2020
Resected Pancreatic Cancer With N2 Node Involvement Is Refractory to Gemcitabine-Based Adjuvant Chemotherapy
Liu C, Cheng H, Jin K, Fan Z, Gong Y, Qian Y, Deng S, Huang Q, Ni Q, Yu X, Luo G. Resected Pancreatic Cancer With N2 Node Involvement Is Refractory to Gemcitabine-Based Adjuvant Chemotherapy. Cancer Control 2020, 27: 1073274820915947. PMID: 32268796, PMCID: PMC7153189, DOI: 10.1177/1073274820915947.Peer-Reviewed Original ResearchConceptsGemcitabine-based adjuvant chemotherapyResectable pancreatic cancerPancreatic cancerAdjuvant chemotherapyN2 node involvementNode involvementCurative resection of pancreatic adenocarcinomaResection of pancreatic adenocarcinomaGemcitabine-based regimenGemcitabine-based treatmentNode-positive subgroupEfficacy of gemcitabineGemcitabine-based chemotherapyN2 tumorsAdjuvant regimenNodal involvementNodal statusNode-negativeCurative resectionPancreatic adenocarcinomaSubgroup patientsLymphatic metastasisChemotherapyPatientsCancer
2019
New advances in diagnosis and treatment of pancreatic cancer
Jin K, Huang Q, Liu C, Yu X. New advances in diagnosis and treatment of pancreatic cancer. Chinese Journal Of Digestive Surgery 2019, 18: 657-661. DOI: 10.3760/cma.j.issn.1673-9752.2019.07.009.Peer-Reviewed Original Research
2018
Application of the Eighth Edition of the American Joint Committee on Cancer Staging for Pancreatic Adenocarcinoma
Liu C, Cheng H, Jin K, Guo M, Lu Y, Wang Z, Yang C, Long J, Ni Q, Yu X, Luo G. Application of the Eighth Edition of the American Joint Committee on Cancer Staging for Pancreatic Adenocarcinoma. Pancreas 2018, 47: 742-747. PMID: 29851752, DOI: 10.1097/mpa.0000000000001073.Peer-Reviewed Original ResearchConceptsAmerican Joint Committee on CancerAmerican Joint Committee on Cancer stageTumor resectionPancreatic cancerEighth editionAmerican Joint Committee on Cancer eighth editionAmerican Joint Committee on Cancer seventh editionStage classificationLymph node involvementEnd Results registrySeventh editionPrognosis to patientsNode involvementTumor diameterPositive nodesInstitutional seriesPancreatic adenocarcinomaCancer stageStage distributionSurvival curvesPatientsSurvival analysisTumorStatistical differenceCancer
2016
Optimize CA19-9 in detecting pancreatic cancer by Lewis and Secretor genotyping
Luo G, Guo M, Jin K, Liu Z, Liu C, Cheng H, Lu Y, Long J, Liu L, Xu J, Ni Q, Yu X. Optimize CA19-9 in detecting pancreatic cancer by Lewis and Secretor genotyping. Pancreatology 2016, 16: 1057-1062. PMID: 27692554, DOI: 10.1016/j.pan.2016.09.013.Peer-Reviewed Original ResearchConceptsDetect pancreatic cancerCut-off valueSensitivity of CA19-9CA19-9Pancreatic cancerEffectiveness of CA19-9Secretor genotypeStaging of pancreatic cancerII pancreatic cancerDetection of stage INegative predictive valueCohort of subjectsCA19Carbohydrate antigenStage IPredictive valueSanger sequencingCancerSecretor statusSecretorEarly detectorGenotypic backgroundGroupCritical 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
2015
Should a standard lymphadenectomy during pancreatoduodenectomy exclude para-aortic lymph nodes for all cases of resectable pancreatic head cancer? A consensus statement by the Chinese Study Group for Pancreatic Cancer (CSPAC)
LIU C, CHEN R, CHEN Y, FU D, HONG D, HAO J, LIU D, LI J, LI S, LI Y, MAI G, MOU Y, NI Q, PENG L, QIAN H, QIN R, SUN B, SHAO C, SUN Y, TIAN B, WANG J, WANG W, WANG W, ZHAO G, YU X. Should a standard lymphadenectomy during pancreatoduodenectomy exclude para-aortic lymph nodes for all cases of resectable pancreatic head cancer? A consensus statement by the Chinese Study Group for Pancreatic Cancer (CSPAC). International Journal Of Oncology 2015, 47: 1512-1516. PMID: 26314752, DOI: 10.3892/ijo.2015.3128.Peer-Reviewed Original ResearchConceptsPara-aortic lymph nodesPancreatic head cancerHead cancerCurative surgeryChinese Study GroupLymph nodesStandard lymphadenectomyPancreatic cancerResectable pancreatic head cancerStudy groupCases of pancreatic head cancerHigh-volume centersPancreatic cancer patientsResection statusTumor burdenPrimary tumorResected casesNode stationsPoor prognosisCancer casesCancer patientsDorsal pancreasConsensus statementSurgeryCancerEffects of Alcohol metabolism on Hepatocellular carcinoma progression
