2022
Integrative molecular and clinical profiling of acral melanoma links focal amplification of 22q11.21 to metastasis
Farshidfar F, Rhrissorrakrai K, Levovitz C, Peng C, Knight J, Bacchiocchi A, Su J, Yin M, Sznol M, Ariyan S, Clune J, Olino K, Parida L, Nikolaus J, Zhang M, Zhao S, Wang Y, Huang G, Wan M, Li X, Cao J, Yan Q, Chen X, Newman AM, Halaban R. Integrative molecular and clinical profiling of acral melanoma links focal amplification of 22q11.21 to metastasis. Nature Communications 2022, 13: 898. PMID: 35197475, PMCID: PMC8866401, DOI: 10.1038/s41467-022-28566-4.Peer-Reviewed Original ResearchConceptsAcral melanomaMelanoma subtypesClinical profilingCommon melanoma subtypeImmune checkpoint blockadeCheckpoint blockadeInferior survivalMelanoma cell linesKey molecular driversPoor prognosisTherapeutic targetAnchorage-independent growthImmunomodulatory genesNon-white individualsHotspot mutationsMolecular driversCandidate oncogeneMelanomaApoptotic cell deathLZTR1Focal amplificationTumor promoterCell linesMetastasisTumor suppressor
2020
Synthetic Lethal Targeting of Mitotic Checkpoints in HPV-Negative Head and Neck Cancer
Deneka AY, Einarson MB, Bennett J, Nikonova AS, Elmekawy M, Zhou Y, Lee JW, Burtness BA, Golemis EA. Synthetic Lethal Targeting of Mitotic Checkpoints in HPV-Negative Head and Neck Cancer. Cancers 2020, 12: 306. PMID: 32012873, PMCID: PMC7072436, DOI: 10.3390/cancers12020306.Peer-Reviewed Original ResearchG1/S checkpointNeck squamous cell carcinomaSingle-agent activitySquamous cell carcinomaHPV-negative headHPV-negative HNSCCHNSCC cell linesWEE1 inhibitor AZD1775S checkpointNegative HNSCCCell carcinomaHuman papillomavirusHNSCC cancerNeck cancerWorse outcomesSubset of drugsCommon mutational eventsDNA damageAnchorage-independent growthDual inhibitionClonogenic capacityClinical agentsSynthetic lethal targetingReduced activationHNSCC
2017
Exome Sequencing of African-American Prostate Cancer Reveals Loss-of-Function ERF Mutations
Huang F, Mosquera J, Garofalo A, Oh C, Baco M, Amin-Mansour A, Rabasha B, Bahl S, Mullane S, Robinson B, Aldubayan S, Khani F, Karir B, Kim E, Chimene-Weiss J, Hofree M, Romanel A, Osborne J, Kim J, Azabdaftari G, Woloszynska-Read A, Sfanos K, De Marzo A, Demichelis F, Gabriel S, Van Allen E, Mesirov J, Tamayo P, Rubin M, Powell I, Garraway L. Exome Sequencing of African-American Prostate Cancer Reveals Loss-of-Function ERF Mutations. Cancer Discovery 2017, 7: 973-983. PMID: 28515055, PMCID: PMC5836784, DOI: 10.1158/2159-8290.cd-16-0960.Peer-Reviewed Original ResearchConceptsProstate cancerRecurrent loss-of-function mutationsSystematic genome sequencingCastration-resistant prostate cancerLethal castration-resistant prostate cancerProstate cancer tumor suppressor geneCancer sequencing studiesCancer genome characterizationLoss-of-function mutationsIncreased anchorage-independent growthPrimary prostate cancerAfrican American menProstate cancer cohortAnchorage-independent growthTumor suppressor geneProstate cancer genesGene expression signaturesTranscriptional repressorGenomic characterizationSequencing studiesExome sequencingCancer genesAndrogen signalingGene mutationsCancer cohortCRISPR/Cas9 mutagenesis invalidates a putative cancer dependency targeted in on-going clinical trials
