2009
Phosphatidylinositol-3-Kinase as a Therapeutic Target in Melanoma
Aziz SA, Davies M, Pick E, Zito C, Jilaveanu L, Camp RL, Rimm DL, Kluger Y, Kluger HM. Phosphatidylinositol-3-Kinase as a Therapeutic Target in Melanoma. Clinical Cancer Research 2009, 15: 3029-3036. PMID: 19383818, PMCID: PMC4431617, DOI: 10.1158/1078-0432.ccr-08-2768.Peer-Reviewed Original ResearchMeSH KeywordsBrain NeoplasmsCell ProliferationChromonesEnzyme InhibitorsHumansImmunoblottingImmunoenzyme TechniquesMelanomaMorpholinesNevus, PigmentedPhosphatidylinositol 3-KinasesPhosphoinositide-3 Kinase InhibitorsPhosphorylationProtein Array AnalysisSkin NeoplasmsTissue Array AnalysisTumor Cells, CulturedConceptsPhosphatidylinositol-3 kinasePI3K inhibitorsExpression of p85PI3KP110alpha subunitPathway membersK inhibitorsCell linesPI3K pathway membersReverse phase protein arrayGood drug targetPhase protein arrayPI3K pathwayTargets of drugsCellular processesPhospho-Akt levelsPI3K inhibitionMelanoma cell linesDrug targetsFull activationP85K pathwayLY294002Protein arraysResistant cell linesAnalysis of Drosophila Segmentation Network Identifies a JNK Pathway Factor Overexpressed in Kidney Cancer
Liu J, Ghanim M, Xue L, Brown CD, Iossifov I, Angeletti C, Hua S, Nègre N, Ludwig M, Stricker T, Al-Ahmadie HA, Tretiakova M, Camp RL, Perera-Alberto M, Rimm DL, Xu T, Rzhetsky A, White KP. Analysis of Drosophila Segmentation Network Identifies a JNK Pathway Factor Overexpressed in Kidney Cancer. Science 2009, 323: 1218-1222. PMID: 19164706, PMCID: PMC2756524, DOI: 10.1126/science.1157669.Peer-Reviewed Original ResearchMeSH KeywordsAmino Acid SequenceAnimalsApoptosisCarcinoma, Renal CellCell LineCompound Eye, ArthropodDrosophila melanogasterDrosophila ProteinsEmbryo, NonmammalianFushi Tarazu Transcription FactorsGene Expression ProfilingGene Regulatory NetworksHomeodomain ProteinsHumansJanus KinasesKidneyKidney NeoplasmsMolecular Sequence DataNervous SystemNuclear ProteinsPhosphoprotein PhosphatasesPhosphorylationRepressor ProteinsSignal TransductionTranscription FactorsTranscription, GeneticConceptsTranscription factorsClear cell renal cell carcinomaCell renal cell carcinomaKey transcription factorDrosophila segmentation networkConserved roleEmbryonic segmentationDrosophila melanogasterUbiquitin E3JNK signalingDependent apoptosisSPOPRenal cell carcinomaSPOP expressionKidney cancerTumor necrosis factorNew roleDrosophilaMelanogasterPuckeredGenesSignalingOverexpressedIdentificationApoptosis
2007
Small bowel carcinoid (enterochromaffin cell) neoplasia exhibits transforming growth factor–β1‐mediated regulatory abnormalities including up‐regulation of C‐Myc and MTA1
Kidd M, Modlin IM, Pfragner R, Eick GN, Champaneria MC, Chan AK, Camp RL, Mane SM. Small bowel carcinoid (enterochromaffin cell) neoplasia exhibits transforming growth factor–β1‐mediated regulatory abnormalities including up‐regulation of C‐Myc and MTA1. Cancer 2007, 109: 2420-2431. PMID: 17469181, DOI: 10.1002/cncr.22725.Peer-Reviewed Original ResearchMeSH KeywordsBlotting, WesternCadherinsCarcinoid TumorCell ProliferationCells, CulturedCyclin-Dependent Kinase Inhibitor p21Enterochromaffin CellsGene Expression Regulation, NeoplasticHistone DeacetylasesHumansIntestinal NeoplasmsMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3PhosphorylationProto-Oncogene Proteins c-mycRepressor ProteinsSignal TransductionSmad ProteinsTrans-ActivatorsTransforming Growth Factor beta1Tumor Cells, CulturedUp-RegulationConceptsEffects of TGFbeta1Normal EC cellsC-MycDownstream targetsEC cellsSmad2 phosphorylationE-cadherinCell proliferationEC cell proliferationProtein expressionGrowth regulatory mechanismsCandidate downstream targetsTranscriptional networksC-Myc pathwayC-myc transcriptsGrowth promotionCytostatic programGene responsesEC cell linesRegulatory mechanismsTranscript expressionTranscriptsNuclear translocationTumor cellsMTA1Phosphorylation of Akt (Ser473) Predicts Poor Clinical Outcome in Oropharyngeal Squamous Cell Cancer
