2021
The Tumor Microenvironment in Cholangiocarcinoma Progression
Fabris L, Sato K, Alpini G, Strazzabosco M. The Tumor Microenvironment in Cholangiocarcinoma Progression. Hepatology 2021, 73: 75-85. PMID: 32500550, PMCID: PMC7714713, DOI: 10.1002/hep.31410.Peer-Reviewed Original Research
2020
Intrahepatic cholangiocarcinoma: Morpho-molecular pathology, tumor reactive microenvironment, and malignant progression
Sirica AE, Strazzabosco M, Cadamuro M. Intrahepatic cholangiocarcinoma: Morpho-molecular pathology, tumor reactive microenvironment, and malignant progression. Advances In Cancer Research 2020, 149: 321-387. PMID: 33579427, PMCID: PMC8800451, DOI: 10.1016/bs.acr.2020.10.005.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBile Duct NeoplasmsCholangiocarcinomaDisease ProgressionHumansTumor MicroenvironmentConceptsIntrahepatic cholangiocarcinomaMalignant progressionCommon primary liver cancerPrimary hepatic malignancyPrimary liver cancerStandard of careHigh mortality rateICCA developmentMalignant aggressivenessHepatic malignanciesHepatobiliary cancersTumor immunobiologyDesmoplastic stromaHepatocellular carcinomaLiver cancerMortality rateTherapy resistanceEpithelial cancersDeleterious roleCell originCancerReactive microenvironmentMicroenvironmental factorsProgressionManagement options
2018
β‐Catenin and interleukin‐1β–dependent chemokine (C‐X‐C motif) ligand 10 production drives progression of disease in a mouse model of congenital hepatic fibrosis
Kaffe E, Fiorotto R, Pellegrino F, Mariotti V, Amenduni M, Cadamuro M, Fabris L, Strazzabosco M, Spirli C. β‐Catenin and interleukin‐1β–dependent chemokine (C‐X‐C motif) ligand 10 production drives progression of disease in a mouse model of congenital hepatic fibrosis. Hepatology 2018, 67: 1903-1919. PMID: 29140564, PMCID: PMC5906178, DOI: 10.1002/hep.29652.Peer-Reviewed Original ResearchConceptsSignal transducerΒ-cateninJanus kinase/signal transducerKinase/signal transducerActivator of transcriptionProtein kinase ATranscription 3 (STAT3) phosphorylationHepatic disease 1 (PKHD1) geneNOD-like receptorsKinase ATranscription 3Novel therapeutic avenuesGenetic diseasesNuclear translocationCognate receptorsFamily 3Nuclear factorMouse modelPKHD1Activated B cellsPhosphorylationActivatorCyst growthTherapeutic avenuesAMG 487
2017
Animal models of biliary injury and altered bile acid metabolism
Mariotti V, Strazzabosco M, Fabris L, Calvisi DF. Animal models of biliary injury and altered bile acid metabolism. Biochimica Et Biophysica Acta (BBA) - Molecular Basis Of Disease 2017, 1864: 1254-1261. PMID: 28709963, PMCID: PMC5764833, DOI: 10.1016/j.bbadis.2017.06.027.Peer-Reviewed Original ResearchConceptsBile acid metabolismBiliary injuryMouse modelAnimal modelsDistinct immune systemCholestatic liver injuryAcid metabolismJesus BanalesMarco MarzioniNicholas LaRussoPeter JansenBiliary repairLiver injuryDuctular reactionLiver repairObstructive cholestasisDisease progressionPeribiliary inflammationMain phenotypic featuresBiliary dysgenesisViral infectionImmune systemLiver homeostasisLiver phenotypeHuman settingDirect‐acting antivirals combination for elderly patients with chronic hepatitis C: A cost‐effectiveness analysis