Lin A, Giuliano C, Sayles N, Sheltzer J. CRISPR/Cas9 mutagenesis invalidates a putative cancer dependency targeted in on-going clinical trials. ELife 2017, 6: e24179. PMID: 28337968, PMCID: PMC5365317, DOI: 10.7554/elife.24179.Peer-Reviewed Original ResearchConceptsMaternal embryonic leucine zipper kinaseClinical trialsCancer cell linesBasal breast cancer cell linesCancer typesCell linesNovel chemotherapy agentsTriple-negative subtypeCurrent clinical trialsBreast cancer cell linesEmbryonic leucine zipper kinaseLeucine zipper kinaseMELK knockdownBreast cancerChemotherapy agentsPreclinical resultsSmall molecule inhibitorsAnchorage-independent growthMELK inhibitorTarget mechanismsPreclinical target validationTrialsDoubling timeTarget validationInhibitors
2015
Cis-eQTL analysis and functional validation of candidate susceptibility genes for high-grade serous ovarian cancer
Lawrenson K, Li Q, Kar S, Seo JH, Tyrer J, Spindler TJ, Lee J, Chen Y, Karst A, Drapkin R, Aben KK, Anton-Culver H, Antonenkova N, Baker H, Bandera E, Bean Y, Beckmann M, Berchuck A, Bisogna M, Bjorge L, Bogdanova N, Brinton L, Brooks-Wilson A, Bruinsma F, Butzow R, Campbell I, Carty K, Chang-Claude J, Chenevix-Trench G, Chen A, Chen Z, Cook L, Cramer D, Cunningham J, Cybulski C, Dansonka-Mieszkowska A, Dennis J, Dicks E, Doherty J, Dörk T, du Bois A, Dürst M, Eccles D, Easton D, Edwards R, Eilber U, Ekici A, Fasching P, Fridley B, Gao Y, Gentry-Maharaj A, Giles G, Glasspool R, Goode E, Goodman M, Grownwald J, Harrington P, Harter P, Hasmad H, Hein A, Heitz F, Hildebrandt M, Hillemanns P, Hogdall E, Hogdall C, Hosono S, Iversen E, Jakubowska A, James P, Jensen A, Ji B, Karlan B, Kruger Kjaer S, Kelemen L, Kellar M, Kelley J, Kiemeney L, Krakstad C, Kupryjanczyk J, Lambrechts D, Lambrechts S, Le N, Lee A, Lele S, Leminen A, Lester J, Levine D, Liang D, Lissowska J, Lu K, Lubinski J, Lundvall L, Massuger L, Matsuo K, McGuire V, McLaughlin J, Nevanlinna H, McNeish I, Menon U, Modugno F, Moysich K, Narod S, Nedergaard L, Ness R, Azmi M, Odunsi K, Olson S, Orlow I, Orsulic S, Weber R, Pearce C, Pejovic T, Pelttari L, Permuth-Wey J, Phelan C, Pike M, Poole E, Ramus S, Risch H, Rosen B, Rossing M, Rothstein J, Rudolph A, Runnebaum I, Rzepecka I, Salvesen H, Schildkraut J, Schwaab I, Sellers T, Shu X, Shvetsov Y, Siddiqui N, Sieh W, Song H, Southey M, Sucheston L, Tangen I, Teo S, Terry K, Thompson P, Timorek A, Tsai Y, Tworoger S, van Altena A, Van Nieuwenhuysen E, Vergote I, Vierkant R, Wang-Gohrke S, Walsh C, Wentzensen N, Whittemore A, Wicklund K, Wilkens L, Woo Y, Wu X, Wu A, Yang H, Zheng W, Ziogas A, Monteiro A, Pharoah P, Gayther S, Freedman M. Cis-eQTL analysis and functional validation of candidate susceptibility genes for high-grade serous ovarian cancer. Nature Communications 2015, 6: 8234. PMID: 26391404, PMCID: PMC4580986, DOI: 10.1038/ncomms9234.Peer-Reviewed Original ResearchMeSH KeywordsCarcinoma, Ovarian EpithelialCell Line, TumorFemaleGene Expression Regulation, NeoplasticGenetic Association StudiesGenetic Predisposition to DiseaseHomeodomain ProteinsHumansNeoplasm ProteinsNeoplasms, Glandular and EpithelialNuchal CordOvarian NeoplasmsProtein BindingQuantitative Trait LociConceptsCandidate