ArticleDiscover oncology2025
Single-cell profiling of ERBB family receptors identifies ERBB3 as a key regulator in head and neck squamous cell carcinoma progression.
Article in Discover oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- Utilizing clinical features, genetic mutations, and a 14-gene molecular assay for optimizing the management of multiple primary lung cancer.Translational lung cancer research · 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
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The ERBB receptor family is widely implicated in epithelial malignancies, yet the functional and immunological significance of ERBB3 in head and neck squamous cell carcinoma (HNSCC) remains insufficiently characterized. In this study, we employed single-cell and bulk transcriptomic analyses to comprehensively map the expression patterns and prognostic value of ERBB family members in HNSCC, identifying ERBB3 as a tumor-specific marker predominantly enriched in malignant epithelial clusters. Notably, high ERBB3 expression was paradoxically associated with favorable overall survival, prompting further mechanistic investigation. Functional assays in SCC9 cells demonstrated that ERBB3 promotes proliferation, colony formation, and invasion. Immune profiling revealed that ERBB3-high tumors displayed enhanced communication with B cell subsets, particularly involving immunosuppressive signals such as TNFRSF13B and IL4R. Flow cytometry analysis in a 4NQO-induced mouse model showed that ERBB3 inhibition reduced CCDC50⁺ B cells while restoring MHC-II expression, indicating a shift toward immune activation. These findings highlight a dual role of ERBB3 in HNSCC, acting both as an oncogenic contributor and an immune-modulatory regulator, and position ERBB3 as a promising context-dependent therapeutic target.
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.