2022
Development of an immunohistochemical assay for Siglec-15
Shafi S, Aung TN, Robbins C, Zugazagoitia J, Vathiotis I, Gavrielatou N, Yaghoobi V, Fernandez A, Niu S, Liu LN, Cusumano ZT, Leelatian N, Cole K, Wang H, Homer R, Herbst RS, Langermann S, Rimm DL. Development of an immunohistochemical assay for Siglec-15. Laboratory Investigation 2022, 102: 771-778. PMID: 35459795, PMCID: PMC9253057, DOI: 10.1038/s41374-022-00785-9.Peer-Reviewed Original ResearchMeSH KeywordsAntibodies, MonoclonalB7-H1 AntigenCarcinoma, Non-Small-Cell LungHumansImmunohistochemistryLung NeoplasmsSialic Acid Binding Immunoglobulin-like LectinsConceptsSiglec-15IHC assaysPD-L1PD-1/PD-L1 inhibitionPD-L1 blockadePD-L1 inhibitionHigh expressionFuture clinical trialsImmunoglobulin-type lectinsSiglec-15 expressionCompanion diagnostic assayPromising new targetTumor histologyImmunotherapeutic targetLung cancerImmune cellsClinical trialsNovel recombinant antibodiesCancer histologyImmunohistochemical assaysMyeloid cellsTumor typesScoring systemNew targetsHigh concordance
2020
Initial Evaluation of Rapid, Direct-to-Digital Prostate Biopsy Pathology.
Torres R, Olson E, Homer R, Martin DT, Levene MJ, Perincheri S, Sprenkle PC, Humphrey PA. Initial Evaluation of Rapid, Direct-to-Digital Prostate Biopsy Pathology. Archives Of Pathology & Laboratory Medicine 2020, 145: 583-591. PMID: 32991670, DOI: 10.5858/arpa.2020-0037-oa.Peer-Reviewed Original Research
2019
Reanalysis of the NCCN PD-L1 companion diagnostic assay study for lung cancer in the context of PD-L1 expression findings in triple-negative breast cancer
Rimm DL, Han G, Taube JM, Yi ES, Bridge JA, Flieder DB, Homer R, Roden AC, Hirsch FR, Wistuba II, Pusztai L. Reanalysis of the NCCN PD-L1 companion diagnostic assay study for lung cancer in the context of PD-L1 expression findings in triple-negative breast cancer. Breast Cancer Research 2019, 21: 72. PMID: 31196152, PMCID: PMC6567382, DOI: 10.1186/s13058-019-1156-6.Peer-Reviewed Original ResearchMeSH KeywordsB7-H1 AntigenBiomarkers, TumorCarcinoma, Non-Small-Cell LungFemaleHumansImmunohistochemistryPrognosisTriple Negative Breast NeoplasmsConceptsPD-L1 expressionImmune cell PD-L1 expressionLung cancerImmune cellsTriple-negative breast cancerEasy scoring methodCompanion diagnostic testsPD-L1Immune therapyBreast cancerImmunohistochemical testsBetter outcomesLarger studyTumor cellsDiagnostic testsCancerExpression findingsCellsExpressionPoor agreementScoring methodTherapyTrials
2017
A Prospective, Multi-institutional, Pathologist-Based Assessment of 4 Immunohistochemistry Assays for PD-L1 Expression in Non–Small Cell Lung Cancer
Rimm DL, Han G, Taube JM, Yi ES, Bridge JA, Flieder DB, Homer R, West WW, Wu H, Roden AC, Fujimoto J, Yu H, Anders R, Kowalewski A, Rivard C, Rehman J, Batenchuk C, Burns V, Hirsch FR, Wistuba II. A Prospective, Multi-institutional, Pathologist-Based Assessment of 4 Immunohistochemistry Assays for PD-L1 Expression in Non–Small Cell Lung Cancer. JAMA Oncology 2017, 3: 1051-1058. PMID: 28278348, PMCID: PMC5650234, DOI: 10.1001/jamaoncol.2017.0013.Peer-Reviewed Original ResearchMeSH KeywordsAntibodiesB7-H1 AntigenBiological AssayCarcinoma, Non-Small-Cell LungHumansImmunohistochemistryLung NeoplasmsPathologistsReproducibility of ResultsConceptsPD-L1 expressionNon-small cell lung cancerDako Link 48 platformIntraclass correlation coefficientCell lung cancerImmune cellsPD-L1Tumor cellsSP142 antibodyLung cancerAnti-programmed cell death 1Less PD-L1 expressionCell death ligand 1Tumour cell assessmentPD-L1 antibodiesDeath ligand 1Cell death 1Cell scoringOwn scoring systemSerial histologic sectionsSP142 assayL1 therapyDeath-1Laboratory-developed testsPatient response
