and 994 somatic mutations of genes with predicted functional conse- quences. We found new recurrent alterations in four genes (ARID1A, RPS6KA3, NFE2L2 and IRF2) not previously described in HCC. Func- tional analyses showed tumor suppressor properties for IRF2, whose inactivation, exclusively found in hepatitis B virus (HBV)-related tumors, led to impaired TP53 function. In contrast, inactivation of chromatin remodelers was frequent and predominant in al…

GeneticsHepatitis B virusARID1AOncogeneTumor suppressor geneHepatologyHCCSBiologymedicine.disease_causemedicine.diseaseGermline mutationHepatocellular carcinomamedicineCancer researchCarcinogenesisJournal of Hepatology
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Transcriptional regulation of miR-224 upregulated in human HCCs by NFκB inflammatory pathways

2012

Background & Aims: miR-224 is up-regulated in human HCCs as compared to both paired peri-tumoral cirrhotic tissues and cirrhotic livers without HCC. Here, we have cloned the miR-224 regulatory region and characterized its transcriptional regulation by the NFκB-dependent inflammatory pathways. Methods: Mature miRNA expression was evaluated by a 2 step stem-loop real-time RT-PCR. The recruitment of polymerase II and transcription factors on the pre-miR-224 promoter has been assessed by ChIPSeq and ChIP. Results: We found miR-224 levels strongly up-regulated in both peri-tumoral cirrhotic livers and HCC samples as compared to normal livers. In silico analysis of the putative miR-224 promoter r…

LipopolysaccharidesLiver CirrhosisMaleCarcinoma HepatocellularTranscription GeneticLiver CirrhosiLipopolysaccharideBiologyCell MovementCell Line TumormicroRNATranscriptional regulationHumansNF kappa BHCCmir-224; nfκb; hcc; mirnas; transcriptionTranscription factorLymphotoxin-alphamiRNAAgedHepatologymiRNAs; HCC; miR-224; Transcription; NF kappa BTumor Necrosis Factor-alphaLiver NeoplasmsNF-kappa BMicroRNAmiR-224HCCSMiddle AgedNFKB1Up-RegulationMicroRNAsIκBαLiverLiver NeoplasmCase-Control StudiesImmunologymiRNAsCancer researchTumor necrosis factor alphaFemaleSignal transductionCase-Control StudieTranscriptionNFκBHumanSignal Transduction
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Frequent genomic imbalances suggest commonly altered tumour genes in human hepatocarcinogenesis

2001

Hepatocellular carcinoma (HCC) is one of the most frequent-occurring malignant tumours worldwide, but molecular changes of tumour DNA, with the exception of viral integrations and p53 mutations, are poorly understood. In order to search for common macro-imbalances of genomic tumour DNA, 21 HCCs and 3 HCC-cell lines were characterized by comparative genomic hybridization (CGH), subsequent database analyses and in selected cases by fluorescence in situ hybridization (FISH). Chromosomal subregions of 1q, 8q, 17q and 20q showed frequent gains of genomic material, while losses were most prevalent in subregions of 4q, 6q, 13q and 16q. Deleted regions encompass tumour suppressor genes, like RB-1 a…

MaleCancer Researchmedicine.medical_specialtyCarcinoma HepatocellularTumor suppressor geneoncogenescomparative genomic hybridizationBiologymedicine.disease_causeTranslocation GeneticFISHGene clustermedicineTumor Cells CulturedHumanstumour suppressor genesGenes Tumor SuppressorGeneIn Situ Hybridization FluorescenceGeneticsmedicine.diagnostic_testhepatocarcinogenesisLiver NeoplasmsCytogeneticsRegular Articlehepatocellular carcinomaHCCSdigestive system diseasesOncologyKaryotypingCancer researchFemaleChromosome DeletionCarcinogenesisComparative genomic hybridizationFluorescence in situ hybridizationBritish Journal of Cancer
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Deficiency of the promyelocytic leukemia protein fosters hepatitis C-associated hepatocarcinogenesis in mice.

2012

Overwhelming lines of epidemiological evidence have indicated that persistent infection with hepatitis C virus (HCV) is a major risk for the development of hepatocellular carcinoma (HCC). We have recently shown that HCV core protein mediates functional inactivation of the promyelocytic leukemia (PML) tumor suppressor pathway. However, the role of PML in HCC development yet remains unclear. To clarify the function of PML in liver carcinogenesis and HCV-associated pathogenesis we crossed PML-deficient mice with HCV transgene (HCV-Tg) expressing mice and treated the resulting animals with DEN/Phenobarbital, an established protocol for liver carcinogenesis. Seven months after treatment, livers …

MalePathologyMouseGastroenterology and hepatologyvirusesMedizinlcsh:MedicineApoptosisPromyelocytic Leukemia Proteinmedicine.disease_causeMiceMolecular Cell BiologyBasic Cancer ResearchTransgeneslcsh:ScienceMultidisciplinarybiologyCell DeathHomozygoteLiver NeoplasmsNuclear Proteinsvirus diseasesCell DifferentiationHepatitis CAnimal ModelsHepatitis CGene Expression Regulation NeoplasticLeukemiaInfectious hepatitismedicine.anatomical_structureLiverOncologyHepatocyteHepatocellular carcinomaMedicineResearch ArticleGene Expression Regulation ViralRiskmedicine.medical_specialtyGenotypeHepatitis C virusMice TransgenicPromyelocytic leukemia proteinModel OrganismsGlutamate-Ammonia LigaseGastrointestinal TumorsmedicineAnimalsBiologyTransaminasesLiver diseasesModels GeneticTumor Suppressor Proteinslcsh:RCancers and NeoplasmsHepatocellular CarcinomaHCCSmedicine.diseasedigestive system diseasesbiology.proteinlcsh:QCarcinogenesisTranscription FactorsPLoS ONE
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Incidence of new foci of hepatocellular carcinoma after radiofrequency ablation: role of multidetector CT