Yu Z, Weinberger PM, Sasaki C, Egleston BL, Speier WF, Haffty B, Kowalski D, Camp R, Rimm D, Vairaktaris E, Burtness B, Psyrri A. Phosphorylation of Akt (Ser473) Predicts Poor Clinical Outcome in Oropharyngeal Squamous Cell Cancer. Cancer Epidemiology Biomarkers & Prevention 2007, 16: 553-558. PMID: 17372251, DOI: 10.1158/1055-9965.epi-06-0121.Peer-Reviewed Original ResearchMeSH KeywordsAdultAgedBiomarkers, TumorCarcinoma, Squamous CellChi-Square DistributionFemaleHumansImmunoenzyme TechniquesMaleMiddle AgedNeoplasm Recurrence, LocalOropharyngeal NeoplasmsPhosphorylationPredictive Value of TestsPrognosisProportional Hazards ModelsProtein Array AnalysisProto-Oncogene Proteins c-aktPTEN PhosphohydrolaseSurvival AnalysisConceptsNuclear p-AktAkt activationP-AktOropharyngeal squamous cell cancerSquamous cell carcinoma progressionPhosphorylated AktCohort of patientsLocal recurrence rateOverall survival rateSquamous cell cancerPoor clinical outcomeAdverse patient outcomesP-AKT levelsPromising molecular targetP-AKT expressionProtein expression levelsPhosphorylation of AktDisease recurrenceLocal recurrenceCell cancerClinical outcomesAdjusted analysisPrognostic significanceRecurrence ratePatient outcomes
2003
Tissue microarray analysis of signal transducers and activators of transcription 3 (Stat3) and phospho-Stat3 (Tyr705) in node-negative breast cancer shows nuclear localization is associated with a better prognosis.
Dolled-Filhart M, Camp RL, Kowalski DP, Smith BL, Rimm DL. Tissue microarray analysis of signal transducers and activators of transcription 3 (Stat3) and phospho-Stat3 (Tyr705) in node-negative breast cancer shows nuclear localization is associated with a better prognosis. Clinical Cancer Research 2003, 9: 594-600. PMID: 12576423.Peer-Reviewed Original ResearchMeSH KeywordsAcute-Phase ProteinsBiomarkersBreast NeoplasmsCell NucleusDNA-Binding ProteinsFemaleHumansImmunohistochemistryLymphatic MetastasisMultivariate AnalysisPhosphorylationPhosphotyrosinePrognosisProportional Hazards ModelsSTAT3 Transcription FactorSurvival AnalysisTime FactorsTrans-ActivatorsConceptsNode-negative breast cancerBreast cancerCytoplasmic expressionNuclear expressionOverall survivalReceptor stainingPrognostic markerPhospho-STAT3Breast cancer tissue microarrayEstrogen receptor stainingProgesterone receptor stainingNode-negative tumorsLarge retrospective studyIndependent prognostic markerBreast cancer specimensTissue microarray analysisCancer tissue microarrayShort-term survivalTranscription 3Breast cancer tumorsHER2 stainingBetter prognosisRetrospective studyRole of STAT3Signal transducer
2002
Alterations of Smad signaling in human breast carcinoma are associated with poor outcome: a tissue microarray study.
Xie W, Mertens JC, Reiss DJ, Rimm DL, Camp RL, Haffty BG, Reiss M. Alterations of Smad signaling in human breast carcinoma are associated with poor outcome: a tissue microarray study. Cancer Research 2002, 62: 497-505. PMID: 11809701.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBreast NeoplasmsCell DivisionCell LineDNA-Binding ProteinsFemaleGenes, BRCA1Genes, BRCA2Germ-Line MutationHeterozygoteHumansImmunohistochemistryKeratinocytesMammary Glands, AnimalMiceMice, Inbred BALB CPhosphorylationPregnancyPrognosisSignal TransductionSmad2 ProteinSmad3 ProteinSmad4 ProteinTrans-ActivatorsTransforming Growth Factor betaTumor Cells, CulturedConceptsHuman breast cancer cell linesBreast cancer cell linesHuman breast carcinomaBreast cancerCancer cell linesBreast carcinomaCell linesStage II breast cancerAxillary lymph node metastasisHuman breast cancer developmentHER2/neu expressionSmad signalingParticular histological subtypeProgesterone receptor expressionLymph node metastasisShorter overall survivalTGF-beta type II receptorTissue microarray studyBreast carcinoma specimensBreast cancer developmentTransgenic mouse modelHuman breast cancerHereditary breast cancerTGF-beta receptor signalingGrowth factor-beta signaling