In one paragraphArticle in Cells, 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
What 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
19 authors.
María LabradorDepartment of Molecular Biotechnology and Health Sciences, University of Turin, 10126 Turin, Italy.ORCID 0000-0001-8934-7235 Sara CozzubboDepartment of Molecular Biotechnology and Health Sciences, University of Turin, 10126 Turin, Italy.
Mariangela PorroDepartment of Molecular Biotechnology and Health Sciences, University of Turin, 10126 Turin, Italy.ORCID 0009-0001-5131-4750 Michela CumerlatoDepartment of Molecular Biotechnology and Health Sciences, University of Turin, 10126 Turin, Italy.
Cecilia BandiniDepartment of Molecular Biotechnology and Health Sciences, University of Turin, 10126 Turin, Italy.
Elisabetta MereuDepartment of Molecular Biotechnology and Health Sciences, University of Turin, 10126 Turin, Italy.
Benedetta DonatiLaboratory of Translational Research, Azienda USL-IRCCS di Reggio Emilia, 42122 Reggio Emilia, Italy.ORCID 0000-0002-9163-8194 Veronica ManicardiLaboratory of Translational Research, Azienda USL-IRCCS di Reggio Emilia, 42122 Reggio Emilia, Italy.ORCID 0000-0003-2490-7283 Domenica RonchettiDepartment of Oncology and Hemato-Oncology, University of Milan, 20122 Milan, Italy.ORCID 0000-0002-4824-3445 Mattia D'AgostinoDepartment of Molecular Biotechnology and Health Sciences, University of Turin, 10126 Turin, Italy.ORCID 0000-0002-1711-6996 Alessandra LaroccaDepartment of Molecular Biotechnology and Health Sciences, University of Turin, 10126 Turin, Italy.
Francesca GayDepartment of Molecular Biotechnology and Health Sciences, University of Turin, 10126 Turin, Italy.ORCID 0000-0002-8619-412X Benedetto BrunoDepartment of Molecular Biotechnology and Health Sciences, University of Turin, 10126 Turin, Italy.ORCID 0000-0002-7299-6770 Alessia CiarrocchiLaboratory of Translational Research, Azienda USL-IRCCS di Reggio Emilia, 42122 Reggio Emilia, Italy.ORCID 0000-0002-5541-2075 Andrew Chatr-AryamontriChemoGenix CRISPR Screening Platform, Institute for Research in Immunology and Cancer, Université de Montréal, Montreal, QC H3T 1J4, Canada.ORCID 0000-0002-1589-9982 Antonino NeriDepartment of Oncology and Hemato-Oncology, University of Milan, 20122 Milan, Italy.
Roberto PivaDepartment of Molecular Biotechnology and Health Sciences, University of Turin, 10126 Turin, Italy.ORCID 0000-0002-2273-3470 Funding
Italian Association for Cancer Research Investigator Grant-21585University of Torino RILO 2022-2025
6 · The paper itselfAbstract
Proteasome inhibitors (PIs) are central to multiple myeloma (MM) therapy; however, resistance remains a major clinical challenge, particularly in relapsed/refractory disease. To identify functional mediators of carfilzomib (CFZ) resistance, we performed complementary gain-of-function CRISPR activation and pharmacological screening approaches. These unbiased strategies converged on the E3 ubiquitin ligase MDM2 as a modulator of PI response. MDM2 transactivation enhanced MM cell survival and accelerated recovery following CFZ exposure, supporting a causal role in proteotoxic stress tolerance. Pharmacologic inhibition of MDM2 with NVP-CGM097 synergized with CFZ across multiple PI-sensitive and PI-resistant MM cell lines, irrespective of
Indexed as
Drug Resistance, NeoplasmMultiple MyelomaProteasome InhibitorsProto-Oncogene Proteins c-mdm2Tumor Suppressor Protein p53Cell Cycle CheckpointsCell Line, TumorHumansOligopeptidescarfilzomibMDM2 protein, humanOligopeptidesProteasome InhibitorsProto-Oncogene Proteins c-mdm2TP53 protein, humanTumor Suppressor Protein p53drug resistanceMDM2multiple myelomaproteasome inhibitorssynthetic lethalityTP53
Identifiers
PMID42121932
PMCPMC13162650
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