2014
The combination of HTATIP2 expression and microvessel density predicts converse survival of hepatocellular carcinoma with or without sorafenib
Wang W, Liu L, Xu H, Sun H, Wu C, Zhu X, Zhang W, Xu J, Liu C, Long J, Ni Q, Tang Z, Yu X. The combination of HTATIP2 expression and microvessel density predicts converse survival of hepatocellular carcinoma with or without sorafenib. Oncotarget 2014, 5: 3895-3906. PMID: 25008315, PMCID: PMC4116529, DOI: 10.18632/oncotarget.2019.Peer-Reviewed Original ResearchConceptsSurvival of hepatocellular carcinomaMicrovessel densityHepatocellular carcinomaSorafenib treatmentDissemination of hepatocellular carcinomaAssociated with inhibition of angiogenesisAdvanced hepatocellular carcinomaMicrovessel density valuesCurative HCC resectionSuppressor of tumor growthInhibition of angiogenesisNegative prognostic indicatorAssociated with inhibitionSorafenib interventionHCC resectionSorafenib administrationOverall survivalDisease recurrencePrognostic factorsTissue microarrayPrognostic indicatorTumor growthSorafenibPersonalized treatmentPredictive value
2005
Defective Jak-Stat Activation in Hepatoma Cells Is Associated with Hepatitis C Viral IFN- Resistance
Zhu H, Nelson D, Crawford J, Liu C. Defective Jak-Stat Activation in Hepatoma Cells Is Associated with Hepatitis C Viral IFN- Resistance. Journal Of Interferon & Cytokine Research 2005, 25: 528-539. PMID: 16181053, DOI: 10.1089/jir.2005.25.528.Peer-Reviewed Original ResearchMeSH KeywordsAntiviral AgentsCarcinoma, HepatocellularCell Line, TumorDNA-Binding ProteinsDrug Resistance, ViralHepacivirusHumansInterferon-alphaLiverLiver NeoplasmsMutationProtein-Tyrosine KinasesRepliconRepressor ProteinsSTAT3 Transcription FactorSuppressor of Cytokine Signaling 3 ProteinSuppressor of Cytokine Signaling ProteinsTrans-ActivatorsTranscription FactorsViral Nonstructural ProteinsConceptsIFN resistanceHCV subgenomic replicon cell culture systemViral infectionChronic hepatitis C viral infectionIFN-sensitive cell linesHepatitis C viral infectionIFN stimulationCell linesRibavirin combination therapyMajority of patientsC viral infectionSTAT3 activationResistant cell linesIFN monotherapyIFN therapySuppressor of cytokineCombination therapyIFN sensitivityJAK-STAT activationIFNPotential mechanismsLong-term cultureCell culture systemExhibit alterationsJAK-STAT
1994
Identification of factor-binding sites in the duck hepatitis B virus enhancer and in vivo effects of enhancer mutations.
Liu C, Mason W, Burch J. Identification of factor-binding sites in the duck hepatitis B virus enhancer and in vivo effects of enhancer mutations. Journal Of Virology 1994, 68: 2286-96. PMID: 8139013, PMCID: PMC236704, DOI: 10.1128/jvi.68.4.2286-2296.1994.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBase SequenceCell NucleusCells, CulturedDNA Mutational AnalysisDNA-Binding ProteinsDNA, ViralDucksEnhancer Elements, GeneticHepatitis B Virus, DuckHepatocyte Nuclear Factor 1Hepatocyte Nuclear Factor 1-betaLiverMolecular Sequence DataMutagenesis, Site-DirectedNuclear ProteinsPancreasProtein BindingTranscription FactorsConceptsHepatitis B virus enhancerVirus replicationDuck hepatitis B virus replicationHepatitis B virus replicationB virus replicationHepatitis B virusCore gene promoterLMH chicken hepatoma cellsHuman growth hormoneB virusLiver-enriched transcription factorsTwo- to fourfoldVivo effectsIntact viral genomeGrowth hormoneVirus enhancerPrimary hepatocyte culturesShort-term assaysProductive infectionSignificant inhibitionVirus RNA synthesisVirusCell linesHepatoma cellsFactor-binding sites