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
2019
Longitudinal molecular trajectories of diffuse glioma in adults
Barthel FP, Johnson KC, Varn FS, Moskalik AD, Tanner G, Kocakavuk E, Anderson KJ, Abiola O, Aldape K, Alfaro KD, Alpar D, Amin SB, Ashley DM, Bandopadhayay P, Barnholtz-Sloan JS, Beroukhim R, Bock C, Brastianos PK, Brat DJ, Brodbelt AR, Bruns AF, Bulsara KR, Chakrabarty A, Chakravarti A, Chuang JH, Claus EB, Cochran EJ, Connelly J, Costello JF, Finocchiaro G, Fletcher MN, French PJ, Gan HK, Gilbert MR, Gould PV, Grimmer MR, Iavarone A, Ismail A, Jenkinson MD, Khasraw M, Kim H, Kouwenhoven MCM, LaViolette PS, Li M, Lichter P, Ligon KL, Lowman AK, Malta TM, Mazor T, McDonald KL, Molinaro AM, Nam DH, Nayyar N, Ng HK, Ngan CY, Niclou SP, Niers JM, Noushmehr H, Noorbakhsh J, Ormond DR, Park CK, Poisson LM, Rabadan R, Radlwimmer B, Rao G, Reifenberger G, Sa JK, Schuster M, Shaw BL, Short SC, Smitt PAS, Sloan AE, Smits M, Suzuki H, Tabatabai G, Van Meir EG, Watts C, Weller M, Wesseling P, Westerman BA, Widhalm G, Woehrer A, Yung WKA, Zadeh G, Huse JT, De Groot JF, Stead LF, Verhaak RGW. Longitudinal molecular trajectories of diffuse glioma in adults. Nature 2019, 576: 112-120. PMID: 31748746, PMCID: PMC6897368, DOI: 10.1038/s41586-019-1775-1.Peer-Reviewed Original ResearchConceptsAdult patientsDiffuse gliomasRecurrent gliomaOverall survivalPoor outcomeCurrent therapiesChromosome arms 1p/19qAcquired alterationsMajor subtypesTherapeutic resistanceGliomasGlioma developmentGene alterationsIDH mutationsGlioma subtypesPatientsHypermutator phenotypeDriver genesSubtypesClinical annotationSurvivalSubclonal selectionCell cycleAlterationsLittle evidence