2024
DNAR-16. TARGETING APOBEC CYTIDINE DEAMINASES TO ENHANCE RADIOSENSITIVITY IN GLIOMA
Marin B, Gujar A, Kocakavuk E, Johnson K, Amin S, Verhaak R. DNAR-16. TARGETING APOBEC CYTIDINE DEAMINASES TO ENHANCE RADIOSENSITIVITY IN GLIOMA. Neuro-Oncology 2024, 26: viii120-viii121. PMCID: PMC11553289, DOI: 10.1093/neuonc/noae165.0467.Peer-Reviewed Original ResearchApolipoprotein B mRNA-editing enzyme catalytic polypeptide-likeRadiation therapyNon-homologous end joiningRecurrent gliomaDNA-dependent protein kinaseMutational signaturesRT-induced DNA damageMonitoring response to treatmentRadiosensitivity in vitroEnhanced radiosensitivity in vitroA3GPromote tumor evolutionResponse to treatmentAutophosphorylation of DNA-dependent protein kinaseAPOBEC mutational signaturesAdult brain tumorsPrimary adult brain tumorGlioma Longitudinal Analysis ConsortiumFamily of cytidine deaminasesRadiosensitizing gliomasAPOBEC3G (A3GNon-homologous end-joining pathwayPost-RTGlioma cell linesWhole-genome sequencing
2021
Radiotherapy is associated with a deletion signature that contributes to poor outcomes in patients with cancer
Kocakavuk E, Anderson K, Varn F, Johnson K, Amin S, Sulman E, Lolkema M, Barthel F, Verhaak R. Radiotherapy is associated with a deletion signature that contributes to poor outcomes in patients with cancer. Nature Genetics 2021, 53: 1088-1096. PMID: 34045764, PMCID: PMC8483261, DOI: 10.1038/s41588-021-00874-3.Peer-Reviewed Original ResearchConceptsWorse clinical outcomesNon-irradiated tumorsClinical outcomesRecurrent cancerPatient survivalPoor outcomeMetastatic tumorsRecurrent gliomaRadiation therapyRadiation-induced DNA damageDNA damageGlioma Longitudinal Analysis ConsortiumMutational signature analysisCancer treatmentDeletion burdenRadiotherapyMedical FoundationAPOBEC mutagenesisSignificant increaseTumorsCancerDNA damage repairDeletion signatureMutational spectrumSmall deletions
2018
Glioma through the looking GLASS: molecular evolution of diffuse gliomas and the Glioma Longitudinal Analysis Consortium
Aldape K, Amin SB, Ashley DM, Barnholtz-Sloan JS, Bates AJ, Beroukhim R, Bock C, Brat DJ, Claus EB, Costello JF, de Groot JF, Finocchiaro G, French PJ, Gan HK, Griffith B, Herold-Mende CC, Horbinski C, Iavarone A, Kalkanis SN, Karabatsou K, Kim H, Kouwenhoven MCM, McDonald KL, Miletic H, Nam DH, Ng HK, Niclou SP, Noushmehr H, Ormond D, Poisson LM, Reifenberger G, Roncaroli F, K J, Smitt P, Smits M, Souza CF, Tabatabai G, Van Meir EG, Verhaak RGW, Watts C, Wesseling P, Woehrer A, Yung WKA, Jungk C, Hau AC, van Dyck E, Westerman BA, Yin J, Abiola O, Zeps N, Grimmond S, Buckland M, Khasraw M, Sulman EP, Muscat AM, Stead L. Glioma through the looking GLASS: molecular evolution of diffuse gliomas and the Glioma Longitudinal Analysis Consortium. Neuro-Oncology 2018, 20: 873-884. PMID: 29432615, PMCID: PMC6280138, DOI: 10.1093/neuonc/noy020.Peer-Reviewed Original ResearchConceptsGlioma Longitudinal Analysis ConsortiumMolecular evolutionAnalysis ConsortiumEvolution of gliomasLethal phenotypeCancer Genome AtlasEpigenetic abnormalitiesTargetable vulnerabilitiesGenome AtlasSomatic alterationsDiverse groupCurrent knowledgeAdult diffuse gliomasComprehensive understandingDiffuse gliomasKnowledge gapsEssential insightsEvolutionMolecular subtypesConsortiumPhenotype