2022
Hormone therapies in meningioma-where are we?
Miyagishima D, Moliterno J, Claus E, Günel M. Hormone therapies in meningioma-where are we? Journal Of Neuro-Oncology 2022, 161: 297-308. PMID: 36418843, PMCID: PMC10371392, DOI: 10.1007/s11060-022-04187-1.Peer-Reviewed Original ResearchConceptsPositive receptor statusReceptor statusSomatostatin analoguesClinical trialsHormone-related risk factorsMajority of patientsNIH Clinical Trials DatabaseClinical trials databasesStratification of patientsHormone therapyTrials databasesFuture trialsHormonal agentsSpecific therapyRisk factorsSomatostatin receptorsInclusion criteriaMEDLINE-PubMedMeningioma growthMost meningiomasTherapeutic potentialMeningiomasPatientsTherapyTrialsInterferon-γ resistance and immune evasion in glioma develop via Notch-regulated co-evolution of malignant and immune cells
Parmigiani E, Ivanek R, Rolando C, Hafen K, Turchinovich G, Lehmann FM, Gerber A, Brkic S, Frank S, Meyer SC, Wakimoto H, Günel M, Louvi A, Mariani L, Finke D, Holländer G, Hutter G, Tussiwand R, Taylor V, Giachino C. Interferon-γ resistance and immune evasion in glioma develop via Notch-regulated co-evolution of malignant and immune cells. Developmental Cell 2022, 57: 1847-1865.e9. PMID: 35803280, DOI: 10.1016/j.devcel.2022.06.006.Peer-Reviewed Original ResearchConceptsTumor-associated microglia/macrophagesGlioma cellsImmune surveillanceMicroglia/macrophagesImmune cell populationsBrain tumor cellsMouse glioma cellsCytokine expressionImmune attackImmune cellsMouse modelImmune evasionSuppression of NotchTumor cellsNotch inhibitionTumor initiationUpregulation of oncogenesNotch activityCell populationsGliomasCellsSurveillanceLow Notch activityNiche controlTherapy
2017
Longitudinal analysis of treatment-induced genomic alterations in gliomas
Erson-Omay EZ, Henegariu O, Omay SB, Harmancı AS, Youngblood MW, Mishra-Gorur K, Li J, Özduman K, Carrión-Grant G, Clark VE, Çağlar C, Bakırcıoğlu M, Pamir MN, Tabar V, Vortmeyer AO, Bilguvar K, Yasuno K, DeAngelis LM, Baehring JM, Moliterno J, Günel M. Longitudinal analysis of treatment-induced genomic alterations in gliomas. Genome Medicine 2017, 9: 12. PMID: 28153049, PMCID: PMC5290635, DOI: 10.1186/s13073-017-0401-9.Peer-Reviewed Original ResearchMeSH KeywordsAntineoplastic AgentsChromosome AberrationsCombined Modality TherapyDisease ProgressionDNA Mismatch RepairDNA Mutational AnalysisDNA, NeoplasmExomeFemaleGeneral SurgeryGenome, HumanGenomicsGlioblastomaHumansImmunotherapyLongitudinal StudiesMiddle AgedMutationNeoplasm Recurrence, LocalPrecision MedicineRadiotherapyTreatment OutcomeConceptsWhole-exome sequencingMismatch repair deficiencyImmune checkpoint inhibitionMalignant brain tumorsMolecular changesLongitudinal analysisMedian survivalCheckpoint inhibitionSubsequent recurrenceMaximal resectionStandard treatmentBackgroundGlioblastoma multiformeBrain tumorsTumor-normal pairsFavorable responsePrimary GBMIndividual tumorsConclusionsOur studyPrecision therapyPersonalized treatmentGenomic profilingRepair deficiencyGenomic alterationsGenomic profilesTherapy
2015
Heparin is an activating ligand of the orphan receptor tyrosine kinase ALK
Murray PB, Lax I, Reshetnyak A, Ligon GF, Lillquist JS, Natoli EJ, Shi X, Folta-Stogniew E, Gunel M, Alvarado D, Schlessinger J. Heparin is an activating ligand of the orphan receptor tyrosine kinase ALK. Science Signaling 2015, 8: ra6. PMID: 25605972, DOI: 10.1126/scisignal.2005916.Peer-Reviewed Original ResearchConceptsAnaplastic lymphoma kinaseReceptor tyrosine kinasesActivation of RTKsCultured neuroblastoma cellsReceptor tyrosine kinase anaplastic lymphoma kinaseActivation of ALKStroma contributesLung adenocarcinomaLymphoma kinaseNervous systemExtracellular domainDrug resistanceNeuroblastoma cellsAberrant activationALK activityHeparinCancerPotential mechanismsGenetic amplificationActivationTyrosine kinaseAdenocarcinomaNeuroblastomaTherapyProgression