ArticleScientific reports2025
Single-cell transcriptomics reveals cellular evolution underlying pleomorphic adenoma recurrence and malignant transformation.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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
3 citing papers in PubMed.
- Patient-derived 3D organotypic co-cultures as a long-term ex vivo model for pleomorphic adenoma of the parotid gland.Scientific reports · 2026Article
- Vascular Endothelial Barrier in Salivary Glands: From Physiological Regulation to Pathological Impairment of Secretion.International journal of molecular sciences · 2026Review
- Deciphering novel targets in salivary gland pleomorphic adenoma by integrating plasma proteomics and parotid transcriptomics analyses.Journal of dental sciences · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
Abstract
Pleomorphic adenoma (PA), the most common benign salivary gland tumor, harbors unpredictable risks of recurrence and malignant transformation into carcinoma ex pleomorphic adenoma (CXPA), posing significant clinical challenges. To better delineate the tumor transformation trajectory, we performed single-cell RNA sequencing of normal salivary gland, primary PA, recurrent PA (rPA), and CXPA. Cell trajectory reconstruction, differential expression gene identification, and key gene network analysis were integrated to characterize molecular transitions and intercellular crosstalk driving PA recurrence and malignant transformation. Immunohistochemistry was used to validate key findings. GALNT13 + myoepithelial cells were identified as CXPA-specific malignant progenitors, delineating early malignant conversion. Concurrently, MIF + myoepithelial cells exhibited enhanced tissue-destructive capabilities. Fibroblasts enforced fibrotic restraint in primary PA and drove extracellular matrix degradation in CXPA. The tumor microenvironment exhibited stage-specific adaptations, with CXPA favoring pro-inflammatory MIF-CD74/CD44 signaling and rPA adopting immunosuppressive traits. Stromal reprogramming and immune-editing dynamics collectively orchestrated microenvironmental adaptation, linking cellular heterogeneity to clinical aggressiveness. This study provides the first comprehensive molecular atlas of PA-to-CXPA transformation, revealing malignant specialization of the myoepithelial subpopulation, fibroblast-mediated stromal reprogramming, and immune-editing driven microenvironmental adaptation. These findings provide a framework for precision stratification of the malignant potential of PA, while positioning microenvironmental intervention as a cornerstone of future clinical strategies.
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.