In one paragraphArticle in Science advances, 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
13 authors.
Emery Di CiccoCutaneous Biology Research Center, Department of Dermatology, Massachusetts General Hospital and Harvard Medical School, Charlestown, MA 02129, USA.ORCID 0000-0001-8507-1809 Jovan IsmaCutaneous Biology Research Center, Department of Dermatology, Massachusetts General Hospital and Harvard Medical School, Charlestown, MA 02129, USA.ORCID 0009-0008-8580-4169 Stefano SolCutaneous Biology Research Center, Department of Dermatology, Massachusetts General Hospital and Harvard Medical School, Charlestown, MA 02129, USA.ORCID 0000-0003-2576-0156 Gaetana RestivoDepartment of Dermatology, University Hospital Zurich, University of Zurich, Zurich, Switzerland.ORCID 0000-0003-4364-2364 Sandro GoruppiCutaneous Biology Research Center, Department of Dermatology, Massachusetts General Hospital and Harvard Medical School, Charlestown, MA 02129, USA.ORCID 0000-0002-2976-8983 Joni Renee WhiteCutaneous Biology Research Center, Department of Dermatology, Massachusetts General Hospital and Harvard Medical School, Charlestown, MA 02129, USA.ORCID 0000-0002-5428-960X Juerg HafnerDepartment of Dermatology, University Hospital Zurich, University of Zurich, Zurich, Switzerland.ORCID 0000-0002-4571-1143 Victor A NeelDepartment of Dermatology, Massachusetts General Hospital and Harvard Medical School, Boston, MA 02114, USA.
Anna MandinovaCutaneous Biology Research Center, Department of Dermatology, Massachusetts General Hospital and Harvard Medical School, Charlestown, MA 02129, USA.ORCID 0000-0001-9273-0972 Mitchell P LevesqueDepartment of Dermatology, University Hospital Zurich, University of Zurich, Zurich, Switzerland.
Gian Paolo DottoCutaneous Biology Research Center, Department of Dermatology, Massachusetts General Hospital and Harvard Medical School, Charlestown, MA 02129, USA.ORCID 0000-0002-1197-8448 Funding
GROWTH DIFFERENTIATION CONTROL IN PRIMARY KERATINOCYTES.R01AR039190 · NIAMS · YALE UNIVERSITY · PI DOTTO, GIAN-PAOLO · 1988 to 2021
$9.5MEpigenetic control of skin homeostasis by the ULK3 nuclear kinaseR01AR078374 · NIAMS · MASSACHUSETTS GENERAL HOSPITAL · PI DOTTO, GIAN-PAOLO · 2021 to 2025
$2.4MAndrogen receptor function in melanomaR01CA269356 · NCI · MASSACHUSETTS GENERAL HOSPITAL · PI DOTTO, GIAN-PAOLO · 2022 to 2025
$2.3MNCI NIH HHS R01 CA269356NIAMS NIH HHS R01 AR039190NIAMS NIH HHS R01 AR078374
6 · The paper itselfAbstract
The molecular mechanisms linking chromosome homeostasis to fibroblast reprogramming into cancer-associated fibroblasts (CAFs) remain poorly understood. Here, we identify a clinically relevant, telomere-associated nuclear pathway driving CAF activation across multiple human cancers. The long noncoding RNA TERRA is consistently elevated in CAFs from skin, lung, and breast tumors. We show that the androgen receptor (AR) represses TERRA transcription through subtelomeric binding, and its loss enables TERRA up-regulation and interaction with the RNA binding protein NONO. This interaction forms a CAF-specific nuclear complex that reprograms gene expression. Mechanistically, NONO is directly recruited to and binds the promoters of key CAF effector genes, where it regulates their transcription in a TERRA-dependent manner. Disrupting the TERRA-NONO axis, via TERRA silencing or pharmacologic NONO inhibition, reverses CAF activation and suppresses tumor-stroma interactions in vitro and in vivo, highlighting its therapeutic potential.
Indexed as
Cancer-Associated FibroblastsCellular ReprogrammingChromosomal Proteins, Non-HistoneDNA-Binding ProteinsNeoplasmsRNA-Binding ProteinsRNA, Long NoncodingAnimalsCell Line, TumorFibroblastsGene Expression Regulation, NeoplasticHumansReceptors, AndrogenChromosomal Proteins, Non-HistoneDNA-Binding ProteinsReceptors, AndrogenRNA-Binding ProteinsRNA, Long Noncoding
Identifiers
PMID42826195
PMCPMC13641401
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