susceptibility genesExpression quantitative trait loci (eQTL) analysisQuantitative trait locus (QTL) analysisChromosome conformation captureGenome-wide association studiesSusceptibility genesCis-eQTL analysisHigh-grade serous epithelial ovarian cancerAnchorage-independent growthConformation captureHOXD9 promoterTranscriptomic profilingCausal variantsFunctional validationRisk lociLocus analysisAssociation studiesBroader roleFunctional roleGenesContact inhibitionRisk variantsPopulation-doubling timePrecursor cellsHOXD9The p53R172H Mutant Does Not Enhance Hepatocellular Carcinoma Development and Progression
Ahronian L, Driscoll D, Klimstra D, Lewis B. The p53R172H Mutant Does Not Enhance Hepatocellular Carcinoma Development and Progression. PLOS ONE 2015, 10: e0123816. PMID: 25885474, PMCID: PMC4401698, DOI: 10.1371/journal.pone.0123816.Peer-Reviewed Original ResearchConceptsAnchorage-independent growthMutant-expressing cellsHCC cell linesP53 mutantsKnockdown of mutant p53Cell linesP53-null counterpartsCell migrationFrequency of p53 mutationsP53-null cellsP73 target genesTA isoforms of p63Analysis of cell linesP53 family membersP53 tumor suppressor geneTumor-free survivalHCC mouse modelHCC cellsIncreased tumor incidenceShRNA-mediated knockdownTumor suppressor geneGain-of-function mutationsDecreased cell migrationHepatocellular carcinoma developmentIsoforms of p63
2014
Reversal of Anchorage-Independent Multicellular Spheroid into a Monolayer Mimics a Metastatic Model
Kunjithapatham R, Karthikeyan S, Geschwind JF, Kieserman E, Lin M, Fu DX, Ganapathy-Kanniappan S. Reversal of Anchorage-Independent Multicellular Spheroid into a Monolayer Mimics a Metastatic Model. Scientific Reports 2014, 4: 6816. PMID: 25351825, PMCID: PMC4212233, DOI: 10.1038/srep06816.Peer-Reviewed Original ResearchConceptsMetastatic phenotypeAnchorage-independent growthMolecular regulationMulticellular spheroidsStem cell markersMolecular eventsCancer stem cell markersVitro modelModel of metastasisMetastatic processSpecific therapeutic targetsTherapeutic targetAntimetastatic agentPhenotypeMetastatic modelRegulationVivo dataExpressionChemoresistanceInvasivenessSpheroidsMajor impedimentInductionMimicsGrowthPhosphorylation of ETS1 by Src Family Kinases Prevents Its Recognition by the COP1 Tumor Suppressor
Lu G, Zhang Q, Huang Y, Song J, Tomaino R, Ehrenberger T, Lim E, Liu W, Bronson RT, Bowden M, Brock J, Krop IE, Dillon DA, Gygi SP, Mills GB, Richardson AL, Signoretti S, Yaffe MB, Kaelin WG. Phosphorylation of ETS1 by Src Family Kinases Prevents Its Recognition by the COP1 Tumor Suppressor. Cancer Cell 2014, 26: 222-234. PMID: 25117710, PMCID: PMC4169234, DOI: 10.1016/j.ccr.2014.06.026.Peer-Reviewed Original ResearchMeSH KeywordsAmino Acid SequenceAnimalsBinding SitesFemaleHCT116 CellsHEK293 CellsHumansMiceMice, Inbred NODMice, SCIDMolecular Sequence DataNeoplasm TransplantationPhosphorylationProtein BindingProto-Oncogene Protein c-ets-1Proto-Oncogene Protein c-ets-2src-Family KinasesTriple Negative Breast NeoplasmsTumor BurdenUbiquitin-Protein LigasesUbiquitinationConceptsSrc family kinasesFamily kinasesTumor suppressorPhosphorylation of ETS1Ubiquitin ligase componentTumor suppressor proteinAnchorage-independent growthNeighboring tyrosine residueCOP1 substratesRegulatory phosphorylationSpecific serineThreonine residuesSrc familySuppressor proteinTyrosine residuesETS1Breast cancer cellsPhosphorylationCancer cellsNeoplastic growthKinaseSuppressorProteinOncoproteinResidues
