Featured Publications
Metabolism of cancer cells commonly responds to irradiation by a transient early mitochondrial shutdown
Krysztofiak A, Szymonowicz K, Hlouschek J, Xiang K, Waterkamp C, Larafa S, Goetting I, Vega-Rubin-de-Celis S, Theiss C, Matschke V, Hoffmann D, Jendrossek V, Matschke J. Metabolism of cancer cells commonly responds to irradiation by a transient early mitochondrial shutdown. IScience 2021, 24: 103366. PMID: 34825138, PMCID: PMC8603201, DOI: 10.1016/j.isci.2021.103366.Peer-Reviewed Original ResearchCommon metabolic responseCompensatory glycolysisDSB repair kineticsMitochondrial respiratory chainRepair kineticsRadiation-induced DNAFuture mechanistic studiesDNA repairDNA repair kineticsRespiratory chainCancer metabolismMitochondrial functionStress conditionsMetabolic vulnerabilitiesCancer cell linesMetabolic targetsCancer cellsCell linesMitochondrial recoveryGlycolysisNew hypothesisMetabolic responseMetabolismMechanistic studiesDiscoveryVulnerability of IDH1-Mutant Cancers to Histone Deacetylase Inhibition via Orthogonal Suppression of DNA Repair
Dow J, Krysztofiak A, Liu Y, Colon-Rios DA, Rogers FA, Glazer PM. Vulnerability of IDH1-Mutant Cancers to Histone Deacetylase Inhibition via Orthogonal Suppression of DNA Repair. Molecular Cancer Research 2021, 19: 2057-2067. PMID: 34535560, PMCID: PMC8642278, DOI: 10.1158/1541-7786.mcr-21-0456.Peer-Reviewed Original ResearchConceptsHistone deacetylase inhibitor vorinostatPatient-derived tumor xenograftsHomology-directed repairIsocitrate dehydrogenase 1/2 mutationsHistone deacetylase inhibitionIDH1 mutant cellsGreater cell deathHDACi treatmentInhibitor vorinostatTumor xenograftsDeacetylase inhibitionIDH1/2 mutationsPotential biomarkersSpecific cancersMutant cancersCancerCancer cellsDNA repair defectsMalignancyVorinostatDNA double-strand breaksGliomasHistone hypermethylationCell deathPARPi
2018
Restraining Akt1 Phosphorylation Attenuates the Repair of Radiation-Induced DNA Double-Strand Breaks and Reduces the Survival of Irradiated Cancer Cells
Szymonowicz K, Oeck S, Krysztofiak A, van der Linden J, Iliakis G, Jendrossek V. Restraining Akt1 Phosphorylation Attenuates the Repair of Radiation-Induced DNA Double-Strand Breaks and Reduces the Survival of Irradiated Cancer Cells. International Journal Of Molecular Sciences 2018, 19: 2233. PMID: 30065170, PMCID: PMC6121313, DOI: 10.3390/ijms19082233.Peer-Reviewed Original ResearchConceptsDSB repairLong-term colony formation assaysDNA double-strand break repairDouble-strand break repairKinase-protein kinase BPhosphorylation-deficient mutantKey phosphorylation sitesDNA damage responseEssential subcellular processesProtein kinase BDSB repair kineticsCancer cellsCellular radiation responseActivation stateMurine prostate cancer cellsColony formation assaysEffector proteinsGenotoxic stressPhosphorylation sitesDamage responseBreak repairGenetic approachesThreonine 308Serine 473Kinase B