Evidence map›Paper›PMID 42465925›Full record

ArticlemedRxiv : the preprint server for health sciences2026

A Single-cell Atlas of Juvenile Nasopharyngeal Angiofibroma Reveals VEGF-Driven Angiogenic Remodeling as a Therapeutic Vulnerability.

Heidi Martini-Stoica, Brittany T Rupp, Meik Kunz, Alessandra Livraghi-Butrico, Kenichi Okuda, Wanda K O'Neal, Scott H Randell, Hong Dang, Hiroaki Murano, Minako Furusho and 9 more

Abstract readPreprint
PubMed Full text at PMC Publisher
In one paragraph

Article in medRxiv : the preprint server for health sciences, 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

19 authors.

Heidi Martini-StoicaDepartment of Otolaryngology-Head and Neck Surgery, University of North Carolina School of Medicine, Chapel Hill, NC, USA.ORCID 0000-0003-1599-9905
Brittany T RuppDepartment of Oral and Craniofacial Molecular Biology, Virginia Commonwealth University, Richmond VA., USA.
Meik KunzThe Bioinformatics CRO, Sanford, FL, USA.
Alessandra Livraghi-ButricoMarsico Lung Institute, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA.
Kenichi OkudaMarsico Lung Institute, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA.
Wanda K O'NealMarsico Lung Institute, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA.
Scott H RandellMarsico Lung Institute, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA.
Hong DangMarsico Lung Institute, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA.
Hiroaki MuranoMarsico Lung Institute, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA.
Minako FurushoMarsico Lung Institute, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA.
Lisa MortonMarsico Lung Institute, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA.
Frederic AskinDepartment of Pathology and Laboratory Medicine, University of North Carolina School of Medicine, Chapel Hill, NC, USA.
Brian D ThorpDepartment of Otolaryngology-Head and Neck Surgery, University of North Carolina School of Medicine, Chapel Hill, NC, USA.
Cristine Klatt-CromwellDepartment of Otolaryngology-Head and Neck Surgery, University of North Carolina School of Medicine, Chapel Hill, NC, USA.
Charles S EbertDepartment of Otolaryngology-Head and Neck Surgery, University of North Carolina School of Medicine, Chapel Hill, NC, USA.
Brent A SeniorDepartment of Otolaryngology-Head and Neck Surgery, University of North Carolina School of Medicine, Chapel Hill, NC, USA.
Jackson R VuncannonDepartment of Otolaryngology-Head and Neck Surgery, University of North Carolina School of Medicine, Chapel Hill, NC, USA.
Adam J KimpleDepartment of Otolaryngology-Head and Neck Surgery, University of North Carolina School of Medicine, Chapel Hill, NC, USA.
Kevin M ByrdDepartment of Oral and Craniofacial Molecular Biology, Virginia Commonwealth University, Richmond VA., USA.

Funding

Virus Vector Shared ResourceP30CA016059 · NCI · VIRGINIA COMMONWEALTH UNIVERSITY · PI Renato Martins · 1985 to 2026
$51.0M
NCI NIH HHS P30 CA016059
6 · The paper itself

Abstract

Background: Juvenile nasopharyngeal angiofibroma (JNA) is a rare locally aggressive vascular sinonasal tumor that primarily affects adolescent males. Despite advances in endoscopic surgery and preoperative embolization, JNA can be associated with major operative bleeding risk and clinically meaningful recurrence, while non-surgical treatment options remain limited. Methods: To define the cellular programs underlying JNA vascularity, we performed single-cell RNA sequencing of JNA tumors (n=2), tumor-adjacent mucosa, and control sinonasal tissue. We analyzed cell composition, differential gene expression, pathway enrichment, and cell-cell communication, followed by Drug2cell-based mapping of transcriptional states to candidate therapeutic targets. Results: JNA contained an expanded fibrovascular compartment composed of endothelial cells, fibroblasts, pericytes, vascular smooth muscle cells, and neural crest-like cells. Neural crest- like cells were enriched in JNA but showed relatively limited transcriptional differences from tumor-adjacent tissue. By contrast, endothelial cells demonstrated the strongest disease-associated remodeling, with enrichment of angiogenesis, extracellular matrix organization, hypoxia response, and cell migration pathways. Endothelial cells also showed downregulation of adaptive immune signaling pathways, suggesting reduced immune engagement within the tumor microenvironment. Intercellular communication analyses revealed dense endothelial-stromal signaling across the JNA fibrovascular network. Drug2cell analysis nominated VEGF/VEGFR signaling as a candidate therapeutic vulnerability, with VEGFR-targeting agents predicted to act primarily on vascular and lymphatic endothelial populations. Conclusions: JNA is organized around an angiogenesis-dominant fibrovascular program driven by endothelial-centered signaling. These data support further investigation of VEGF/VEGFR-directed therapy as a potential adjunctive strategy for patients with recurrent, unresectable, or surgically high-risk JNA.

Indexed as

AngiogenesisBiomarkersCell-cell communicationJuvenile nasopharyngeal angiofibromaSingle-cell transcriptomicsTumor microenvironment

Identifiers

PMID42465925
PMCPMC13370528

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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Registered trials

None linked

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.