2018
Genomic Heterogeneity and the Small Renal Mass
Ueno D, Xie Z, Boeke M, Syed J, Nguyen KA, McGillivray P, Adeniran A, Humphrey P, Dancik GM, Kluger Y, Liu Z, Kluger H, Shuch B. Genomic Heterogeneity and the Small Renal Mass. Clinical Cancer Research 2018, 24: 4137-4144. PMID: 29760223, PMCID: PMC6125159, DOI: 10.1158/1078-0432.ccr-18-0214.Peer-Reviewed Original Research
2015
NFATc1 promotes prostate tumorigenesis and overcomes PTEN loss-induced senescence
Manda K, Tripathi P, Hsi A, Ning J, Ruzinova M, Liapis H, Bailey M, Zhang H, Maher C, Humphrey P, Andriole G, Ding L, You Z, Chen F. NFATc1 promotes prostate tumorigenesis and overcomes PTEN loss-induced senescence. Oncogene 2015, 35: 3282-3292. PMID: 26477312, PMCID: PMC5012433, DOI: 10.1038/onc.2015.389.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBlotting, WesternCell LineCell Line, TumorCell ProliferationCell Transformation, NeoplasticCellular SenescenceCytokinesGene Expression Regulation, NeoplasticHumansImmunohistochemistryMaleMice, KnockoutMice, NudeMice, TransgenicNFATC Transcription FactorsProstateProstatic NeoplasmsPTEN PhosphohydrolaseReverse Transcriptase Polymerase Chain ReactionTransplantation, HomologousTumor Cells, CulturedTumor MicroenvironmentConceptsProstate tumorigenesisHuman PCaNFATc1 activationNon-tumorigenic prostate cellsActivated T cells c1Cultured PCa cellsT cells c1Cellular senescenceRole of NFATc1Number of cytokinesActivation of NFATc1Proinflammatory cytokinesPCa cellsProstate cancerProstatic adenocarcinomaLuminal epitheliumMouse prostateCells c1Normal prostateOncogenic roleOncogene c-mycProstate tissueProstate cellsSoluble factorsNuclear factor
2009
Loss of Nkx3.1 leads to the activation of discrete downstream target genes during prostate tumorigenesis
Song H, Zhang B, Watson M, Humphrey P, Lim H, Milbrandt J. Loss of Nkx3.1 leads to the activation of discrete downstream target genes during prostate tumorigenesis. Oncogene 2009, 28: 3307-3319. PMID: 19597465, PMCID: PMC2746257, DOI: 10.1038/onc.2009.181.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAtrophyClusterinDisease Models, AnimalDisease ProgressionDown-RegulationGene DeletionGene Expression ProfilingGene Expression Regulation, NeoplasticHomeodomain ProteinsHumansLasersMaleMiceMicrodissectionOxidoreductases Acting on Sulfur Group DonorsProstateProstatic NeoplasmsProto-Oncogene Proteins c-aktProto-Oncogene Proteins c-mycPTEN PhosphohydrolaseSignal TransductionThioredoxinsTranscription FactorsTranscription, GeneticTranscriptional ActivationConceptsNKX3.1 lossMolecular consequencesGene expressionProstate tumorigenesisPTEN-AKTCancer initiationProstate cancer initiationCohort of genesNumber of genesC-Myc signaling pathwayDownstream target genesHuman prostate tumorigenesisLoss of NKX3.1NKX3.1 expressionTumor suppressor geneGene expression data setsExpression data setsQuiescin Q6Transcriptional regulatorsIndependent lossesExpression of NKX3.1Laser capture microdissectionTarget genesCancer gene expression data setsSignaling pathways
2001
Frequent and early loss of the EGR1 corepressor NAB2 in human prostate carcinoma
Abdulkadir S, Carbone J, Naughton C, Humphrey P, Catalona W, Milbrandt J. Frequent and early loss of the EGR1 corepressor NAB2 in human prostate carcinoma. Human Pathology 2001, 32: 935-939. PMID: 11567222, DOI: 10.1053/hupa.2001.27102.Peer-Reviewed Original ResearchMeSH KeywordsAdenocarcinomaDown-RegulationGene Expression Regulation, NeoplasticHumansImmunohistochemistryMaleNeoplasm ProteinsProstatic Intraepithelial NeoplasiaProstatic NeoplasmsRepressor ProteinsConceptsHuman prostate cancerHuman prostate carcinomaProstate cancerProstate carcinomaProstatic intraepithelial neoplasia lesionsIntraepithelial neoplasia lesionsProstate carcinoma specimensExpression of Nab2Prostate tumor suppressorNeoplasia lesionsTumor gradeCarcinoma specimensProstate tumorigenesisTumor progressionTranscription factor EGR1Protein expressionEarly lossEGR1 levelsCarcinomaTumorigenic processCancerTumor suppressorSame stimuliEGR1Transcriptional activityImpaired prostate tumorigenesis in Egr1-deficient mice