2013
Hyperoxia and Interferon-γ–Induced Injury in Developing Lungs Occur via Cyclooxygenase-2 and the Endoplasmic Reticulum Stress–Dependent Pathway
Choo-Wing R, Syed MA, Harijith A, Bowen B, Pryhuber G, Janér C, Andersson S, Homer RJ, Bhandari V. Hyperoxia and Interferon-γ–Induced Injury in Developing Lungs Occur via Cyclooxygenase-2 and the Endoplasmic Reticulum Stress–Dependent Pathway. American Journal Of Respiratory Cell And Molecular Biology 2013, 48: 749-757. PMID: 23470621, PMCID: PMC3727872, DOI: 10.1165/rcmb.2012-0381oc.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAnimals, NewbornBronchopulmonary DysplasiaCelecoxibCell DeathCyclooxygenase 2Cyclooxygenase 2 InhibitorsEndoplasmic Reticulum StressHumansHyperoxiaImmunohistochemistryInfant, NewbornInterferon-gammaLungMiceMice, Inbred C57BLMice, TransgenicPyrazolesRNA, Small InterferingSulfonamidesTranscription Factor CHOPConceptsBronchopulmonary dysplasiaCyclooxygenase-2Endoplasmic reticulum stress-dependent pathwaysER stress pathway activationPathway mediatorsHuman bronchopulmonary dysplasiaFinal common pathwayAlveolar epithelial cellsImpaired alveolarizationStress pathway activationCOX2 inhibitionMurine modelMurine lungClinical relevanceIFNVivo modelHyperoxiaLungHuman lungPathway activationCHOP siRNAStress-dependent pathwaysInjuryEpithelial cellsCommon pathway
2007
P21 Regulates TGF-β1–Induced Pulmonary Responses via a TNF-α–Signaling Pathway
Yamasaki M, Kang HR, Homer RJ, Chapoval SP, Cho SJ, Lee BJ, Elias JA, Lee CG. P21 Regulates TGF-β1–Induced Pulmonary Responses via a TNF-α–Signaling Pathway. American Journal Of Respiratory Cell And Molecular Biology 2007, 38: 346-353. PMID: 17932374, PMCID: PMC2258454, DOI: 10.1165/rcmb.2007-0276oc.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsApoptosisCrosses, GeneticCyclin-Dependent Kinase Inhibitor p21DoxycyclineFibrosisImmunohistochemistryInflammationLungMiceMice, Inbred C57BLMice, TransgenicRandom AllocationRNA, MessengerSignal TransductionStatistics as TopicTransforming Growth Factor beta1Tumor Necrosis Factor-alphaConceptsMurine lungCyclin-dependent kinase inhibitorAbsence of p21Caspase-3 activationP21 locusKey regulatorTNF-alpha expressionEffects of TGFExpression of p21Negative modulatorAlveolar destructionLung inflammationTransgenic overexpressionParenchymal destructionPulmonary responseApoptosisRepair responseP21 expressionRegulatory cytokinesMyofibroblast accumulationP21TGF-β1Epithelial cellsEpithelial apoptosisKinase inhibitorsPrimary Malignant Melanoma of the Transverse Colon: Report of a Case and Review of the Literature
Kenney B, Dotto J, Homer R, Shafi N, Davydova L. Primary Malignant Melanoma of the Transverse Colon: Report of a Case and Review of the Literature. International Journal Of Surgical Pathology 2007, 15: 401-407. PMID: 17913951, DOI: 10.1177/1066896907302370.Peer-Reviewed Original ResearchConceptsPrimary malignant melanomaMalignant melanomaTransverse colonAfrican American male patientGastrointestinal involvementMale patientsOphthalmologic examinationSmall bowelPrimary lesionResection specimenPrimary melanomaImmunohistochemical positivityGastrointestinal tractMelanomaColonMicroscopic examinationMetastatic phenomenonExaminationMost casesBowelAnorectumPatientsEsophagusLesionsTumorsSemaphorin 7A plays a critical role in TGF-β1–induced pulmonary fibrosis
