ArticlePloS one2026
Cell-cell junction gene signatures as subtype-specific prognostic biomarkers in breast cancer.
Article in PloS one, 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
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cell-cell junctions (CCJs) are essential for maintaining epithelial integrity, and adhesion-related molecules have long been implicated in breast cancer progression. However, the subtype-specific prognostic significance of CCJ-related gene expression patterns within individual intrinsic breast cancer subtypes has not been systematically characterized. We analyzed 179 genes annotated to the Gene Ontology term "cell-cell junction organization" (GO:0045216) across intrinsic breast cancer subtypes using the METABRIC and The Cancer Genome Atlas (TCGA) datasets. Subtype-specific prognostic CCJ genes were identified using multivariate Cox proportional hazards models for disease-specific survival and integrated into CCJ gene expression signatures. The prognostic performance was validated in an independent cohort (SCAN-B). Elevated CCJ signature scores were associated with poorer survival across subtypes, with particularly strong effects in Luminal B (LumB) and Basal-like (Basal) tumors. Person-year analyses indicated that high CCJ scores predicted an increased incidence of early recurrence (0-5 years) in these aggressive subtypes. Pathway enrichment analyses revealed that high-score tumors exhibited upregulation of extracellular matrix organization and matrisome-related pathways. Single-cell RNA sequencing further demonstrated that LumB CCJ genes (e.g., PARD6B, CDH3) were predominantly expressed in tumor epithelial cells, whereas the Basal CCJ signature reflected contributions from epithelial (e.g., MARVELD2) and endothelial (e.g., RAMP2) cells. Collectively, CCJ signatures stratify prognosis and capture subtype-specific cellular and microenvironmental features in breast cancer.
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.