Abdulkadir S, Qu Z, Garabedian E, Song S, Peters T, Svaren J, Carbone J, Naughton C, Catalona W, Ackerman J, Gordon J, Humphrey P, Milbrandt J. Impaired prostate tumorigenesis in Egr1-deficient mice. Nature Medicine 2001, 7: 101-107. PMID: 11135623, DOI: 10.1038/83231.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsDNA-Binding ProteinsEarly Growth Response Protein 1Gene Expression Regulation, NeoplasticImmediate-Early ProteinsMaleMiceMice, TransgenicNeoplasm ProteinsPrecancerous ConditionsProstatic NeoplasmsRepressor ProteinsTranscription FactorsConceptsEarly growth response protein 1Prostate cancerTumor progressionProstatic intra-epithelial neoplasiaEgr1 deficiencyIntra-epithelial neoplasiaHigh-resolution magnetic resonance imagingTransgenic mouse modelHuman prostate cancerTumor growth rateEgr1-deficient miceMagnetic resonance imagingProstate tumor progressionMouse modelProstate tumorigenesisSurvival analysisResonance imagingCarcinomaTumor developmentProtein 1ProgressionCancerMiceDeficiencyEGR1
2000
Overexpression and regulation of expression of scatter factor/hepatocyte growth factor in prostatic carcinoma
Zhu X, Humphrey P. Overexpression and regulation of expression of scatter factor/hepatocyte growth factor in prostatic carcinoma. Urology 2000, 56: 1071-1074. PMID: 11113771, DOI: 10.1016/s0090-4295(00)00795-0.Peer-Reviewed Original ResearchMeSH KeywordsBlotting, WesternCarcinomaGene Expression Regulation, NeoplasticHepatocyte Growth FactorHumansImmunoenzyme TechniquesMaleProstateProstatic NeoplasmsTumor Cells, CulturedConceptsPlatelet-derived growth factorVascular endothelial growth factorHGF expressionSF/HGF expressionEndothelial growth factorGrowth factorProstatic carcinomaIL-1betaStromal myofibroblastsProstatic tissueSF/HGFCarcinoma tissuesGrowth factors basic fibroblast growth factorCell linesProstatic epithelial cell linesHuman prostatic carcinoma tissueHuman prostatic tissue samplesProstatic tissue samplesProstatic carcinoma tissueBenign prostatic tissueHuman prostatic carcinomaHuman prostatic tissueMalignant human prostatic tissuesMultifunctional polypeptide growth factorsEnzyme-linked immunosorbent
1997
Effect of Canarypox Virus (ALVAC)-Mediated Cytokine Expression on Murine Prostate Tumor Growth
Kawakita M, Rao G, Ritchey J, Ornstein D, Hudson M, Harmon T, Ratliff T, Humphrey P, Tartaglia J, Paoletti E. Effect of Canarypox Virus (ALVAC)-Mediated Cytokine Expression on Murine Prostate Tumor Growth. Journal Of The National Cancer Institute 1997, 89: 428-436. PMID: 9091644, DOI: 10.1093/jnci/89.6.428.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAvipoxvirusB7-1 AntigenCytokinesDisease Models, AnimalFlow CytometryGene Expression Regulation, NeoplasticGene Expression Regulation, ViralGene Transfer TechniquesGenetic VectorsImmunotherapyInterferon-gammaInterleukin-2MaleMiceMice, Inbred C57BLMice, SCIDProstatic NeoplasmsTime FactorsTumor Necrosis Factor-alphaConceptsRM-1 cellsTumor cell expressionMouse prostate cancer cellsIL-2TNF-alphaC57BL/6 miceProstate cancer cellsTumor growthCell expressionTumor sizeB7-1Gene product expressionCo-stimulatory molecules B7-1Canarypox virusCytotoxic T lymphocyte activityKaplan-Meier survival methodMeasurable tumor sizeNonspecific antitumor activitySubsequent tumor challengeT lymphocyte activityCancer cellsCytotoxic T cellsInfected cellsProstate tumor growthMouse prostate tumor model
1994
Phorbol ester-induced apoptosis is accompanied by NGFI-A and c-fos activation in androgen-sensitive prostate cancer cells.