Kang HR, Lee CG, Homer RJ, Elias JA. Semaphorin 7A plays a critical role in TGF-β1–induced pulmonary fibrosis. Journal Of Experimental Medicine 2007, 204: 1083-1093. PMID: 17485510, PMCID: PMC2118575, DOI: 10.1084/jem.20061273.Peer-Reviewed Original ResearchMeSH KeywordsAnalysis of VarianceAnimalsAntigens, CDApoptosisCollagenDNA DamageImmunoblottingImmunohistochemistryIn Situ HybridizationIn Situ Nick-End LabelingIntegrin beta1MiceMice, TransgenicNerve Tissue ProteinsPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktPulmonary AlveoliPulmonary FibrosisReceptors, Cell SurfaceReverse Transcriptase Polymerase Chain ReactionSemaphorinsTransforming Growth Factor beta1ConceptsProtein kinase BSEMA 7APKB/Akt inhibitionAkt-dependent pathwayCritical roleSemaphorin 7ACCN proteinsFibroblast growth factor-2Kinase BCritical regulatorApoptosis regulatorMatrix proteinsGrowth factor 2Akt inhibitionBeta1 integrinReceptor componentsTissue remodelingFactor 2Fibrotic stimuliSmad 2/3Myofibroblast hyperplasiaGrowth factorRegulatorCentral roleProtein
2005
Role of CCR5 in IFN-γ–induced and cigarette smoke–induced emphysema
Ma B, Kang MJ, Lee CG, Chapoval S, Liu W, Chen Q, Coyle AJ, Lora JM, Picarella D, Homer RJ, Elias JA. Role of CCR5 in IFN-γ–induced and cigarette smoke–induced emphysema. Journal Of Clinical Investigation 2005, 115: 3460-3472. PMID: 16284650, PMCID: PMC1280966, DOI: 10.1172/jci24858.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAnnexin A5ApoptosisBronchoalveolar LavageCell DeathChemokinesDNADNA PrimersEmphysemaEnzyme-Linked Immunosorbent AssayFemaleImmunohistochemistryIn Situ Nick-End LabelingInflammationInterferon-gammaLigandsLungMacrophagesMatrix Metalloproteinase 9MiceMice, Inbred C57BLMice, TransgenicMutationPhenotypePulmonary AlveoliReceptors, CCR5Reverse Transcriptase Polymerase Chain ReactionRNA, MessengerSmokingTime FactorsConceptsCCR5 ligandsIFN-gammaPotent stimulatorCigarette smoke-induced inflammationCigarette smoke-induced emphysemaSecretory leukocyte protease inhibitorImportance of CCR5Murine emphysema modelPathogenesis of IFNRANTES/CCLSmoke-induced inflammationDNA injuryRole of CCR5Smoke-induced emphysemaLeukocyte protease inhibitorSelect chemokinesTh1 inflammationPulmonary inflammationEmphysema modelCXC chemokinesTissue destructionIFN-gamma stimulationMMP-9CCR5Cigarette smoke
2002
Pulmonary type II cell hypertrophy and pulmonary lipoproteinosis are features of chronic IL-13 exposure
Homer RJ, Zheng T, Chupp G, He S, Zhu Z, Chen Q, Ma B, Hite RD, Gobran LI, Rooney SA, Elias JA. Pulmonary type II cell hypertrophy and pulmonary lipoproteinosis are features of chronic IL-13 exposure. American Journal Of Physiology - Lung Cellular And Molecular Physiology 2002, 283: l52-l59. PMID: 12060560, DOI: 10.1152/ajplung.00438.2001.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAsthmaBronchoalveolar Lavage FluidGene ExpressionHypertrophyImmunohistochemistryInterleukin-13MiceMice, Inbred C57BLMice, Inbred CBAMice, TransgenicProteolipidsPulmonary AlveoliPulmonary FibrosisPulmonary Surfactant-Associated Protein APulmonary Surfactant-Associated ProteinsPulmonary SurfactantsRNA, MessengerConceptsType II cell hypertrophyIL-13Cell hypertrophyChronic pulmonary conditionsPathogenesis of asthmaBronchoalveolar lavage fluidTh2-mediated immunityIL-13 exposureProminent interstitial fibrosisWild-type miceAirway hyperresponsivenessMucus metaplasiaEosinophilic inflammationPulmonary diseaseInterstitial fibrosisLavage fluidPulmonary conditionsTwo- to threefold increaseSurfactant accumulationLittermate controlsPotent stimulatorSurfactant phospholipidsFibrosisKey mediatorHypertrophy
