2023
Exercise Does Not Independently Improve Histological Outcomes in Biopsy-Proven Non-Alcoholic Fatty Liver Disease: A Systematic Review and Meta-Analysis
Chen G, Banini B, Do A, Gunderson C, Zaman S, Lim J. Exercise Does Not Independently Improve Histological Outcomes in Biopsy-Proven Non-Alcoholic Fatty Liver Disease: A Systematic Review and Meta-Analysis. Genes 2023, 14: 1811. PMID: 37761951, PMCID: PMC10531443, DOI: 10.3390/genes14091811.Peer-Reviewed Original ResearchConceptsNon-alcoholic fatty liver diseaseBiopsy-proven non-alcoholic fatty liver diseaseEffects of exerciseFatty liver diseaseHistological outcomesLiver histologyLiver diseaseClinical trialsHistological endpointsSystematic reviewSignificant histopathological improvementNAFLD activity scoreImpact of exerciseIndependent effectsRandom-effects modelSystematic literature searchHistopathological improvementExercise interventionActivity scoreClinical endpointsPooled estimatesMeta-AnalysisTotal participantsLiterature searchComparison groupNonalcoholic liver disease: Epidemiology, risk factors, natural history, and management strategies
Agyapong G, Dashti F, Banini B. Nonalcoholic liver disease: Epidemiology, risk factors, natural history, and management strategies. Annals Of The New York Academy Of Sciences 2023, 1526: 16-29. PMID: 37400359, PMCID: PMC10524684, DOI: 10.1111/nyas.15012.Peer-Reviewed Reviews, Practice Guidelines, Standards, and Consensus StatementsConceptsNonalcoholic fatty liver diseaseNonalcoholic fatty liverLiver diseaseRisk factorsCommon chronic liver diseaseEnd-stage liver diseaseNatural historyNAFLD risk factorsChronic liver diseaseFatty liver diseaseCurrent management strategiesClinicopathologic spectrumLiver transplantationNonalcoholic steatohepatitisProgressive fibrosisFatty liverHepatocellular cancerLeading indicationDiseaseUnited StatesManagement strategiesCirrhosisSteatohepatitisTransplantationFibrosisNew uses for an old remedy: Digoxin as a potential treatment for steatohepatitis and other disorders
Jamshed F, Dashti F, Ouyang X, Mehal W, Banini B. New uses for an old remedy: Digoxin as a potential treatment for steatohepatitis and other disorders. World Journal Of Gastroenterology 2023, 29: 1824-1837. PMID: 37032732, PMCID: PMC10080697, DOI: 10.3748/wjg.v29.i12.1824.Peer-Reviewed Reviews, Practice Guidelines, Standards, and Consensus Statements
2022
The Independent Effect of Exercise on Biopsy-Proven Non-Alcoholic Fatty Liver Disease: A Systematic Review
Chen G, Banini B, Do A, Lim J. The Independent Effect of Exercise on Biopsy-Proven Non-Alcoholic Fatty Liver Disease: A Systematic Review. Clinical And Molecular Hepatology 2022, 29: s319-s332. PMID: 36517000, PMCID: PMC10029942, DOI: 10.3350/cmh.2022.0366.Peer-Reviewed Original ResearchConceptsNon-alcoholic fatty liver diseaseBiopsy-proven non-alcoholic fatty liver diseaseNon-invasive testsFatty liver diseaseHepatic steatosisLiver fibrosisLiver diseaseHistological endpointsIndependent effectsSystematic reviewNon-randomized interventional studyMagnetic resonance imaging-based techniquesAdditional large RCTsChronic liver diseaseSignificant histological improvementEffects of exerciseClinical outcome endpointsSystematic literature searchHistological improvementExercise interventionHepatocyte ballooningOriginal research studiesLarge RCTsOutcome endpointsInterventional studyDigoxin as an emerging therapy in noncardiac diseases
Dashti F, Jamshed F, Ouyang X, Mehal W, Banini B. Digoxin as an emerging therapy in noncardiac diseases. Trends In Pharmacological Sciences 2022, 44: 199-203. PMID: 36396496, DOI: 10.1016/j.tips.2022.10.002.Peer-Reviewed Reviews, Practice Guidelines, Standards, and Consensus StatementsHepatic Hydrothorax: An Independent Predictor of Mortality in Cirrhosis? Is the MELD-Na Score Worth Its Salt?
