2020
Kras mutation correlating with circulating regulatory T cells predicts the prognosis of advanced pancreatic cancer patients
Cheng H, Luo G, Jin K, Fan Z, Huang Q, Gong Y, Xu J, Yu X, Liu C. Kras mutation correlating with circulating regulatory T cells predicts the prognosis of advanced pancreatic cancer patients. Cancer Medicine 2020, 9: 2153-2159. PMID: 32017404, PMCID: PMC7064028, DOI: 10.1002/cam4.2895.Peer-Reviewed Original ResearchMeSH KeywordsAdultAgedBiomarkers, TumorCD4 Lymphocyte CountCirculating Tumor DNADNA Mutational AnalysisFemaleFollow-Up StudiesHumansKaplan-Meier EstimateMaleMiddle AgedMutationNeoplasm StagingPancreatic NeoplasmsPolymerase Chain ReactionPrognosisProto-Oncogene Proteins p21(ras)Retrospective StudiesT-Lymphocytes, RegulatoryTime FactorsConceptsCell-free circulating tumor DNAAdvanced pancreatic cancer patientsPancreatic cancer patientsCirculating regulatory T cellsCirculating T-cell subsetsCA19-9 levelsRegulatory T cellsKRAS mutation statusT cell subsetsTumor-node-metastasisCancer patientsMutation statusTumor DNAKRAS mutationsT cellsAssociated with extremely poor survivalRegulatory T cell levelsAdvanced pancreatic cancerLevels of TregsProportion of TregsAbnormal immune statusCirculating tumor DNAT cell levelsPredicted worse prognosisTumor-node-metastasis stage
2016
Critical role of oncogenic KRAS in pancreatic cancer (Review)
LIU J, JI S, LIANG C, QIN Y, JIN K, LIANG D, XU W, SHI S, ZHANG B, LIU L, LIU C, XU J, NI Q, YU X. Critical role of oncogenic KRAS in pancreatic cancer (Review). Molecular Medicine Reports 2016, 13: 4943-4949. PMID: 27121414, DOI: 10.3892/mmr.2016.5196.Peer-Reviewed Original ResearchConceptsPancreatic ductal adenocarcinomaPancreatic cancerGenetically engineered mouse modelsPancreatic intraepithelial neoplasiaDevelopment of pancreatic ductal adenocarcinomaFormation of pancreatic intraepithelial neoplasiaProgression of pancreatic ductal adenocarcinomaIntraepithelial neoplasiaHigher mortality rateMutated KRASDuctal adenocarcinomaMouse modelHuman malignanciesKRASKRAS signalingPharmacological inhibitionOncogenic KRASPharmacological targetsMortality rateCancerTargeting KRASMolecular mechanismsProgression
2014
The UPF1 RNA surveillance gene is commonly mutated in pancreatic adenosquamous carcinoma
Liu C, Karam R, Zhou Y, Su F, Ji Y, Li G, Xu G, Lu L, Wang C, Song M, Zhu J, Wang Y, Zhao Y, Foo W, Zuo M, Valasek M, Javle M, Wilkinson M, Lu Y. The UPF1 RNA surveillance gene is commonly mutated in pancreatic adenosquamous carcinoma. Nature Medicine 2014, 20: 596-598. PMID: 24859531, PMCID: PMC4048332, DOI: 10.1038/nm.3548.Peer-Reviewed Original ResearchMeSH KeywordsAlternative SplicingBase SequenceCarcinoma, AdenosquamousGene ComponentsHEK293 CellsHumansImmunohistochemistryIn Situ Nick-End LabelingMolecular Sequence DataMutagenesisMutationNonsense Mediated mRNA DecayPancreatic NeoplasmsReal-Time Polymerase Chain ReactionReverse Transcriptase Polymerase Chain ReactionRNA HelicasesSequence Analysis, DNATrans-Activators
2013
Deep Sequencing Analysis of HCV NS3 Resistance-Associated Variants and Mutation Linkage in Liver Transplant Recipients