2000
IL-13 stimulates vascular endothelial cell growth factor and protects against hyperoxic acute lung injury
Corne J, Chupp G, Lee C, Homer R, Zhu Z, Chen Q, Ma B, Du Y, Roux F, McArdle J, Waxman A, Elias J. IL-13 stimulates vascular endothelial cell growth factor and protects against hyperoxic acute lung injury. Journal Of Clinical Investigation 2000, 106: 783-791. PMID: 10995789, PMCID: PMC381393, DOI: 10.1172/jci9674.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntibodiesBlotting, WesternBronchoalveolar Lavage FluidEndothelial Growth FactorsEpithelial CellsFibroblast Growth Factor 10Fibroblast Growth Factor 7Fibroblast Growth FactorsGene Expression RegulationGrowth SubstancesHyperoxiaImmunohistochemistryInterleukin-13LungLymphokinesMacrophagesMiceMice, TransgenicMuscle, SmoothOxygenProtein IsoformsSurvival RateVascular Endothelial Growth Factor AVascular Endothelial Growth FactorsConceptsAcute lung injuryHyperoxic acute lung injuryIL-13Lung injuryVEGF accumulationProtective effectTransgenic miceRoom airNontransgenic littermate controlsBreathing room airAcid isoformEndothelial cell growth factorVascular endothelial cell growth factorMice breathing room airCell growth factorBronchoalveolar lavageNontransgenic miceLittermate controlsImportant causeAntibody neutralizationMiceGrowth factorInjuryHyperoxiaSurvivalEvidence for the Neoplastic Transformation of Von-Meyenburg Complexes
Jain D, Sarode V, Abdul–Karim F, Homer R, Robert M. Evidence for the Neoplastic Transformation of Von-Meyenburg Complexes. The American Journal Of Surgical Pathology 2000, 24: 1131-1139. PMID: 10935654, DOI: 10.1097/00000478-200008000-00011.Peer-Reviewed Original ResearchConceptsVon Meyenburg complexesAdenomatous lesionsNeoplastic transformationTumor-like nodulesCongenital hepatic fibrosisDuctal plate malformationPattern of fibrosisBackground of fibrosisCases of cholangiocarcinomaEpithelial membrane antigenYears of ageSmall renal cystsPortal hypertensionDuctular proliferationMicronodular cirrhosisHepatic fibrosisTomographic scanHistologic examinationImmunohistochemical stainingRenal cystsCentral veinMembrane antigenCarcinoembryonic antigenCirrhosisCholangiocarcinoma
1996
Targeted expression of IL-11 in the murine airway causes lymphocytic inflammation, bronchial remodeling, and airways obstruction.
Tang W, Geba GP, Zheng T, Ray P, Homer RJ, Kuhn C, Flavell RA, Elias JA. Targeted expression of IL-11 in the murine airway causes lymphocytic inflammation, bronchial remodeling, and airways obstruction. Journal Of Clinical Investigation 1996, 98: 2845-2853. PMID: 8981933, PMCID: PMC507752, DOI: 10.1172/jci119113.Peer-Reviewed Original ResearchMeSH KeywordsAirway ObstructionAirway ResistanceAnimalsBlotting, NorthernBlotting, SouthernCloning, MolecularDisease Models, AnimalGene Expression RegulationHistocytochemistryImmunohistochemistryInterleukin-11LungMethacholine ChlorideMiceMice, TransgenicMicroscopy, ElectronPromoter Regions, GeneticProteinsPulmonary FibrosisUteroglobinConceptsIL-11Fibrotic responseTransgene miceAlpha-smooth muscle actinMononuclear cell infiltratePotential effector functionsSmooth muscle actinTargeted expressionSmooth muscle cellsHuman airway disordersType IIILung stromal cellsAirway disordersLymphocytic inflammationCell infiltrateSubepithelial fibrosisAirway resistanceRespiratory virusesMouse airwaysMurine airwaysInflammatory fociPhysiologic evaluationInflammatory responseBronchial remodelingMHC class