Asotibe JC, Banini BA. Hepatic Hydrothorax: An Independent Predictor of Mortality in Cirrhosis? Is the MELD-Na Score Worth Its Salt? Digestive Diseases And Sciences 2022, 67: 4609-4611. PMID: 35534743, DOI: 10.1007/s10620-022-07523-7.Commentaries, Editorials and LettersDerivation and Validation of a Model to Predict Clinically Significant Portal Hypertension Using Transient Elastography and FIB-4
Banini BA, Patel S, Yu JW, Kang L, Bailey C, Strife BJ, Siddiqui MS, Patel V, Matherly SC, Lee H, Lewis S, Cherian R, Stravitz RT, Luketic V, Sanyal AJ, Sterling RK. Derivation and Validation of a Model to Predict Clinically Significant Portal Hypertension Using Transient Elastography and FIB-4. Journal Of Clinical Gastroenterology 2022, 57: 189-197. PMID: 34999644, PMCID: PMC9271129, DOI: 10.1097/mcg.0000000000001664.Peer-Reviewed Original ResearchConceptsHepatic venous pressure gradientSignificant portal hypertensionFIB-4Chronic liver diseaseAdvanced fibrosisPortal hypertensionLiver biopsyLiver diseasePlatelet countPositive predictive value 27Negative predictive value 99Venous pressure gradientTransjugular liver biopsyGold standardInternal bootstrap validationExternal validationLiver histologyFibrosis indexCurrent gold standardTransient elastographyOptimal cutoffBootstrap validationPatientsSpecificity 67Value 99
2021
Role of candidate gene variants in modulating the risk and severity of alcoholic hepatitis
Beaudoin JJ, Liang T, Tang Q, Banini BA, Shah VH, Sanyal AJ, Chalasani NP, Gawrieh S. Role of candidate gene variants in modulating the risk and severity of alcoholic hepatitis. Alcohol Clinical And Experimental Research 2021, 45: 709-719. PMID: 33616244, PMCID: PMC8076096, DOI: 10.1111/acer.14581.Peer-Reviewed Original ResearchConceptsPatatin-like phospholipase domain-containing protein 3Effects of variantsCopy number variantsAcyltransferase domainDomain-containing protein 3Genetic basisCandidate genesCandidate gene variantsGenetic variantsNumber variantsHaptoglobin geneIndividual variantsProtein 3Member 2AllelesGenesGene variantsRisk allelesTransmembrane 6Affected individualsVariantsIdentification of a Metabolic, Transcriptomic, and Molecular Signature of Patatin‐Like Phospholipase Domain Containing 3–Mediated Acceleration of Steatohepatitis
Banini BA, Kumar DP, Cazanave S, Seneshaw M, Mirshahi F, Santhekadur PK, Wang L, Guan HP, Oseini AM, Alonso C, Bedossa P, Koduru SV, Min H, Sanyal AJ. Identification of a Metabolic, Transcriptomic, and Molecular Signature of Patatin‐Like Phospholipase Domain Containing 3–Mediated Acceleration of Steatohepatitis. Hepatology 2021, 73: 1290-1306. PMID: 33131062, PMCID: PMC8046714, DOI: 10.1002/hep.31609.Peer-Reviewed Original ResearchNAFLD-related HCC
Banini BA, Sanyal AJ. NAFLD-related HCC. Advances In Cancer Research 2021, 149: 143-169. PMID: 33579423, DOI: 10.1016/bs.acr.2020.11.001.ChaptersConceptsNonalcoholic fatty liver diseaseHepatocellular carcinomaType 2 diabetes mellitusFatty liver diseaseNumber of patientsDiabetes mellitusMetabolic syndromeLiver diseaseCurrent evidenceMain molecular mechanismsMetabolic perturbationsTwo- toUnites StatesMolecular mechanismsMellitusObesityPatientsCarcinomaGlobal increaseSyndromeDiseaseIncidenceHepatocarcinogenesis
2020
Multidisciplinary Management of Hepatic Hydrothorax in 2020: An Evidence‐Based Review and Guidance
