ArticleFrontiers in endocrinology2026
Complex landscape of somatic copy number alterations in head and neck paragangliomas.
Article in Frontiers in endocrinology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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.
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.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Copy number alterations (CNAs) drive cancer by amplifying oncogenes and deleting tumor suppressor genes. Although CNA patterns are well-studied in common cancers, they remain poorly characterized in rare tumors. Methods: In this study, we employed an allele-specific copy number analysis using ASCAT on 25 head and neck paragangliomas (HNPGLs) with high tumor cell purity (≥70%) and available clinicopathologic and mutation data. Results: The majority of HNPGLs exhibited a near-diploid state. The recurrent somatic CNAs were predominantly hemizygous deletions, frequently affecting chromosomal regions 7q11, 1p36, 1p34, and 1p21.1-1p13.2, and involving key tumor suppressor genes associated with paragangliomas/pheochromocytomas (PPGLs), including Conclusion: Collectively, our study reveals a complex landscape of somatic CNAs in HNPGLs. The presence of recurrent alterations in hotspot genomic loci and PPGLs-associated genes suggests that genomic instability may be a significant contributing factor to tumor development and progression.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.