2010
A Variant in a MicroRNA complementary site in the 3′ UTR of the KIT oncogene increases risk of acral melanoma
Godshalk SE, Paranjape T, Nallur S, Speed W, Chan E, Molinaro AM, Bacchiocchi A, Hoyt K, Tworkoski K, Stern DF, Sznol M, Ariyan S, Lazova R, Halaban R, Kidd KK, Weidhaas JB, Slack FJ. A Variant in a MicroRNA complementary site in the 3′ UTR of the KIT oncogene increases risk of acral melanoma. Oncogene 2010, 30: 1542-1550. PMID: 21119596, PMCID: PMC3069149, DOI: 10.1038/onc.2010.536.Peer-Reviewed Original ResearchConceptsMessenger RNAsComplementary sitesNovel genetic markersKIT oncogeneTarget genesRegulatory relationshipsUntranslated regionGenetic markersHeritable riskFunctional variantsGenetic variantsOncogeneMultifaceted roleProtein levelsProtein expressionVariant resultsComplementary sequencesReporter dataUTRMelanoma pathogenesisMiR-221KIT variantsSeed regionExpressionVariants
1999
Melanoma Cell Autonomous Growth: The Rb/E2F Pathway
Halaban R. Melanoma Cell Autonomous Growth: The Rb/E2F Pathway. Cancer And Metastasis Reviews 1999, 18: 333-343. PMID: 10721488, DOI: 10.1023/a:1006396104073.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCarrier ProteinsCell CycleCell Cycle ProteinsCell DivisionCyclin-Dependent KinasesDNA-Binding ProteinsE2F Transcription FactorsHumansMelanocytesMelanomaPhosphorylationRetinoblastoma ProteinRetinoblastoma-Binding Protein 1Signal TransductionTranscription Factor DP1Transcription FactorsConceptsPocket proteinsExternal growth factorsNormal melanocytesE2F activityTarget genesRb/E2F pathwayE2F transcription factorsCell surface receptor stimulationMelanoma cellsCell-autonomous growthTumor suppressor proteinClass of enzymesCyclin-dependent kinasesInactivation of pRbConstitutive high expressionGrowth factorCell cycle progressionSurface receptor stimulationMetastatic melanoma cellsRetinoblastoma familySuppressive complexE2F pathwayPositive regulatorTranscription factorsMouse melanocytes
1998
Release of cell cycle constraints in mouse melanocytes by overexpressed mutant E2F1E132, but not by deletion of p16INK4A or p21WAF1/CIP1
Halaban R, Cheng E, Zhang Y, Mandigo C, Miglarese M. Release of cell cycle constraints in mouse melanocytes by overexpressed mutant E2F1E132, but not by deletion of p16INK4A or p21WAF1/CIP1. Oncogene 1998, 16: 2489-2501. PMID: 9627115, DOI: 10.1038/sj.onc.1201773.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCarrier ProteinsCell CycleCell Cycle ProteinsCell SurvivalCyclin-Dependent Kinase Inhibitor p16Cyclin-Dependent Kinase Inhibitor p21CyclinsDNA-Binding ProteinsE2F Transcription FactorsE2F1 Transcription FactorGene Expression RegulationHumansMelanocytesMiceMice, NudeMutagenesisProtein BiosynthesisRecombinant Fusion ProteinsRetinoblastoma ProteinRetinoblastoma-Binding Protein 1Tetradecanoylphorbol AcetateTranscription Factor DP1Transcription FactorsConceptsP21WAF1/CIP1Cell cycle progressionMouse melanocytesTarget genesCycle progressionRetinoblastoma tumor suppressor proteinE2F-mediated transactivationCell cycle constraintsTumor suppressor proteinRole of E2F1Deletion of p16INK4AFree E2FExpression of RbGene disruptionSuppressor proteinEctopic expressionHallmark of melanomaTetradecanoyl phorbol 13Loss of p16INK4aConstitutive expressionMelanoma cell linesCell deathNormal melanocytesIndependent growthMelanocyte growthMelanomas, from the cell cycle point of view (Review).
Halaban R, Miglarese M, Smicun Y, Puig S. Melanomas, from the cell cycle point of view (Review). International Journal Of Molecular Medicine 1998, 1: 419-25. PMID: 9852245, DOI: 10.3892/ijmm.1.2.419.Peer-Reviewed Original ResearchConceptsRetinoblastoma tumor suppressor proteinTransformation of melanocytesTumor suppressor proteinCyclin-dependent kinase inhibitorCell cycle progressionDependent kinase inhibitorCell cycle pointMetastatic melanoma cellsCDK regulatorsCDK activitySuppressor proteinTarget genesGenetic lossCycle progressionRb phosphorylationUnrestricted proliferationAutocrine growth factorReduced expressionKinase inhibitorsMelanoma cellsGrowth factorAberrant productionExpressionE2FCKI