Banini BA, Alwatari Y, Stovall M, Ogden N, Gershman E, Shah RD, Strife BJ, Shojaee S, Sterling RK. Multidisciplinary Management of Hepatic Hydrothorax in 2020: An Evidence‐Based Review and Guidance. Hepatology 2020, 72: 1851-1863. PMID: 32585037, DOI: 10.1002/hep.31434.Peer-Reviewed Reviews, Practice Guidelines, Standards, and Consensus StatementsThe extracellular sulfatase SULF2 promotes liver tumorigenesis by stimulating assembly of a promoter-looping GLI1-STAT3 transcriptional complex
Carr RM, Romecin Duran PA, Tolosa EJ, Ma C, Oseini AM, Moser CD, Banini BA, Huang J, Asumda F, Dhanasekaran R, Graham RP, Toruner MD, Safgren SL, Almada LL, Wang S, Patnaik MM, Roberts LR, Fernandez-Zapico ME. The extracellular sulfatase SULF2 promotes liver tumorigenesis by stimulating assembly of a promoter-looping GLI1-STAT3 transcriptional complex. Journal Of Biological Chemistry 2020, 295: 2698-2712. PMID: 31988246, PMCID: PMC7049957, DOI: 10.1074/jbc.ra119.011146.Peer-Reviewed Original ResearchConceptsGLI family zinc finger 1Transcriptional complexTarget genesSer/ThrSTAT3 target genesSULF2 overexpressionZinc finger 1Suppressor of cytokineTyrosine kinase 4Promoter conformationSpecific gene signaturesSTAT3 functionHuman orthologPromoter bindingTranscriptomic analysisConsensus sitesGli1 knockdownTransgenic mice overexpressingSignal transducerTranscription 3Molecular mechanismsFinger 1Kinase 4Hepatocellular carcinoma growthOverexpression
2019
Haptoglobin 2 Allele is Associated With Histologic Response to Vitamin E in Subjects With Nonalcoholic Steatohepatitis
Banini BA, Cazanave SC, Yates KP, Asgharpour A, Vincent R, Mirshahi F, Le P, Contos MJ, Tonascia J, Chalasani NP, Kowdley KV, McCullough AJ, Behling CA, Schwimmer JB, Lavine JE, Sanyal AJ. Haptoglobin 2 Allele is Associated With Histologic Response to Vitamin E in Subjects With Nonalcoholic Steatohepatitis. Journal Of Clinical Gastroenterology 2019, 53: 750-758. PMID: 30586008, PMCID: PMC6588507, DOI: 10.1097/mcg.0000000000001142.Peer-Reviewed Original ResearchConceptsNonalcoholic fatty liver disease activity scoreNonalcoholic steatohepatitisLiver enzymesHistologic responseHp genotypeVitamin ENonalcoholic fatty liver diseaseResolution of steatohepatitisSignificant histologic improvementDisease Activity ScoreFatty liver diseaseHp 1 alleleRegression analysisEffect of VitEHaptoglobin 2 alleleDifferential treatment effectsGreater histologicCardiovascular outcomesHistologic improvementDiabetes mellitusLaboratory markersActivity scoreLiver diseaseHistologic featuresFibrosis stage
2017
Current and future pharmacologic treatment of nonalcoholic steatohepatitis
Banini BA, Sanyal AJ. Current and future pharmacologic treatment of nonalcoholic steatohepatitis. Current Opinion In Gastroenterology 2017, 33: 134-141. PMID: 28346237, PMCID: PMC5491795, DOI: 10.1097/mog.0000000000000356.Peer-Reviewed Reviews, Practice Guidelines, Standards, and Consensus StatementsConceptsNonalcoholic fatty liver diseaseEnd-stage liver diseaseNonalcoholic steatohepatitisLiver diseaseTrend of NAFLDChemokine receptor type 2Future pharmacologic treatmentsCornerstone of therapyStage liver diseaseFatty liver diseasePeroxisome proliferator activator receptorProgression of fibrosisAnti-inflammatory agentsDietary caloric restrictionGlucagon-like peptide 1 pathwayReceptor type 2Liver histologyMetabolic endotoxemiaPharmacologic treatmentTherapeutic optionsHepatocellular cancerAntifibrotic agentsIntestinal microbiomeAggressive formPharmacologic targetTreatment of NASH: What Helps Beyond Weight Loss?