Ciaccio A, Cortesi PA, Bellelli G, Rota M, Conti S, Okolicsanyi S, Rota M, Cesana G, Mantovani LG, Annoni G, Strazzabosco M. Direct‐acting antivirals combination for elderly patients with chronic hepatitis C: A cost‐effectiveness analysis. Liver International 2017, 37: 982-994. PMID: 27943549, DOI: 10.1111/liv.13339.Peer-Reviewed Original ResearchMeSH KeywordsAge FactorsAgedAged, 80 and overAntiviral AgentsComputer SimulationCost-Benefit AnalysisDecision Support TechniquesDisease ProgressionDrug CostsDrug Therapy, CombinationFemaleFrail ElderlyGeriatric AssessmentHepatitis C, ChronicHumansLiver CirrhosisMaleMarkov ChainsModels, EconomicQuality-Adjusted Life YearsRisk FactorsTime FactorsTreatment OutcomeConceptsIncremental cost-effectiveness ratioChronic hepatitis CQuality-adjusted life yearsCost-effectiveness ratioElderly patientsCHC patientsHepatitis CFrailty phenotypeFrailty statusFibrosis stageLife yearsElderly CHC patientsMild fibrosis stageInterferon-free treatmentHealthcare system perspectiveLifetime time horizonCost-effectiveness analysisDAA treatmentDAA combinationsAdvanced fibrosisFrail subjectsClinical variablesLiver fibrosisF2 patientsAge 75
2011
Polycystic Liver Diseases: Congenital Disorders of Cholangiocyte Signaling
Strazzabosco M, Somlo S. Polycystic Liver Diseases: Congenital Disorders of Cholangiocyte Signaling. Gastroenterology 2011, 140: 1855-1859.e1. PMID: 21515270, PMCID: PMC3109236, DOI: 10.1053/j.gastro.2011.04.030.Peer-Reviewed Original ResearchMeSH KeywordsBiliary TractCystsDisease ProgressionEpithelial CellsGenetic Predisposition to DiseaseHumansLiver DiseasesSignal TransductionConceptsPolycystic liver diseaseLiver cyst formationClinical featuresLiver diseaseMultiple cystsDisease progressionBiliary epitheliumLiver parenchymaProgressive enlargementCongenital diseaseCyst formationCholangiocyte physiologyCongenital disorderPotential targetGenetic defectsDiseaseProgressionDisordersInheritance patternSignalingIntracellular organellesDifferent entitiesTherapyKidneyPathway
2010
Insulin resistance and necroinflammation drives ductular reaction and epithelial-mesenchymal transition in chronic hepatitis C
Svegliati-Baroni G, Faraci G, Fabris L, Saccomanno S, Cadamuro M, Pierantonelli I, Trozzi L, Bugianesi E, Guido M, Strazzabosco M, Benedetti A, Marchesini G. Insulin resistance and necroinflammation drives ductular reaction and epithelial-mesenchymal transition in chronic hepatitis C. Gut 2010, 60: 108. PMID: 20966027, PMCID: PMC3784835, DOI: 10.1136/gut.2010.219741.Peer-Reviewed Original ResearchConceptsChronic hepatitis CFibroblast-specific protein-1Epithelial-mesenchymal transitionInsulin resistanceDuctular reactionHepatitis CHepatic fibrosisEpithelial componentOral glucose insulin sensitivityOral glucose tolerance testTertiary care academic centerEpithelial-mesenchymal transition (EMT) markersNuclear Snail expressionProspective observational studyGlucose insulin sensitivityGlucose tolerance testDegree of necroinflammationStage of fibrosisTissue repairCK7-positive cellsNecroinflammatory activityNecroinflammatory scoreAdvanced fibrosisConsecutive patientsTotal inflammationPrediction of progression‐free survival in patients presenting with hepatocellular carcinoma within the Milan criteria
De Giorgio M, Vezzoli S, Cohen E, Armellini E, Lucà MG, Verga G, Pinelli D, Nani R, Valsecchi MG, Antolini L, Colledan M, Fagiuoli S, Strazzabosco M. Prediction of progression‐free survival in patients presenting with hepatocellular carcinoma within the Milan criteria. Liver Transplantation 2010, 16: 503-512. PMID: 20373461, DOI: 10.1002/lt.22039.Peer-Reviewed Original ResearchConceptsMilan criteriaProgression rateHepatocellular carcinomaRisk factorsObserved progression rateT2 patientsBarcelona Clinic Liver Cancer (BCLC) algorithmEnd-Stage Liver Disease exceptionOrgan allocationTumor persistence/recurrenceStage T2 patientsT2 hepatocellular carcinomaConsecutive HCC patientsProgression-free survivalChronic liver diseasePersistence/recurrenceDistinct natural historyTreatment of choiceBCLC guidelinesMELD scoreMELD exceptionsLocal therapyTransarterial chemoembolizationLiver diseaseTumor diameter