ArticleThyroid research2025
Discriminating epigenetic landscapes: multi-omics characterization of benign thyroid nodules versus papillary thyroid carcinomas.
Article in Thyroid research, 2025. 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
6 authors.
Funding
Abstract
backgroundDiscriminating the epigenetic landscapes of coincidental benign thyroid nodules (particularly follicular adenoma subtypes) from papillary thyroid carcinoma (PTC) remains a critical unresolved challenge, impeding mechanistic insights into their divergent pathogenic trajectories.
methodsTo address this knowledge gap, we performed integrative multi-omics profiling of histologically paired benign thyroid nodules and PTC lesions from the same patients, synergizing chromatin accessibility mapping (ATAC-seq), whole-exome sequencing, transcriptomics, and ATAC-seq-derived extrachromosomal circular DNA (eccDNA) detection.
resultsThree pivotal mechanisms emerged from our cross-omics analyses to delineate the benign-malignant dichotomy. First, chromatin architecture interrogation revealed spatially colocalized PTC-specific accessible regions with somatic mutation hotspots, suggesting coordinated interplay between epigenetic remodeling and genomic instability in malignant transformation. Second, we uncovered ARHGEF28 and ARHGEF24 as novel potential benign-specific master regulators, where TEAD4-binding motif enrichment in benign-hyperaccessible chromatin drives their coordinated overexpression, forming a self-reinforcing regulatory loop unique to benign thyroid nodules. Third, eccDNA-centric profiling delineated a different regulatory paradigm: benign thyroid noduless exhibited preferential enrichment of T-cell signaling related elements on eccDNA scaffolds, whereas PTCs eccDNA were enriched in the DNA replication signaling pathways. This multidimensional atlas not only maps lineage-specific regulatory topologies of thyroid neoplasms but also establishes the ARHGEF28/24-TEAD4 axis as potential association with benign lineage.
conclusionsBy elucidating chromatin-based thresholds of malignant progression, our findings provide a molecular framework for differential diagnosis and mechanistic dissection of transformation checkpoints.
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.