Banini BA, Sanyal AJ. Treatment of NASH: What Helps Beyond Weight Loss? The American Journal Of Gastroenterology 2017, 112: 821. PMID: 28397875, DOI: 10.1038/ajg.2017.83.Peer-Reviewed Reviews, Practice Guidelines, Standards, and Consensus StatementsTranscriptional Induction of Periostin by a Sulfatase 2–TGFβ1–SMAD Signaling Axis Mediates Tumor Angiogenesis in Hepatocellular Carcinoma
Chen G, Nakamura I, Dhanasekaran R, Iguchi E, Tolosa EJ, Romecin PA, Vera RE, Almada LL, Miamen AG, Chaiteerakij R, Zhou M, Asiedu MK, Moser CD, Han S, Hu C, Banini BA, Oseini AM, Chen Y, Fang Y, Yang D, Shaleh HM, Wang S, Wu D, Song T, Lee JS, Thorgeirsson SS, Chevet E, Shah VH, Fernandez-Zapico ME, Roberts LR. Transcriptional Induction of Periostin by a Sulfatase 2–TGFβ1–SMAD Signaling Axis Mediates Tumor Angiogenesis in Hepatocellular Carcinoma. Cancer Research 2017, 77: 632-645. PMID: 27872089, PMCID: PMC5429157, DOI: 10.1158/0008-5472.can-15-2556.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBiomarkers, TumorBlotting, WesternCarcinoma, HepatocellularCell Adhesion MoleculesChromatin ImmunoprecipitationEnzyme-Linked Immunosorbent AssayGene Expression Regulation, NeoplasticGene Knockdown TechniquesHumansImmunohistochemistryKaplan-Meier EstimateLiver NeoplasmsMiceMice, KnockoutNeovascularization, PathologicOligonucleotide Array Sequence AnalysisReal-Time Polymerase Chain ReactionSignal TransductionSmad ProteinsSulfatasesSulfotransferasesTransforming Growth Factor beta1ConceptsHepatocellular carcinomaSulfatase 2Protein periostinMicrovascular densityHCC cellsExtracellular matrix protein periostinTGFβ1/Smad pathwayMetastatic hepatocellular carcinomaLower microvascular densityPoor patient survivalWild-type miceClinical HCC specimensHuman HCC cellsPatient survivalPOSTN levelsAntiangiogenic approachesKO miceRational drug developmentParacrine fashionNumerous tumorsHCC angiogenesisTumor growthEndothelial proliferationTumor angiogenesisHCC specimens
2016
A diet-induced animal model of non-alcoholic fatty liver disease and hepatocellular cancer
Asgharpour A, Cazanave SC, Pacana T, Seneshaw M, Vincent R, Banini BA, Kumar DP, Daita K, Min HK, Mirshahi F, Bedossa P, Sun X, Hoshida Y, Koduru SV, Contaifer D, Warncke UO, Wijesinghe DS, Sanyal AJ. A diet-induced animal model of non-alcoholic fatty liver disease and hepatocellular cancer. Journal Of Hepatology 2016, 65: 579-588. PMID: 27261415, PMCID: PMC5012902, DOI: 10.1016/j.jhep.2016.05.005.Peer-Reviewed Original ResearchConceptsNon-alcoholic steatohepatitisNon-alcoholic fatty liver diseaseDiet-induced animal modelsProgressive non-alcoholic steatohepatitisHuman non-alcoholic steatohepatitisFatty liver diseaseHepatocellular cancerLiver diseaseAnimal modelsDiet-induced mouse modelGene signatureHigh-fat dietSimilar histological phenotypesAd libitum consumptionProgressive fibrosisLDL cholesterolChow dietMice fedInsulin resistanceFat dietClinical endpointsHuman NAFLDObesogenic dietPreclinical modelsMouse modelMolecular mechanisms of lipotoxicity and glucotoxicity in nonalcoholic fatty liver disease
