Evidence map›Paper›PMID 41323280›Full record

ArticleiScience2025

Epigenetic profiling reveals key super-enhancer networks driving oncogenesis in HPV-positive HNSCC.

Fernando T Zamuner, Spencer S Chan, Michael D Kessler, Ilya E Vorontsov, Andrey Loginov, Rossin Erbe, Eddie Imada, Deborah X Xie, Theresa Guo, Elana J Fertig and 4 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in iScience, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Review
  2. Article
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.

Fernando T ZamunerDepartment of Otolaryngology-Head and Neck Surgery, Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA.
Spencer S ChanCenter for Bioinformatics and Computational Biology, University of Maryland, College Park, MD 20910, USA.
Michael D KesslerInstitute for Genome Sciences, University of Maryland School of Medicine, Baltimore, MD 21201, USA.
Ilya E VorontsovVavilov Institute of General Genetics, Russian Academy of Sciences, Moscow 119991, Russia.
Andrey LoginovInstitute for Genome Sciences, University of Maryland School of Medicine, Baltimore, MD 21201, USA.
Rossin ErbeDepartment of Oncology, Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University, Baltimore, MD 21231, USA.
Eddie ImadaDepartment of Pathology and Laboratory Medicine, Weill Cornell Medicine, New York, NY 10065, USA.
Deborah X XieDepartment of Otolaryngology-Head and Neck Surgery, Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA.
Theresa GuoDepartment of Otolaryngology-Head and Neck Surgery, University of California, San Diego Health, La Jolla, San Diego, CA 92037, USA.
Elana J FertigSidney Kimmel Comprehensive Cancer Center, Johns Hopkins University School of Medicine, Baltimore, MD 21231, USA.
Ivan V KulakovskiyVavilov Institute of General Genetics, Russian Academy of Sciences, Moscow 119991, Russia.
Ludmila DanilovaSidney Kimmel Comprehensive Cancer Center, Johns Hopkins University School of Medicine, Baltimore, MD 21231, USA.
Alexander V FavorovVavilov Institute of General Genetics, Russian Academy of Sciences, Moscow 119991, Russia.
Daria A GaykalovaInstitute for Genome Sciences, University of Maryland School of Medicine, Baltimore, MD 21201, USA.

Funding

Comprehensive Analysis and Multi-Omics Data Integration for Cancer-Related StudiesR50CA243627 · NCI · JOHNS HOPKINS UNIVERSITY · PI Ludmila Danilova · 2019 to 2026
$975k
NCI NIH HHS R50 CA243627
6 · The paper itself

Abstract

Human papillomavirus-positive (HPV+) head and neck squamous cell carcinoma (HNSCC) is a growing subset of cancer cases distinct from HPV-negative by fewer genetic mutations and prevalent epigenetic dysregulation. We mapped H3K27ac-marked super-enhancers (SEs) via ChIP-seq in HPV+ patient-derived xenografts (PDXs) and normal oropharyngeal mucosa, identifying tumor-specific SE domains (T-SEDs) enriched for transcription factors (TFs) including TP63, FOSL1, and JUND. These SE-associated TFs regulate key oncogenic pathways and are downregulated by BRD4 inhibition with JQ1, highlighting sensitivity to epigenetic modulation. RNA-seq data revealed coordinated dysregulation of enhancer RNAs and mRNAs near T-SEDs, linked to upregulated pathways including epithelial-mesenchymal transition and E2F targets. JQ1 treatment significantly repressed these tumor-specific pathways, suggesting a therapeutic potential for targeting SE-driven transcription in HPV+ HNSCC. This study underscores the critical role of SEs in epigenetic and transcriptional dysregulation in HPV+ HNSCC, revealing therapeutic targets and providing a framework for future mechanistic studies in this area.

Indexed as

BioinformaticsCancerEpigeneticsMolecular network

Identifiers

PMID41323280
PMCPMC12664489

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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.