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
2011
In Vivo Identification of Tumor- Suppressive PTEN ceRNAs in an Oncogenic BRAF-Induced Mouse Model of Melanoma
Karreth FA, Tay Y, Perna D, Ala U, Tan SM, Rust AG, DeNicola G, Webster KA, Weiss D, Perez-Mancera PA, Krauthammer M, Halaban R, Provero P, Adams DJ, Tuveson DA, Pandolfi PP. In Vivo Identification of Tumor- Suppressive PTEN ceRNAs in an Oncogenic BRAF-Induced Mouse Model of Melanoma. Cell 2011, 147: 382-395. PMID: 22000016, PMCID: PMC3236086, DOI: 10.1016/j.cell.2011.09.032.Peer-Reviewed Original ResearchConceptsMicroRNA recognition elementsLow PTEN levelsPTEN protein levelsZEB2 expressionBeauty insertional mutagenesisMicroRNA decoysPI3K/Akt pathwayLoss of PTENCeRNA activityInsertional mutagenesisZeb2 transcriptTumor suppressorCell transformationCeRNAsPTEN levelsAkt pathwayFunctional roleMRNA transcriptsSignificant enrichmentZEB2 mRNAProtein levelsMouse modelCeRNATranscriptsPTEN
2006
RB/E2F Regulation and Dual Activity in the Melanocytic System
Halaban R. RB/E2F Regulation and Dual Activity in the Melanocytic System. 2006, 223-245. DOI: 10.1007/978-1-59259-994-3_13.Peer-Reviewed Original ResearchE2F transcriptional activityE2F interactionTranscriptional activityRb/E2F pathwayChromatin modification activitiesCyclin-dependent kinase activityE2F-regulated genesRb-binding proteinCell cycle genesE2F complex formationMelanoma cellsCell cycle progressionCell surface receptorsGene repressionE2F regulationCycle genesE2F pathwayCDK activityApoptosis genesKinase activityB-RafCycle progressionTumor suppressorCDK inhibitorsN-ras
2005
Rb/E2F: A two-edged sword in the melanocytic system
Halaban R. Rb/E2F: A two-edged sword in the melanocytic system. Cancer And Metastasis Reviews 2005, 24: 339-356. PMID: 15986142, DOI: 10.1007/s10555-005-1582-z.Peer-Reviewed Original ResearchConceptsE2F transcriptional activityTranscriptional activityActivated cell surface receptorsRb/E2F pathwayRb-E2F interactionCyclin-dependent kinase activityCell cycle genesE2F complex formationMelanoma cellsCdk inhibitors p16INK4ACell cycle progressionDependent kinase activityExpression of E2FCell surface receptorsGene repressionCycle genesE2F pathwayCDK activityApoptosis genesKinase activityB-RafCycle progressionRb interactionPhosphorylated RbTumor suppressor
2002
Signal Transduction Abnormalities as Therapeutic Targets
Halaban R, von Willebrand M. Signal Transduction Abnormalities as Therapeutic Targets. Current Clinical Oncology 2002, 287-323. DOI: 10.1007/978-1-59259-159-6_11.Peer-Reviewed Original ResearchGrowth factor-mediated signalingNormal melanocytesChronic myelogenous leukemiaSignal transduction targetsSpecific kinase inhibitorsCell cycle regulatorsCell cycle progressionAutonomous cell proliferationEpidermal growth factor receptor familyEffective tumor suppressorSignal transduction abnormalitiesGrowth factor receptor familyMelanoma cellsTyrosine kinase receptorsFactor receptor familyReceptor kinaseEnvironmental cuesRegulatory proteinsActive Abl kinasesCycle regulatorsCycle progressionTumor suppressorAbl kinaseKinase receptorsOncogenic mutations