Puszyk W, Hlady R, Tiedemann R, Robertson K, Liu C. Effects of Alcohol metabolism on Hepatocellular carcinoma progression. The FASEB Journal 2015, 29 DOI: 10.1096/fasebj.29.1_supplement.45.8.Peer-Reviewed Original ResearchHepatocellular carcinomaTumor progressionModel of HCCRisk of developmentHepatocellular carcinoma progressionEffects of alcoholCancer deathCommon causeAlcohol consumptionCell culture modelCarcinoma progressionCIMP cancersAlcohol metabolismEthanol metabolismTumor developmentProgressionCancerCulture modelPrimary tissuesDNA methylationMethylation abnormalitiesGene targetsMetabolismCarcinomaAbnormalitiesMetabolic tumor burden is associated with major oncogenomic alterations and serum tumor markers in patients with resected pancreatic cancer
Shi S, Ji S, Qin Y, Xu J, Zhang B, Xu W, Liu J, Long J, Liu C, Liu L, Ni Q, Yu X. Metabolic tumor burden is associated with major oncogenomic alterations and serum tumor markers in patients with resected pancreatic cancer. Cancer Letters 2015, 360: 227-233. PMID: 25687883, DOI: 10.1016/j.canlet.2015.02.014.Peer-Reviewed Original ResearchConceptsMetabolic tumor burdenMetabolic tumor volumeSerum tumor markersTumor burdenTumor markersPancreatic cancerAbnormal expressions of TP53Abnormal expressionMonitoring treatment responsePancreatic cancer patientsProgression of pancreatic cancerExpression of TP53Tumor volumeCA19-9SMAD4/DPC4 geneTreatment responseCancer patientsDisease progressionPET/CTPredictive significanceSurvival rateLethal diseasePatientsCancerSerum
2013
Linking metabolism and epigenetic regulation in development of hepatocellular carcinoma
Puszyk W, Le Trinh T, Chapple S, Liu C. Linking metabolism and epigenetic regulation in development of hepatocellular carcinoma. Laboratory Investigation 2013, 93: 983-990. PMID: 23917878, PMCID: PMC4028619, DOI: 10.1038/labinvest.2013.94.Peer-Reviewed Original ResearchConceptsHepatocellular carcinomaLate-stage hepatocellular carcinomaDevelopment of HCCAltered liver metabolismHepatitis B virusMajor risk factorProgression of HCCHepatitis CLiver functionB virusMicro RNA expressionRisk factorsLiver metabolismMetabolic organSurvival rateCancerRNA expressionCommon formCarcinomaUnderlying metabolic processesLiverExogenous environmental factorsEnvironmental factorsExcessive consumptionExposure
2011
Therapeutic and prognostic importance of epithelial–mesenchymal transition in liver cancers: Insights from experimental models
Ogunwobi O, Liu C. Therapeutic and prognostic importance of epithelial–mesenchymal transition in liver cancers: Insights from experimental models. Critical Reviews In Oncology/Hematology 2011, 83: 319-328. PMID: 22178416, DOI: 10.1016/j.critrevonc.2011.11.007.Peer-Reviewed Original ResearchConceptsEpithelial-mesenchymal transitionHepatocellular carcinomaHepatic metastasesPrognostic importanceExperimental modelColon cancerTreatment of patientsRole of EMTHuman cancer patientsPotential therapeutic targetHuman malignant diseaseSignificant morbidityCancer patientsMalignant diseaseMalignant conditionsLiver cancerTherapeutic targetBasic scientistsCancerFurther studiesPatientsCarcinomaMetastasisLiverHuman tissues
2010
DNA Aptamers as Molecular Probes for Colorectal Cancer Study
Sefah K, Meng L, Lopez-Colon D, Jimenez E, Liu C, Tan W. DNA Aptamers as Molecular Probes for Colorectal Cancer Study. PLOS ONE 2010, 5: e14269. PMID: 21170319, PMCID: PMC3000811, DOI: 10.1371/journal.pone.0014269.Peer-Reviewed Original ResearchConceptsColorectal cancerAppropriate therapeutic regimensCell-based systematic evolutionColorectal Cancer StudyMolecular featuresMultistep carcinogenic processCancer cell linesCell line DLD-1Therapeutic regimensNormal colon cellsPrognostic markerDifferent tumorsSpecific tumorsFlow cytometrySpecific biomarkersEarly disease detectionCarcinogenic processTumorsCancerSpecific markersCancer studiesColon cellsDLD-1Cell linesDisease development
2008
Identification of Liver Cancer-Specific Aptamers Using Whole Live Cells
Shangguan D, Meng L, Cao Z, Xiao Z, Fang X, Li Y, Cardona D, Witek R, Liu C, Tan W. Identification of Liver Cancer-Specific Aptamers Using Whole Live Cells. Analytical Chemistry 2008, 80: 721-728. PMID: 18177018, DOI: 10.1021/ac701962v.Peer-Reviewed Original ResearchConceptsLiver cancerLiver cancer cellsEarly diagnosisCell linesBALB/cJ miceCancer cellsSurgical resectionClinical outcomesLiver cell lineEffective treatmentMouse modelWhole live cellsDeadly cancerCurrent studyCancer-specific aptamersTumor selectionBasic mechanism studiesCancerMost cancersBNL CLCancer early diagnosisCell-SELEX methodNoncancer cell linesDiagnosisCancer recognition