{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Belenki D"],"funding":["Bundesministerium für Bildung und Forschung (Federal Ministry of Education and Research)","Bundesministerium für Bildung und Forschung","Deutsche Forschungsgemeinschaft","Deutsche Forschungsgemeinschaft (German Research Foundation)","Bundesministerium für Gesundheit","Deutsche Krebshilfe","Bundesministerium für Gesundheit (Federal Ministry of Health, Germany)","Deutsche Krebshilfe (German Cancer Aid)"],"pagination":["3079"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11955568"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["16(1)"],"pubmed_abstract":["Cellular senescence is a stress-inducible state switch relevant in aging, tumorigenesis and cancer therapy. Beyond a lasting arrest, senescent cells are characterized by profound chromatin remodeling and transcriptional reprogramming. We show here myeloid-skewed aberrant lineage plasticity and its immunological ramifications in therapy-induced senescence (TIS) of primary human and murine B-cell lymphoma. We find myeloid transcription factor (TF) networks, specifically AP-1-, C/EBPβ- and PU.1-governed transcriptional programs, enriched in TIS but not in equally chemotherapy-exposed senescence-incapable cancer cells. Dependent on these master TF, TIS lymphoma cells adopt a lineage-promiscuous state with properties of monocytic-dendritic cell (DC) differentiation. TIS lymphoma cells are prefe"],"journal":["Nature communications"],"pubmed_title":["Senescence-associated lineage-aberrant plasticity evokes T-cell-mediated tumor control."],"pmcid":["PMC11955568"],"funding_grant_id":["e:Med program project SeneSys: 031L0189A","European Union ERA PerMed, HiRisk-HiGain","GO 2688/1 1","SCHM 1633/9-2","7011377629","SCHM 1633/11-1"],"pubmed_authors":["Lee S","Kandler G","Scharnagl E","Reimann M","Dorr JR","Brzezicha B","Shao Z","Pardon K","Schonlein M","Wolf J","Bischof O","Yu Y","Belenki D","Nabuco Leva Ferreira de Freitas JA","Hick TP","Chapuy B","Schmitt CA","Milanovic M","Leser U","Scheidereit C","Bhattacharya A","Fan DNY","Bittner A","Kase J","Du J","Richter-Pechanska P","Lau A","Cai X","Thiessen N"],"additional_accession":[]},"is_claimable":false,"name":"Senescence-associated lineage-aberrant plasticity evokes T-cell-mediated tumor control.","description":"Cellular senescence is a stress-inducible state switch relevant in aging, tumorigenesis and cancer therapy. Beyond a lasting arrest, senescent cells are characterized by profound chromatin remodeling and transcriptional reprogramming. We show here myeloid-skewed aberrant lineage plasticity and its immunological ramifications in therapy-induced senescence (TIS) of primary human and murine B-cell lymphoma. We find myeloid transcription factor (TF) networks, specifically AP-1-, C/EBPβ- and PU.1-governed transcriptional programs, enriched in TIS but not in equally chemotherapy-exposed senescence-incapable cancer cells. Dependent on these master TF, TIS lymphoma cells adopt a lineage-promiscuous state with properties of monocytic-dendritic cell (DC) differentiation. TIS lymphoma cells are prefe","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 Mar","modification":"2026-06-01T07:44:10.44Z","creation":"2026-04-08T10:29:46.775Z"},"accession":"S-EPMC11955568","cross_references":{"pubmed":["40159497"],"doi":["10.1038/s41467-025-57429-x"]}}