Kirst M, Li E, Wang C, Dong H, Liu C, Fried M, Nelson D, Wang G. Deep Sequencing Analysis of HCV NS3 Resistance-Associated Variants and Mutation Linkage in Liver Transplant Recipients. PLOS ONE 2013, 8: e69698. PMID: 23922778, PMCID: PMC3726766, DOI: 10.1371/journal.pone.0069698.Peer-Reviewed Original ResearchConceptsResistance-associated variantsProtease inhibitorsChronic HCV infectionLiver transplant recipientsHCV drug resistanceFuture therapeutic strategiesHCV protease inhibitorsMutation linkageHigh-level resistanceLow levelsPI monotherapyTransplant recipientsHCV infectionLiver transplantLiver transplantationAntiviral therapyHCV populationTherapeutic strategiesViral variantsDrug resistanceDecreased susceptibilityQuasispecies populationPatientsDominant variantDeep sequencing analysis
2011
Concurrent loss of the PTEN and RB1 tumor suppressors attenuates RAF dependence in melanomas harboring V600EBRAF
Xing F, Persaud Y, Pratilas C, Taylor B, Janakiraman M, She Q, Gallardo H, Liu C, Merghoub T, Hefter B, Dolgalev I, Viale A, Heguy A, De Stanchina E, Cobrinik D, Bollag G, Wolchok J, Houghton A, Solit D. Concurrent loss of the PTEN and RB1 tumor suppressors attenuates RAF dependence in melanomas harboring V600EBRAF. Oncogene 2011, 31: 446-457. PMID: 21725359, PMCID: PMC3267014, DOI: 10.1038/onc.2011.250.Peer-Reviewed Original ResearchConceptsHeterogeneity of clinical outcomesSpectrum of genetic alterationsLoss of p16INK4aDiversity of clinical phenotypesLoss of RB1Prevent tumor formationMEK-selective inhibitorsRB1 tumor suppressorV600EBRAF mutationRB1 alterationsMutant BRAFClinical benefitMitogen-activated protein kinase pathwayClinical outcomesBRAF signalingGenetic alterationsGenomic alterationsOncogenic BRAFClinical phenotypePTEN inactivationProtein kinase pathwayCritical oncogenesTumor formationBRAFHuman cancers
2010
Developmental plasticity of stem cells and diseases
Luo G, Long J, Zhang B, Liu C, Xu J, Yu X, Ni Q. Developmental plasticity of stem cells and diseases. Medical Hypotheses 2010, 75: 507-510. PMID: 20691545, DOI: 10.1016/j.mehy.2010.07.007.Peer-Reviewed Original Research
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
2004
Stabilized β-catenin promotes hepatocyte proliferation and inhibits TNFα-induced apoptosis
Shang X, Zhu H, Lin K, Tu Z, Chen J, Nelson D, Liu C. Stabilized β-catenin promotes hepatocyte proliferation and inhibits TNFα-induced apoptosis. Laboratory Investigation 2004, 84: 332-341. PMID: 14767485, DOI: 10.1038/labinvest.3700043.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsApoptosisBeta CateninCarcinoma, HepatocellularCell DivisionCell LineCell Line, TumorCell Transformation, NeoplasticCyclin D1Cytoskeletal ProteinsDrug StabilityGene Expression RegulationGenes, mycHepatocytesHumansLiver NeoplasmsMiceMice, SCIDMutationTrans-ActivatorsTransfectionTumor Necrosis Factor-alphaConceptsHuman hepatocellular carcinomaHepatocyte proliferationCell linesCommon malignant tumorCell proliferationImmune-deficient miceCell survival abilityLiver cell growthMurine hepatocyte cell lineCell growthHepatocyte cell lineAnchorage-independent cell growthMalignant tumorsHepatocellular carcinomaLiver cancerCyclin D1Inhibits TNFαOncogenic transformationCell apoptosisBeta-catenin mutationsAct DΒ-cateninPotential roleC-MycTumors