ArticleNature communications2026
Oncogene inactivation-induced senescence facilitates tumor relapse.
Philipp Schmitt, Katrin Hönig, Maria Teresa Norcia, Marta F Nogueira, Viktoria Flore, Inés Simó Vesperinas, Maria Villoro-Agud, Lushan Peng, Zuhal Safyürek, Mehreen Tariq and 10 more
Abstract read
In one paragraphArticle in Nature communications, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from itWhat it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
2 · The registryThe trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
3 · Its place in the literatureWho cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
4 · The recordCorrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
5 · Who and what moneyAuthors and funding
20 authors.
Philipp SchmittMax-Delbrück Center for Molecular Medicine in the Helmholtz Association, Berlin, Germany.ORCID 0009-0008-1643-0079 Katrin HönigMax-Delbrück Center for Molecular Medicine in the Helmholtz Association, Berlin, Germany.
Maria Teresa NorciaMax-Delbrück Center for Molecular Medicine in the Helmholtz Association, Berlin, Germany.
Marta F NogueiraMax-Delbrück Center for Molecular Medicine in the Helmholtz Association, Berlin, Germany.
Viktoria FloreBerlin Institute of Health (BIH) at Charité Universitätsmedizin Berlin, Berlin, Germany.ORCID 0009-0001-3023-433X Inés Simó VesperinasBerlin Institute of Health (BIH) at Charité Universitätsmedizin Berlin, Berlin, Germany.
Maria Villoro-AgudMax-Delbrück Center for Molecular Medicine in the Helmholtz Association, Berlin, Germany.
Lushan PengMax-Delbrück Center for Molecular Medicine in the Helmholtz Association, Berlin, Germany.
Zuhal SafyürekMax-Delbrück Center for Molecular Medicine in the Helmholtz Association, Berlin, Germany.ORCID 0009-0004-8412-5069 Mehreen TariqMax-Delbrück Center for Molecular Medicine in the Helmholtz Association, Berlin, Germany.ORCID 0009-0003-5217-2226 Ana MilojkovicMax-Delbrück Center for Molecular Medicine in the Helmholtz Association, Berlin, Germany.
Kathleen AndersMax-Delbrück Center for Molecular Medicine in the Helmholtz Association, Berlin, Germany.
Evelin SchröckInstitute for Clinical Genetics, University Hospital Carl Gustav Carus at TUD Dresden University of Technology and Faculty of Medicine of TUD Dresden University of Technology, Dresden, Germany.
Sascha SauerMax-Delbrück Center for Molecular Medicine in the Helmholtz Association, Berlin, Germany.ORCID 0000-0002-4794-3693 Altuna AkalinMax-Delbrück Center for Molecular Medicine in the Helmholtz Association, Berlin, Germany.ORCID 0000-0002-0468-0117 Gerald WillimskyMax-Delbrück Center for Molecular Medicine in the Helmholtz Association, Berlin, Germany.ORCID 0000-0002-9693-948X Inmaculada Martínez-Reyes *Max-Delbrück Center for Molecular Medicine in the Helmholtz Association, Berlin, Germany. i.m.reyes@dkfz-heidelberg.de.ORCID 0000-0003-0479-1535 Thomas Blankenstein *Max-Delbrück Center for Molecular Medicine in the Helmholtz Association, Berlin, Germany. tblanke@mdc-berlin.de.ORCID 0000-0002-3357-4321 Funding
No grant is acknowledged in the PubMed record.
6 · The paper itselfAbstract
Oncogene-directed therapies can induce profound tumor regression in oncogene-addicted cancers, but their long-term benefit is often limited by resistance and relapse. Here we show that oncogene inactivation rapidly induces senescence and a pro-inflammatory senescence-associated secretory phenotype (SASP). In vivo, oncogene inactivation-induced senescence (OIIS) predisposes tumors to relapse, accompanied by polyploidy, chromosomal instability, acquisition of alternative oncogenic pathways including mouse double minute 2 homolog (Mdm2) upregulation, and tumor microenvironmental remodeling toward neovascularization and immunosuppression. Spectral flow cytometry reveals a shift from an immune-activated to an immunosuppressive milieu during relapse. OIIS features are also observed in human BRAF
Indexed as
Cellular SenescenceMelanomaNeoplasm Recurrence, LocalOncogenesAnimalsCell Line, TumorChromosomal InstabilityHumansMicePolyploidyProto-Oncogene Proteins B-rafProto-Oncogene Proteins c-mdm2Senescence-Associated Secretory PhenotypeTumor MicroenvironmentVemurafenibBRAF protein, humanProto-Oncogene Proteins B-rafProto-Oncogene Proteins c-mdm2Vemurafenib
Identifiers
PMID42457681
PMCPMC13373164
What OpenQuestion holds
Textmetadata
LicenceCC BY
Read underepoch 390