2012

Purpose. The authors sought to assess the incidence of new foci of hepatocellular carcinoma (HCC) using multidetector computed tomography (MDCT) in patients treated with radiofrequency ablation (RFA). Materials and methods. Two readers retrospectively reviewed by consensus the follow-up MDCT studies of 125 patients (88 men and 37 women; mean age 68 years) with 141 HCCs (size 1–5.2 cm; mean 2.2 cm) treated with RFA. MDCT follow-up was performed at 1 and 3 months and every 6–12 months thereafter. Reviewers assessed: (1) the presence of new HCC foci in the same liver segment or in a different segment; (2) complete or incomplete tumor ablation; (3) tumour progression. Results. A total of 113 ne…

Malemedicine.medical_specialtyCarcinoma HepatocellularRadiofrequency ablationMultidetector ctSettore MED/01 - Statistica Medicalaw.inventionLiver neoplasmslawMultidetector Computed TomographymedicineHumansRadiology Nuclear Medicine and imagingAgedRetrospective StudiesNeuroradiologyChi-Square Distributionmedicine.diagnostic_testbusiness.industryIncidenceIncidence (epidemiology)Radiofrequency ablation (RFA)UltrasoundInterventional radiologyGeneral MedicineMiddle AgedHCCSmedicine.diseasedigestive system diseasesTreatment OutcomeLiverHepatocellular carcinomaCatheter AblationDisease ProgressionRadiofrequency ablation (RFA); Liver; CT; Liver neoplasmsFemaleRadiologyNeoplasm Recurrence LocalSettore MED/36 - Diagnostica Per Immagini E RadioterapiabusinessFollow-Up StudiesCTLa radiologia medica
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Expression of T-cadherin in tumor cells influences invasive potential of human hepatocellular carcinoma

2006

Overexpression of T-cadherin (T-cad) transcripts occurs in approximately 50% of human hepatocellular carcinomas (HCCs). To elucidate T-cad functions in HCC, we examined T-cad protein expression in normal and tumoral human livers and hepatoma cell lines and investigated its influence on invasive potential of HCC using RNA interference silencing of T-cad expression in Mahlavu cells. Whereas T-cad expression was restricted to endothelial cells (EC) from large blood vessels in normal livers, it was up-regulated in sinusoidal EC from 8/15 invasive HCCs. Importantly, in three of them (38%) T-cad was detected in tumor cells within regions in which E-cadherin expression was absent. Among six hepato…

Pathologymedicine.medical_specialtyCarcinoma HepatocellularTranscription GeneticLiver cytologyCell Culture TechniquesMotilityBiologyTransfectionBiochemistryRNA interferenceCell MovementCell Line TumorGeneticsmedicineGene silencingAnimalsHumansNeoplasm Invasivenesscardiovascular diseasesRNA Small InterferingMolecular BiologyDNA PrimersWound Healingprimary tumors cadherin switch cell invasion hepatoma cell lines RNA interferenceLiver NeoplasmsEndothelial CellsTransfectionHCCSFibroblastsCadherinsdigestive system diseasesT-cadherinLiverCell cultureCancer researchHepatocytesRabbitsCell DivisionBiotechnology
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Targeting HSP90 with the small molecule inhibitor AUY922 (luminespib) as a treatment strategy against hepatocellular carcinoma

2018

Hepatocellular carcinoma (HCC) is a highly malignant tumor that responds very poorly to existing therapies, most probably due to its extraordinary inter- and intra-tumor molecular heterogeneity. The modest therapeutic response to molecular targeted agents underlines the need for new therapeutic approaches for HCC. In our study, we took advantage of well-characterized human HCC cell lines, differing in transcriptomic subtypes, DNA mutation and amplification alterations, reflecting the heterogeneity of primary HCCs, to provide a preclinical evaluation of the specific heat shock protein 90 (HSP90) inhibitor AUY922 (luminespib). Indeed, HSP90 is highly expressed in different tumor types, but it…

p53MaleCancer ResearchCellTranscriptome0302 clinical medicineHCCbeta CateninAged 80 and overLuminespibAUY922Liver NeoplasmsHep G2 CellsSorafenibMiddle AgedUp-RegulationGene Expression Regulation Neoplasticmedicine.anatomical_structureOncologyCaspases030220 oncology & carcinogenesisHepatocellular carcinomaFemaleNUPR1medicine.drugAdultSorafenibCarcinoma Hepatocellularβ-CateninMice NudeAntineoplastic AgentsSmall Molecule Libraries03 medical and health sciencesDownregulation and upregulationIn vivoCell Line TumormedicineHSP90AnimalsHumansHSP90 Heat-Shock ProteinsAgedCell growthbusiness.industryMcl-1IsoxazolesResorcinolsHCCSmedicine.diseasedigestive system diseasesMutationCancer researchTranscriptomebusinessInternational Journal of Cancer
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