2024
ASCL1 Drives Tolerance to Osimertinib in EGFR Mutant Lung Cancer in Permissive Cellular Contexts.
Hu B, Wiesehöfer M, de Miguel F, Liu Z, Chan L, Choi J, Melnick M, Arnal Estape A, Walther Z, Zhao D, Lopez-Giraldez F, Wurtz A, Cai G, Fan R, Gettinger S, Xiao A, Yan Q, Homer R, Nguyen D, Politi K. ASCL1 Drives Tolerance to Osimertinib in EGFR Mutant Lung Cancer in Permissive Cellular Contexts. Cancer Research 2024, 84: 1303-1319. PMID: 38359163, DOI: 10.1158/0008-5472.can-23-0438.Peer-Reviewed Original ResearchTyrosine kinase inhibitorsPatient-derived xenograftsEGFR mutant lung cancerMutant lung cancerPre-treatment tumorsResidual diseaseDrug toleranceLung cancerResidual tumor cells in vivoEGFR mutant lung adenocarcinomaTyrosine kinase inhibitor osimertinibEGFR tyrosine kinase inhibitorsTyrosine kinase inhibitor treatmentTumor cells in vivoMutant lung adenocarcinomaMaximal tumor regressionTranscription factor Ascl1Drug-tolerant cellsTime of maximal responseEvidence of cellsCells in vivoOsimertinib treatmentTumor regressionSingle cell transcriptional profilingTumor cells
2019
The Ulp2 SUMO protease promotes transcription elongation through regulation of histone sumoylation
Ryu H, Su D, Wilson‐Eisele N, Zhao D, López‐Giráldez F, Hochstrasser M. The Ulp2 SUMO protease promotes transcription elongation through regulation of histone sumoylation. The EMBO Journal 2019, 38: embj2019102003. PMID: 31313851, PMCID: PMC6694223, DOI: 10.15252/embj.2019102003.Peer-Reviewed Original ResearchConceptsSmall ubiquitin-like modifierRNA polymerase IIC-terminal domainHistone sumoylationTranscription elongationActive genesSUMO proteaseRNAPII C-terminal domainChromatin regulatory mechanismsTranscriptional elongation defectsUbiquitin-like modifierCtk1 kinaseH2B ubiquitylationEukaryotic proteinsNucleosome associationElongation defectsPolySUMO chainsPolymerase IITranscript elongationCUP1 geneUlp2Saccharomyces cerevisiaeRegulatory mechanismsImpaired associationSerine 2
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