Day M, Zhao X, Wu S, Swanson P, Humphrey P. Phorbol ester-induced apoptosis is accompanied by NGFI-A and c-fos activation in androgen-sensitive prostate cancer cells. Molecular Cancer Research 1994, 5: 735-41. PMID: 7947388.Peer-Reviewed Original ResearchMeSH KeywordsAlkaloidsAndrogensApoptosisCarcinomaDNA DamageDNA-Binding ProteinsDNA, NeoplasmEarly Growth Response Protein 1Enzyme InductionGene Expression Regulation, NeoplasticHumansImmediate-Early ProteinsMaleNeoplasms, Hormone-DependentProstatic NeoplasmsProtein KinasesProto-Oncogene Proteins c-fosStaurosporineTetradecanoylphorbol AcetateTranscription FactorsTranscriptional ActivationTumor Cells, CulturedConceptsTranscription factor NGFIPhorbol ester-induced apoptosisC-fos gene activationEarly transcriptional regulationKinase signal transductionC-fosProtein kinase activatorsProstate cellsTranscriptional regulationGene activationSignal transductionProtein kinaseInduction of deathKinase activatorLNCaP cellsProstate cancer cellsProstate linesApoptotic bodiesCell deathDNA ladderTransient activationTransient inductionIntracellular pathwaysTPA-induced expressionNGFI
1992
Clonal Origin of Epithelial Ovarian Carcinoma: Analysis by Loss of Heterozygosity, p53 Mutation, and X-Chromosome Inactivation
Jacobs I, Kohler M, Wiseman R, Marks J, Whitaker R, Kerns B, Humphrey P, Berchuck A, Ponder B, Bast R. Clonal Origin of Epithelial Ovarian Carcinoma: Analysis by Loss of Heterozygosity, p53 Mutation, and X-Chromosome Inactivation. Journal Of The National Cancer Institute 1992, 84: 1793-1798. PMID: 1433368, DOI: 10.1093/jnci/84.23.1793.Peer-Reviewed Original ResearchMeSH KeywordsAllelesCarcinomaClone CellsDNA, NeoplasmDosage Compensation, GeneticFemaleGene Expression Regulation, NeoplasticGenes, p53HeterozygoteHumansMutationOvarian NeoplasmsConceptsEpithelial ovarian carcinomaOvarian cancerOvarian carcinomaTumor depositsPrimary tumorPolyclonal diseaseLoss of heterozygosityClonal originSporadic epithelial ovarian carcinomaMultiple tumour depositsMonoclonal originMultiple primary tumorsPrimary ovarian tumorsPrimary ovarian cancerHereditary ovarian cancerPeripheral blood lymphocytesP53 gene mutationsX-chromosome inactivation analysisMetastatic depositsOvarian tumorsBlood lymphocytesPeritoneal surfacePeritoneal mesotheliumClinical strategiesP53 mutations