Evidence map›Paper›PMID 41865105›Full record

ArticleScientific reports2026

Single-nucleus ATAC-seq analysis resolves chromatin and transcriptional features of fibrolamellar carcinoma.

Alaa R Farghli, Marc S Sherman, Bo Shui, Andreas Stephanou, Brian J Pepe-Mooney, Colton J Smith, Donald Long, Paul R Munn, Adrian McNairn, Jennifer K Grenier and 4 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Scientific reports, 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 it

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 registry

The 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 literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

14 authors.

Alaa R FarghliDepartment of Biomedical and Translational Sciences, College of Veterinary Medicine, Cornell University, Ithaca, NY, USA.
Marc S ShermanDivision of Genetics, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA.
Bo ShuiDepartment of Biomedical and Translational Sciences, College of Veterinary Medicine, Cornell University, Ithaca, NY, USA.
Andreas StephanouDepartment of Biomedical and Translational Sciences, College of Veterinary Medicine, Cornell University, Ithaca, NY, USA.
Brian J Pepe-MooneyDivision of Genetics, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA.
Colton J SmithDivision of Genetics, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA.
Donald LongDepartment of Biomedical and Translational Sciences, College of Veterinary Medicine, Cornell University, Ithaca, NY, USA.
Paul R MunnGenomics Innovation Hub, Institute of Biotechnology, Cornell University, Ithaca, NY, USA.
Adrian McNairnGenomics Innovation Hub, Institute of Biotechnology, Cornell University, Ithaca, NY, USA.
Jennifer K GrenierGenomics Innovation Hub, Institute of Biotechnology, Cornell University, Ithaca, NY, USA.
Michael KarskiGenomics Innovation Hub, Institute of Biotechnology, Cornell University, Ithaca, NY, USA.
Wolfram GoesslingDivision of Genetics, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA.
Khashayar VakiliDepartment of Surgery, Boston Children's Hospital, Boston, MA, USA. Khashayar.Vakili@childrens.harvard.edu.
Praveen SethupathyDepartment of Biomedical and Translational Sciences, College of Veterinary Medicine, Cornell University, Ithaca, NY, USA. pr46@cornell.edu.

Funding

Dysregulation of the unfolded protein response in the pathogenesis of non-alcoholic steatohepatitisK08DK139370 · NIDDK · MASSACHUSETTS GENERAL HOSPITAL · PI MARC S SHERMAN · 2025 to 2026
$342k
NIDDK NIH HHS K08 DK139370
6 · The paper itself

Abstract

Fibrolamellar carcinoma (FLC) is a rare malignancy disproportionately affecting adolescents and young adults with no curative therapy. FLC is characterized by thick stroma, which has long suggested an important role of the tumor microenvironment. Over the past decade, several studies have revealed aberrant chromatin activity and gene expression in FLC. However, an important limitation of these efforts is that they were conducted on bulk tumor samples. Consequently, the cell types that contribute to the different epigenomic and transcriptional features of FLC have remained unknown. In this study we primarily leverage single nucleus ATAC-seq, along with supporting single nucleus RNA-seq, to unveil cell-type specific signal for chromatin activity, microRNAs, transcription factor networks (such as CREB3L1), and super enhancers including those nearby to notable FLC-enriched genes such as CDH11 and SLC16A14. The results provide a high resolution map of chromatin features of FLC, which in turn affords the opportunity to study cell type specific transcriptional reprogramming in the FLC tumor microenvironment.

Indexed as

Cell NucleusChromatinLiver NeoplasmsTranscription, GeneticCarcinoma, HepatocellularChromatin Immunoprecipitation SequencingGene Expression Regulation, NeoplasticHumansMicroRNAsSuper EnhancersTumor MicroenvironmentChromatinMicroRNAs

Identifiers

PMID41865105
PMCPMC13144680

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.