Mota M, Banini BA, Cazanave SC, Sanyal AJ. Molecular mechanisms of lipotoxicity and glucotoxicity in nonalcoholic fatty liver disease. Metabolism 2016, 65: 1049-1061. PMID: 26997538, PMCID: PMC4931958, DOI: 10.1016/j.metabol.2016.02.014.Peer-Reviewed Reviews, Practice Guidelines, Standards, and Consensus StatementsConceptsCCAAT/enhancer-binding homologous proteinNonalcoholic fatty liver diseasePKR-like ER kinaseFatty liver diseaseP53 upregulated modulatorEndoplasmic reticulum stressGlucose intoleranceHepatocellular injuryPharmacological therapyLiver diseaseMetabolic derangementsInsulin resistanceHepatocyte injuryLipotoxic stateC-Jun NH2-terminal kinase 1Exposure of hepatocytesHigh fructoseProtective roleEnergy homeostasisUpregulated modulatorGlucose dietLipotoxicityMitochondrial impairmentOxidative stressReticulum stress
2014
Brivanib Attenuates Hepatic Fibrosis In Vivo and Stellate Cell Activation In Vitro by Inhibition of FGF, VEGF and PDGF Signaling
Nakamura I, Zakharia K, Banini BA, Mikhail DS, Kim TH, Yang JD, Moser CD, Shaleh HM, Thornburgh SR, Walters I, Roberts LR. Brivanib Attenuates Hepatic Fibrosis In Vivo and Stellate Cell Activation In Vitro by Inhibition of FGF, VEGF and PDGF Signaling. PLOS ONE 2014, 9: e92273. PMID: 24710173, PMCID: PMC3977817, DOI: 10.1371/journal.pone.0092273.Peer-Reviewed Original ResearchMeSH KeywordsAlanineAnimalsCarbon Tetrachloride PoisoningCell LineCell ProliferationCell SurvivalCollagen Type ICollagen Type I, alpha 1 ChainFibroblast Growth FactorsHepatic Stellate CellsHumansImmunohistochemistryLiver CirrhosisLiver NeoplasmsMicePlatelet-Derived Growth FactorProtein Kinase InhibitorsSignal TransductionTriazinesVascular Endothelial Growth Factor AConceptsVascular endothelial growth factor receptorHuman hepatic stellate cellsBile duct ligationLiver fibrosisStellate cell activationPlatelet-derived growth factorCell activationHuman hepatic stellate cell activationChronic thioacetamide administrationHepatic stellate cell activationInhibition of VEGFREndothelial growth factor receptorChronic carbon tetrachlorideNovel therapeutic approachesHepatic stellate cellsStellate cell proliferationSmooth muscle actinDifferent animal modelsLX-2 human hepatic stellate cellsGrowth factor receptorHepatic fibrosisBrivanibDuct ligationLiver cancerTherapeutic approaches
2006
Transcriptional regulatory network analysis of developing human erythroid progenitors reveals patterns of coregulation and potential transcriptional regulators
Keller MA, Addya S, Vadigepalli R, Banini B, Delgrosso K, Huang H, Surrey S. Transcriptional regulatory network analysis of developing human erythroid progenitors reveals patterns of coregulation and potential transcriptional regulators. Physiological Genomics 2006, 28: 114-128. PMID: 16940433, DOI: 10.1152/physiolgenomics.00055.2006.Peer-Reviewed Original ResearchConceptsTranscriptional regulatory network analysisRegulatory network analysisTranscriptional regulatorsErythroid differentiation systemProbe setsCluster of genesPotential transcriptional regulatorsBlood cell lineagesDifferent expression patternsHuman erythroid progenitorsMRNA expression profilingBlood cell transcriptomeNetwork analysisErythroid developmentHematopoietic stem cellsCell transcriptomeDE genesTranscription factorsHematopoietic progenitor cellsEvi-1Target genesMolecular basisExpression profilingHuman erythropoiesisCell lineages