2009
RalA-Exocyst Complex Regulates Integrin-Dependent Membrane Raft Exocytosis and Growth Signaling
Balasubramanian N, Meier JA, Scott DW, Norambuena A, White MA, Schwartz MA. RalA-Exocyst Complex Regulates Integrin-Dependent Membrane Raft Exocytosis and Growth Signaling. Current Biology 2009, 20: 75-79. PMID: 20005108, PMCID: PMC2822103, DOI: 10.1016/j.cub.2009.11.016.Peer-Reviewed Original ResearchConceptsPlasma membraneRecycling endosomesGrowth signalingActivation of Arf6Small GTPase RalACaveolin-dependent internalizationLipid raft microdomainsAnchorage-independent growthEffects of integrinsExocyst complexActive RalARaft microdomainsMembrane raftsRaft markersIntegrin signalingPancreatic cancer cellsRalAAnchorage dependenceAnchorage independenceCell growthSignalingCell detachmentCancer cellsEndosomesExocytosis
2008
Suppressor role of activating transcription factor 2 (ATF2) in skin cancer
Bhoumik A, Fichtman B, DeRossi C, Breitwieser W, Kluger HM, Davis S, Subtil A, Meltzer P, Krajewski S, Jones N, Ronai Z. Suppressor role of activating transcription factor 2 (ATF2) in skin cancer. Proceedings Of The National Academy Of Sciences Of The United States Of America 2008, 105: 1674-1679. PMID: 18227516, PMCID: PMC2234203, DOI: 10.1073/pnas.0706057105.Peer-Reviewed Original ResearchMeSH Keywords9,10-Dimethyl-1,2-benzanthraceneActivating Transcription Factor 2AnimalsApoptosisbeta CateninCarcinogensCell ProliferationCyclin D1DNAEpidermisKeratinocytesMiceMice, KnockoutPapillomaPresenilin-1Proto-Oncogene Proteins c-mybReceptor, Notch1Skin NeoplasmsTetradecanoylphorbol AcetateTissue Array AnalysisTumor Suppressor ProteinsConceptsSkin tumor formationTranscription factor 2Two-stage skin carcinogenesis protocolTumor formationBasal cell carcinomaSkin carcinogenesis protocolFactor 2K14-Cre miceCell carcinomaCarcinogenesis protocolMouse modelBeta-catenin expressionPapilloma developmentSkin cancerExhibit reduced expressionAnchorage-independent growthNormal skinNotch1 expressionCyclin D1MiceReduced expressionSuppressor roleSuppressor activitySelective expressionBasal layer
2000
Loss of p19 ARF Eliminates the Requirement for the pRB-Binding Motif in Simian Virus 40 Large T Antigen-Mediated Transformation
Chao H, Buchmann A, DeCaprio J. Loss of p19 ARF Eliminates the Requirement for the pRB-Binding Motif in Simian Virus 40 Large T Antigen-Mediated Transformation. Molecular And Cellular Biology 2000, 20: 7624-7633. PMID: 11003658, PMCID: PMC86324, DOI: 10.1128/mcb.20.20.7624-7633.2000.Peer-Reviewed Original ResearchMeSH KeywordsAmino Acid MotifsAnimalsAntigens, Viral, TumorBlotting, WesternCarrier ProteinsCell CountCell Cycle ProteinsCell DivisionCell Line, TransformedCell Transformation, NeoplasticContact InhibitionCyclin-Dependent Kinase Inhibitor p16DNA-Binding ProteinsE2F Transcription FactorsFibroblastsGene DeletionGene Expression Regulation, NeoplasticGenes, ReporterMicePromoter Regions, GeneticProtein BindingProteinsRetinoblastoma ProteinRetinoblastoma-Binding