2021
Congenital Cystic Lesions of the Biliary Tree
Lasagni A, Morana G, Strazzabosco M, Fabris L, Cadamuro M. Congenital Cystic Lesions of the Biliary Tree. 2021, 19-46. DOI: 10.1007/978-3-030-65908-0_2.Peer-Reviewed Original ResearchFibropolycystic liver diseasePolycystic liver diseaseFibrocystic liver diseaseHepatorenal fibrocystic diseaseIntrahepatic bile ductsCholedochal cystLiver diseaseBile ductBiliary treeLarge intrahepatic bile ductsSmall intrahepatic bile ductsBile duct dilationRenal function impairmentEarly surgical interventionOnly curative approachCongenital cystic lesionsExtrahepatic bile ductDuctal plate malformationRecessive polycystic kidney diseasePotential therapeutic targetSpectrum of disordersGrowth of cystsPolycystic kidney diseaseBiliary microhamartomasLiver transplantation
2015
Epithelial-to-Mesenchymal Transition and Cancer Invasiveness: What Can We Learn from Cholangiocarcinoma?
Brivio S, Cadamuro M, Fabris L, Strazzabosco M. Epithelial-to-Mesenchymal Transition and Cancer Invasiveness: What Can We Learn from Cholangiocarcinoma? Journal Of Clinical Medicine 2015, 4: 2028-2041. PMID: 26703747, PMCID: PMC4693158, DOI: 10.3390/jcm4121958.Peer-Reviewed Original ResearchMesenchymal transitionAbundant stromal reactionEarly metastatic behaviorPrimary liver cancerEMT-like changesPotential therapeutic targetPro-invasive phenotypeSpecific disease mechanismsDismal prognosisBile ductChronic inflammationEMT biomarkersEpithelial malignanciesStromal reactionLiver cancerTumor stromaTherapeutic targetCholangiocarcinomaNew biomarkersTumor metastatizationMetastatic behaviorCCA cellsTherapeutic opportunitiesTumor microenvironmentStromal cells
2013
Protein kinase a‐dependent pSer675‐β‐catenin, a novel signaling defect in a mouse model of congenital hepatic fibrosis
Spirli C, Locatelli L, Morell CM, Fiorotto R, Morton SD, Cadamuro M, Fabris L, Strazzabosco M. Protein kinase a‐dependent pSer675‐β‐catenin, a novel signaling defect in a mouse model of congenital hepatic fibrosis. Hepatology 2013, 58: 1713-1723. PMID: 23744610, PMCID: PMC3800498, DOI: 10.1002/hep.26554.Peer-Reviewed Original ResearchConceptsAutosomal recessive polycystic kidney diseaseCongenital hepatic fibrosisCaroli's diseaseΒ-cateninHepatic fibrosisRac-1 inhibitionIntrahepatic bile ductsRecessive polycystic kidney diseasePotential therapeutic targetPolycystic kidney diseaseStimulation of cAMPRac-1 activityE-cadherin expressionBile ductKidney diseaseLiver pathologyCystic dysplasiaMouse modelTherapeutic targetTranscriptional activityNuclear translocationDiseasePKA blockerCholangiocytesFibrosisPlatelet‐derived growth factor‐D and Rho GTPases regulate recruitment of cancer‐associated fibroblasts in cholangiocarcinoma
Cadamuro M, Nardo G, Indraccolo S, Dall'Olmo L, Sambado L, Moserle L, Franceschet I, Colledan M, Massani M, Stecca T, Bassi N, Morton S, Spirli C, Fiorotto R, Fabris L, Strazzabosco M. Platelet‐derived growth factor‐D and Rho GTPases regulate recruitment of cancer‐associated fibroblasts in cholangiocarcinoma. Hepatology 2013, 58: 1042-1053. PMID: 23505219, PMCID: PMC3732815, DOI: 10.1002/hep.26384.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntineoplastic AgentsBenzamidesBile Duct NeoplasmsBile Ducts, IntrahepaticCell Line, TumorCell MovementCell ProliferationCells, CulturedCholangiocarcinomaEpithelial-Mesenchymal TransitionFibroblastsHeterograftsHumansImatinib MesylateIn Vitro TechniquesLymphokinesMaleMiceMice, SCIDPiperazinesPlatelet-Derived Growth FactorPyrimidinesRho GTP-Binding ProteinsSignal TransductionConceptsCancer-associated fibroblastsPlatelet-derived growth factorEpithelial-mesenchymal transitionCCA cellsSecretion of PDGFRole of PDGFGrowth factorAbundant stromal reactionAlpha-smooth muscle actinPDGF-D expressionNovel therapeutic approachesPotential therapeutic targetSmooth muscle actinCCA cell linesPDGF-D signalingFibroblast migrationC-Jun N-terminal kinaseEMT biomarkersImmunodeficient miceStromal reactionTherapeutic approachesStroma interactionsTherapeutic targetCholangiocarcinomaMesenchymal markers
2011
Nuclear expression of S100A4 calcium‐binding protein increases cholangiocarcinoma invasiveness and metastasization
Fabris L, Cadamuro M, Moserle L, Dziura J, Cong X, Sambado L, Nardo G, Sonzogni A, Colledan M, Furlanetto A, Bassi N, Massani M, Cillo U, Mescoli C, Indraccolo S, Rugge M, Okolicsanyi L, Strazzabosco M. Nuclear expression of S100A4 calcium‐binding protein increases cholangiocarcinoma invasiveness and metastasization. Hepatology 2011, 54: 890-899. PMID: 21618579, PMCID: PMC3753582, DOI: 10.1002/hep.24466.Peer-Reviewed Original ResearchMeSH KeywordsAgedAnimalsApoptosisBile Duct NeoplasmsBile Ducts, IntrahepaticCell MovementCell NucleusCell ProliferationCholangiocarcinomaFemaleHumansMaleMatrix Metalloproteinase 2Matrix Metalloproteinase 9MiceMiddle AgedNeoplasm InvasivenessNeoplasm MetastasisPrognosisS100 Calcium-Binding Protein A4S100 ProteinsConceptsSurgical resectionCCA cellsNuclear expressionCCA patientsMetastatic propertiesSevere combined immunodeficiency miceTFK-1Time of surgeryRole of S100A4Log-rank testCombined immunodeficiency miceExpression of S100A4EGI-1 cellsHuman CCA cell linesPotential therapeutic targetMMP-9 secretionCCA cell linesHuman liver samplesCholangiocarcinoma invasivenessNuclear S100A4Severe prognosisPatient survivalPoor prognosisNeoplastic ductsImmunodeficiency mice