2012
c-Met is a prognostic marker and potential therapeutic target in clear cell renal cell carcinoma
Gibney GT, Aziz SA, Camp RL, Conrad P, Schwartz BE, Chen CR, Kelly WK, Kluger HM. c-Met is a prognostic marker and potential therapeutic target in clear cell renal cell carcinoma. Annals Of Oncology 2012, 24: 343-349. PMID: 23022995, PMCID: PMC3551486, DOI: 10.1093/annonc/mds463.Peer-Reviewed Original ResearchMeSH KeywordsAdultAgedAged, 80 and overAntineoplastic AgentsBiomarkers, TumorCarcinoma, Renal CellCell Line, TumorCell ProliferationFemaleHepatocyte Growth FactorHumansIndolesKidney NeoplasmsMaleMiddle AgedPiperazinesPrognosisProto-Oncogene Proteins c-metPyrrolidinonesQuinolinesSulfonamidesTissue Array AnalysisConceptsRenal cell carcinomaClear cell renal cell carcinomaC-Met expressionCell renal cell carcinomaHigh c-Met expressionAdjacent normal renal tissuesNormal renal tissueARQ 197Cell carcinomaRenal tissueRCC tumorsTissue microarrayWorse disease-specific survivalC-MetClear cell RCC cell linesC-Met protein expressionCell linesPoor pathologic featuresCell subset analysisDisease-specific survivalPapillary renal cell carcinomaRange of malignanciesC-Met pathwayC-Met inhibitionPotential therapeutic targetMulti-Level Targeting of the Phosphatidylinositol-3-Kinase Pathway in Non-Small Cell Lung Cancer Cells
Zito CR, Jilaveanu LB, Anagnostou V, Rimm D, Bepler G, Maira SM, Hackl W, Camp R, Kluger HM, Chao HH. Multi-Level Targeting of the Phosphatidylinositol-3-Kinase Pathway in Non-Small Cell Lung Cancer Cells. PLOS ONE 2012, 7: e31331. PMID: 22355357, PMCID: PMC3280285, DOI: 10.1371/journal.pone.0031331.Peer-Reviewed Original ResearchMeSH KeywordsAdenocarcinomaAdultAgedAged, 80 and overAntineoplastic AgentsBlotting, WesternCarcinoma, Non-Small-Cell LungCarcinoma, Squamous CellCell Line, TumorCell ProliferationClass Ia Phosphatidylinositol 3-KinaseDrug SynergismFemaleFluorescent Antibody TechniqueHumansImmunoenzyme TechniquesLung NeoplasmsMaleMiddle AgedPhosphoinositide-3 Kinase InhibitorsProtein Kinase InhibitorsProto-Oncogene Proteins c-aktSignal TransductionTissue Array AnalysisTOR Serine-Threonine KinasesConceptsNon-small cell lung cancerNSCLC cell linesDual PI3K/mTOR inhibitorPI3K/AKT/mTOR pathwayPI3K/mTOR inhibitorAKT/mTOR pathwayPI3K inhibitorsNVP-BEZ235MTOR inhibitorsNVP-BKM120MTOR expressionAdvanced stageCell linesMTOR pathwayPI3K subunitsNon-small cell lung cancer cellsK inhibitorsCell lung cancer cellsCell lung cancerSquamous cell carcinomaP85 expressionSynergistic growth inhibitionRegulation of pAktExpression of p85Lung cancer cellsPunctate LC3B Expression Is a Common Feature of Solid Tumors and Associated with Proliferation, Metastasis, and Poor Outcome
Lazova R, Camp RL, Klump V, Siddiqui SF, Amaravadi RK, Pawelek JM. Punctate LC3B Expression Is a Common Feature of Solid Tumors and Associated with Proliferation, Metastasis, and Poor Outcome. Clinical Cancer Research 2012, 18: 370-379. PMID: 22080440, PMCID: PMC4825867, DOI: 10.1158/1078-0432.ccr-11-1282.Peer-Reviewed Original ResearchConceptsMelanoma tissue microarrayTissue microarrayBreast cancerLC3B expressionClinical outcomesNuclear gradeKi-67Solid tumorsHigh LC3B expressionHigh nuclear gradeMultitumor tissue microarrayTypes of cancerHigh LC3BCutaneous metastasesPoor outcomeWorse outcomesHistopathologic gradingLC3B stainingTherapeutic vulnerabilitiesTumorsCancerCancer progressionMetastasisMitotic figuresLC3B levels
2009
C-Raf Is Associated with Disease Progression and Cell Proliferation in a Subset of Melanomas
Jilaveanu LB, Zito CR, Aziz SA, Conrad PJ, Schmitz JC, Sznol M, Camp RL, Rimm DL, Kluger HM. C-Raf Is Associated with Disease Progression and Cell Proliferation in a Subset of Melanomas. Clinical Cancer Research 2009, 15: 5704-5713. PMID: 19737955, PMCID: PMC2763114, DOI: 10.1158/1078-0432.ccr-09-0198.Peer-Reviewed Original ResearchMeSH KeywordsAdolescentAdultAgedAged, 80 and overBenzenesulfonatesCell Line, TumorCell ProliferationCell SurvivalCohort StudiesDisease ProgressionFemaleGene SilencingHumansIndolesMaleMelanomaMiddle AgedNevusNiacinamidePhenolsPhenylurea CompoundsProtein Kinase InhibitorsProto-Oncogene Proteins c-rafPyridinesRNA, Small InterferingSensitivity and SpecificitySkin NeoplasmsSorafenibYoung AdultConceptsExtracellular signal-regulated kinaseC-RafC-Raf expressionSubset of melanomasPhospho-c-RafSignal-regulated kinaseCell linesProtein kinase inhibitionMitogen-activated protein kinase inhibitionDecreased viabilityDecreased Bcl-2 expressionProtein kinaseCell signalingBcl-2 inhibitionRaf kinaseB-RafMelanoma cell linesPhospho-MEKSpecific siRNAsSitu protein expressionGW5074Major isoformsKinasePhospho-ERKBcl-2 expressionPhosphatidylinositol-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 lines
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 cellsMTA1