Protein 1Transcription Factor DP1Transcription FactorsTumor Suppressor Protein p14ARFTumor Suppressor Protein p53ConceptsMouse embryo fibroblastsLXCXE motifP53-binding domainJ-domainT antigenCellular transformationSequence-specific transcription factorsWild-type T antigenRetinoblastoma protein familyN-terminal 70 residuesHsp40/DnaJPRB family membersSimian virus 40 large T antigenAbility of p53Anchorage-independent growthLarge T antigenProtein familySignificant homologyTranscription factorsTerminal domainPRB-bindingPRb familyMutant derivativesMutant formsTumor suppressor
1998
Cell surface density of p185(c-erbB-2) determines susceptibility to anti-p185(c-erbB-2)-ricin A chain (RTA) immunotoxin therapy alone and in combination with anti-p170(EGFR)-RTA in ovarian cancer cells.
Dean G, Pusztai L, Xu F, O'Briant K, DeSombre K, Conaway M, Boyer C, Mendelsohn J, Bast R. Cell surface density of p185(c-erbB-2) determines susceptibility to anti-p185(c-erbB-2)-ricin A chain (RTA) immunotoxin therapy alone and in combination with anti-p170(EGFR)-RTA in ovarian cancer cells. Clinical Cancer Research 1998, 4: 2545-50. PMID: 9796989.Peer-Reviewed Original ResearchConceptsOvarian cancer cellsReceptors/cellCancer cellsC-erbBSynergistic cytotoxicityCopies/cellTumor cellsSKOV3 human ovarian cancer cellsHuman ovarian cancer cellsClonogenic tumor cellsCell surface densityBreast cancerRTA immunotoxinsNude miceSame immunotoxinFirst treatmentAnchorage-independent growthAnchorage-dependent growthVivo growthClonogenic cellsImmunotoxinExpression levelsSignificant correlationCell linesNormal cells
1997
Growth factor activation of MAP kinase requires cell adhesion
Renshaw M, Ren X, Schwartz M. Growth factor activation of MAP kinase requires cell adhesion. The EMBO Journal 1997, 16: 5592-5599. PMID: 9312018, PMCID: PMC1170191, DOI: 10.1093/emboj/16.18.5592.Peer-Reviewed Original ResearchMeSH Keywords3T3 CellsAnimalsCalcium-Calmodulin-Dependent Protein KinasesCell AdhesionCell Transformation, NeoplasticEnzyme ActivationExtracellular Matrix ProteinsGenes, rasKineticsMAP Kinase Kinase Kinase 1MiceMitogen-Activated Protein Kinase 1Platelet-Derived Growth FactorProtein Serine-Threonine KinasesProto-Oncogene Proteins c-rafProto-OncogenesConceptsCell adhesionGrowth factor-regulated pathwaysMAP kinase ERK2Mutants of RasActivation of ERK2MAP kinase pathwayRas-transformed cellsGrowth factor activationExtracellular matrix proteinsSoluble growth factorsAnchorage-independent growthKinase ERK2Growth factorMAP kinaseOncogenic growthEndogenous RasKinase pathwayOncogenic activationMEK activityMatrix proteinsMajor regulatorERK2Factor activationRafMEKRecognition of activated CSF-1 receptor in breast carcinomas by a tyrosine 723 phosphospecific antibody
Flick M, Sapi E, Perrotta P, Maher M, Halaban R, Carter D, Kacinski B. Recognition of activated CSF-1 receptor in breast carcinomas by a tyrosine 723 phosphospecific antibody. Oncogene 1997, 14: 2553-2561. PMID: 9191055, DOI: 10.1038/sj.onc.1201092.Peer-Reviewed Original ResearchMeSH KeywordsAmino Acid SequenceAnimalsAntibodiesAntibody SpecificityBreast NeoplasmsCarcinoma in SituCells, CulturedCross ReactionsEpitopesFibroblastsGenes, fmsHumansImmunohistochemistryMacrophagesMiceMice, Inbred BALB CPhosphopeptidesPhosphorylationPhosphotyrosineProto-Oncogene MasReceptor, Macrophage Colony-Stimulating FactorTumor Cells, CulturedConceptsCSF-1RMultiple signal transduction pathwaysC-fms proto-oncogenePhosphorylation state-specific antibodiesSignal transduction pathwaysCSF-1 receptorAnchorage-independent growthImmunoblots of lysatesActivation/phosphorylationEffector proteinsVivo phosphorylationCytoplasmic domainDifferentiation of macrophagesPhosphospecific antibodiesTransduction pathwaysCellular phenotypesInvasive human breast tumoursSpecific phosphopeptidesC-fms oncogeneCSF-1Proto-oncogeneHuman breast carcinomaFirst direct evidenceNormal proliferationFactor receptor
1990
Cytoplasmic pH and anchorage-independent growth induced by v-Ki-ras, v-src or polyoma middle T.
Schwartz M, Rupp E, Frangioni J, Lechene C. Cytoplasmic pH and anchorage-independent growth induced by v-Ki-ras, v-src or polyoma middle T. Oncogene 1990, 5: 55-8. PMID: 2181378.Peer-Reviewed Original ResearchConceptsAnchorage-independent growthNormal cellsCytoplasmic pHPolyoma middle T oncogeneRas-transformed cellsCell linesExtracellular matrix proteinsMiddle T oncogeneV-SrcSrc oncogeneTissue culture plasticMatrix proteinsCellular requirementsCell growthControl growthOncogeneV-KiAlkaline pHiSeries of cellsCulture plasticGrowth factorCellsGrowthRAMutants
1989
Open reading frames E6 and E7 of bovine papillomavirus type 1 are both required for full transformation of mouse C127 cells
Neary K, DiMaio D. Open reading frames E6 and E7 of bovine papillomavirus type 1 are both required for full transformation of mouse C127 cells. Journal Of Virology 1989, 63: 259-266. PMID: 2535732, PMCID: PMC247680, DOI: 10.1128/jvi.63.1.259-266.1989.Peer-Reviewed Original ResearchConceptsBovine papillomavirus type 1Open reading frames E6Mouse C127 cellsFull-length viral genomesAnchorage-independent growthPapillomavirus type 1Focus-forming activityC127 cellsORF E6First methionine codonViral genomeColony formationRetrovirus long terminal repeatsSeries of mutationsE6/E7Second ATG codonLong terminal repeatBPV1 genomeMethionine codonATG codonNumber plasmidE5 geneSpecific proteinsSimultaneous disruptionE6 protein
1986
Differential Responsiveness of myc- and ras-Transfected Cells to Growth Factors: Selective Stimulation of myc-Transfected Cells by Epidermal Growth Factor
Stern D, Roberts A, Roche N, Sporn M, Weinberg R. Differential Responsiveness of myc- and ras-Transfected Cells to Growth Factors: Selective Stimulation of myc-Transfected Cells by Epidermal Growth Factor. Molecular And Cellular Biology 1986, 6: 870-877. DOI: 10.1128/mcb.6.3.870-877.1986.Peer-Reviewed Original ResearchEpidermal growth factorSoft agarPlatelet-derived growth factorRas oncogeneEGF-like factorsMyc-like genesControl cellsAnchorage-independent growthPresence of epidermal growth factorPresence of platelet-derived growth factorCells to growth factorsTGF-betaRas-transfected cellsGrowth factorExogenous growth factorsResponse of cellsMYCAgarTransforming growth factor-betaOncogeneGrowth factor-betaRasDifferential responseCellsColoniesDifferential responsiveness of myc- and ras-transfected cells to growth factors: selective stimulation of myc-transfected cells by epidermal growth factor.
Stern DF, Roberts AB, Roche NS, Sporn MB, Weinberg RA. Differential responsiveness of myc- and ras-transfected cells to growth factors: selective stimulation of myc-transfected cells by epidermal growth factor. Molecular And Cellular Biology 1986, 6: 870-877. PMID: 3022135, PMCID: PMC367587, DOI: 10.1128/mcb.6.3.870.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntigens, Polyomavirus TransformingAntigens, Viral, TumorCell DivisionCell Transformation, NeoplasticCells, CulturedEpidermal Growth FactorGenesGenes, ViralGrowth SubstancesOncogene Proteins, ViralOncogenesPeptidesPlatelet-Derived Growth FactorPolyomavirusRatsRats, Inbred F344TransfectionTransforming Growth FactorsConceptsEpidermal growth factorPlatelet-derived growth factorExogenous growth factorsSoft agarRas oncogeneGrowth factorEGF-like factorsPresence of PDGFControl cellsAnchorage-independent growthMyc-transfected cellsRas-transfected cellsPresence of EGFLike genesMYCResponsiveness of cellsGrowth factor productionOncogeneAutocrine stimulationNumerous coloniesTGF betaLack of responsivenessGenesSelective stimulationStimulatory effect
1985
Down-modulation of an oncogene protein product and reversion of the transformed phenotype by monoclonal antibodies
Drebin J, Link V, Stern D, Weinberg R, Greene M. Down-modulation of an oncogene protein product and reversion of the transformed phenotype by monoclonal antibodies. Cell 1985, 41: 695-706. PMID: 2860972, DOI: 10.1016/s0092-8674(85)80050-7.Peer-Reviewed Original ResearchConceptsNIH 3T3 cellsAnchorage-independent growthAnti-p185 monoclonal antibodiesColony formationSoft agar colony formationAgar colony formationOncogene protein productGene productsNontransformed phenotypeProtein productsAntibody treatmentRas oncogeneDNA transfectionMonoclonal antibodiesNeu gene productSoft agarOncogenePhenotypeCellsP185P185 levelsNeuroblastoma linesUnrelated specificityControl antibodyNeu oncogeneType beta transforming growth factor: a bifunctional regulator of cellular growth.
Roberts AB, Anzano MA, Wakefield LM, Roche NS, Stern DF, Sporn MB. Type beta transforming growth factor: a bifunctional regulator of cellular growth. Proceedings Of The National Academy Of Sciences Of The United States Of America 1985, 82: 119-123. PMID: 3871521, PMCID: PMC396983, DOI: 10.1073/pnas.82.1.119.Peer-Reviewed Original ResearchConceptsGrowth factorEpidermal growth factorColony formationAnchorage-independent growthNRK fibroblastsType betaPlatelet-derived growth factorHuman lung carcinoma cellsLung carcinoma cellsBreast carcinoma cell linesCarcinoma cell linesCellular myc geneLung carcinomaHuman tumor cellsHuman melanomaAnchorage-dependent growthHuman placentaTumor cellsCarcinoma cellsCell cycle timeHuman plateletsCell linesSoft agarTwo-chain polypeptideBifunctional regulator
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